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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(Wnt1-cre)11Rth
transgene insertion 11, David H Rowitch
MGI:2386570
Summary 182 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Fgfr1tm5.1Sor/Fgfr1tm10.1Sor
Tg(Wnt1-cre)11Rth/0
129S4.Cg-Fgfr1tm5.1Sor Fgfr1tm10.1Sor Tg(Wnt1-cre)11Rth MGI:5882546
cn2
Fgfr1tm5.1Sor/Fgfr1tm9.1Sor
Tg(Wnt1-cre)11Rth/0
129S4.Cg-Fgfr1tm5.1Sor Fgfr1tm9.1Sor Tg(Wnt1-cre)11Rth MGI:5882544
cn3
Fgfr1tm5.1Sor/Fgfr1tm5.1Sor
Tg(Wnt1-cre)11Rth/0
129S4.Cg-Fgfr1tm5.1Sor Tg(Wnt1-cre)11Rth MGI:5882528
cn4
Ext1tm1Yama/Ext1tm1Yama
Tg(Wnt1-cre)11Rth/0
B6.Cg-Ext1tm1Yama Tg(Wnt1-cre)11Rth MGI:4360747
cn5
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sor+
Ptpn11tm1.1Rbns/Ptpn11tm1.1Rbns
Tg(Wnt1-cre)11Rth/0
B6.Cg-Ptpn11tm1.1Rbns Gt(ROSA)26Sortm1Sor Tg(Wnt1-cre)11Rth MGI:3852467
cn6
Ptpn11tm1.1Rbns/Ptpn11tm1.1Rbns
Tg(Wnt1-cre)11Rth/0
B6.Cg-Ptpn11tm1.1Rbns Tg(Wnt1-cre)11Rth MGI:3852466
cn7
Ext1tm1Yama/Ext1+
Tg(Wnt1-cre)11Rth/0
Tgfb2tm1Doe/Tgfb2+
B6.Cg-Tgfb2tm1Doe Ext1tm1Yama Tg(Wnt1-cre)11Rth MGI:4360749
cn8
Chd7Gt(XK403)Byg/Chd7+
Tg(Wnt1-cre)11Rth/0
either: (involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J * CBA/J) or (involves: 129P2/OlaHsd * C57BL/6J * CBA/J * CD-1) MGI:4410359
cn9
Gt(ROSA)26Sortm1(DTA)Jpmb/Gt(ROSA)26Sor+
Tg(Wnt1-cre)11Rth/0
either: (involves: 129S/SvEv * C57BL/6 * CBA) or (involves: 129S/SvEv * C57BL/6 * CBA * CD-1) MGI:3611573
cn10
Tbx1tm2.1Bem/Tbx1tm2.1Bem
Tg(Wnt1-cre)11Rth/0
either: (involves: 129/Sv * C57BL/6 * C57BL/6J * CBA/J * SJL) or (involves: 129/Sv * C57BL/6J * CBA/J * CD-1 * SJL) MGI:4410368
cn11
Lmo4tm1Sho/Lmo4tm1Sho
Tg(Wnt1-cre)11Rth/0
either: (involves: 129/Sv * CD-1) or (involves: 129/Sv * C57BL/6) MGI:3035941
cn12
Mrgprdtm1Mjz/?
Rettm1Ddg/Rettm1Ddg
Tg(Wnt1-cre)11Rth/0
involves: 129 * 129S1/Sv * C57BL/6 * C57BL/6J * CBA/J MGI:4413446
cn13
Mfn2tm1Dcc/Mfn2tm3Dcc
Tg(Wnt1-cre)11Rth/0
involves: 129 * 129S4/SvJaeSor * Black Swiss MGI:3779094
cn14
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sor+
Sox11tm2.1Weg/Sox11tm2.1Weg
Sox4tm1Vlf/Sox4tm1Vlf
Tg(Wnt1-cre)11Rth/0
involves: 129 * C57BL/6 * C57BL/6J * CBA/J MGI:5285375
cn15
Rettm1Ddg/Rettm1Ddg
Tg(Wnt1-cre)11Rth/0
involves: 129 * C57BL/6 * C57BL/6J * CBA/J MGI:4413445
cn16
Hdac2tm1.1Eno/Hdac2tm1.1Eno
Tg(Wnt1-cre)11Rth/?
involves: 129 * C57BL/6 * CBA MGI:3851919
cn17
Hdac1tm1.1Eno/Hdac1tm1.1Eno
Tg(Wnt1-cre)11Rth/?
involves: 129 * C57BL/6 * CBA MGI:3851918
cn18
Hdac8tm1.1Eno/Y
Tg(Wnt1-cre)11Rth/0
involves: 129 * C57BL/6 * CBA * CD-1 MGI:3851920
cn19
Ctnnb1tm2Kem/Ctnnb1tm2Kem
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sor+
Tg(Wnt1-cre)11Rth/0
involves: 129 * C57BL/6 * CBA/J MGI:5308958
cn20
Dicer1tm1Bdh/Dicer1tm1Bdh
Tg(Wnt1-cre)11Rth/0
involves: 129 * C57BL/6 * CBA/J MGI:4868120
cn21
Dicer1tm1Bdh/Dicer1+
Tg(Wnt1-cre)11Rth/0
involves: 129 * C57BL/6 * CBA/J MGI:4868201
cn22
Ctnnb1tm2Kem/Ctnnb1tm3Kba
Tg(Wnt1-cre)11Rth/0
involves: 129 * C57BL/6 * CBA/J MGI:5308953
cn23
Ctnnb1tm2Kem/Ctnnb1tm2Kem
Tg(Wnt1-cre)11Rth/0
involves: 129 * C57BL/6 * CBA/J MGI:5308955
cn24
Ctnnb1tm2Kem/Ctnnb1tm3Kba
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sor+
Tg(Wnt1-cre)11Rth/0
involves: 129 * C57BL/6 * CBA/J MGI:5308956
cn25
Cited2tm1Bha/Cited2tm2Bha
Tg(Wnt1-cre)11Rth/0
involves: 129 * C57BL/6 * CBA * SJL MGI:3804086
cn26
Hs2st1tm1.1Je/Hs2st1tm1.1Je
Hs6st1tm1Wvc/Hs6st1tm1Wvc
Hs6st2tm1Lex/Hs6st2tm1Lex
Tg(Wnt1-cre)11Rth/0
involves: 129 * C57BL/6J * CBA/J MGI:5430387
cn27
Mapttm2Arbr/?
Runx1tm3Spe/Runx1tm3Spe
Tg(Wnt1-cre)11Rth/?
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6J * CBA/J MGI:5702481
cn28
Fgfr1tm5.1Sor/Fgfr1tm10.1Sor
Stat3tm2Aki/Stat3tm2Aki
Tg(Wnt1-cre)11Rth/0
involves: 129P2/OlaHsd * 129S4/SvJaeSor MGI:5882547
cn29
Stat3tm2Aki/Stat3tm2Aki
Tg(Wnt1-cre)11Rth/0
involves: 129P2/OlaHsd * 129S4/SvJaeSor MGI:5882548
cn30
Cbfbtm2.1Ddg/Cbfbtm2.1Ddg
Mapttm2Arbr/?
Tg(Wnt1-cre)11Rth/?
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6J * CBA/J MGI:5702479
cn31
Pbx1tm1Koss/Pbx1tm1Koss
Pbx2tm1Mlc/Pbx2+
Tg(Wnt1-cre)11Rth/0
involves: 129P2/OlaHsd * 129S/Sv * C57BL/6J * CBA/J MGI:5305927
cn32
Nrg1tm4Cbm/Nrg1tm4.1Cbm
Tg(Wnt1-cre)11Rth/0
involves: 129P2/OlaHsd * BALB/cJ * C57BL/6J * CBA/J MGI:5524256
cn33
Ptpn11tm1.1Wbm/Ptpn11tm1.1Wbm
Tg(Wnt1-cre)11Rth/0
involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J * SJL * SJL/J MGI:4365544
cn34
Pkd1tm3Jzh/Pkd1tm3Jzh
Tg(Wnt1-cre)11Rth/?
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:3811608
cn35
Gja1tm1Kwi/Gja1tm1Kwi
Tg(Wnt1-cre)11Rth/0
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:3653215
cn36
Mkl2Gt(RRJ478)Byg/Mkl2Gt(RRJ478)Byg
Tg(Wnt1-cre)11Rth/0
involves: 129P2/OlaHsd * C57BL/6J * CBA/J MGI:3697616
cn37
Braftm1Wds/Braftm1Wds
Raf1tm2Bacc/Raf1tm2Bacc
Tg(Wnt1-cre)11Rth/0
involves: 129P2/OlaHsd * C57BL/6J * CBA/J MGI:5659950
cn38
Hic2Gt(E225A08)1.1Wrst/Hic2Gt(E225A08)1.1Wrst
Tg(Wnt1-cre)11Rth/?
involves: 129P2/OlaHsd * C57BL/6J * CBA/J MGI:5707466
cn39
Gt(ROSA)26Sortm2(DTA)Riet/Gt(ROSA)26Sor+
Tg(Wnt1-cre)11Rth/0
involves: 129P2/OlaHsd * C57BL/6J * CBA/J MGI:4438212
cn40
Pitx2tm1.1Sac/Pitx2tm2Sac
Tg(Wnt1-cre)11Rth/?
Gt(ROSA)26Sortm1Sor/?
involves: 129S1/Sv * 129S4/SvJaeSor * 129X1/SvJ * C57BL/6 * CBA MGI:5298219
cn41
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sor+
HhatTg(TFAP2A-cre)1Will/HhatTg(TFAP2A-cre)1Will
Tg(Wnt1-cre)11Rth/0
involves: 129S1/Sv * 129S4/SvJaeSor * 129X1/SvJ * C57BL/6 * CBA MGI:5447985
cn42
Fgf15tm1Sms/Fgf15tm1Sms
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sor+
Tg(Wnt1-cre)11Rth/0
involves: 129S1/Sv * 129S4/SvJaeSor * 129X1/SvJ * C57BL/6 * CBA MGI:3639491
cn43
Ednrbtm1Nrd/Ednrbtm1Nrd
Gt(ROSA)26Sortm14(CAG-tdTomato)Hze/Gt(ROSA)26Sor+
Tg(Wnt1-cre)11Rth/0
involves: 129S1/Sv * 129S6/SvEvTac * 129X1/SvJ * C57BL/6 * CBA/J MGI:5896991
cn44
Ctnnb1tm2Kem/Ctnnb1tm2.1Kem
Gt(ROSA)26Sortm1(Ctnnb1)Kem/Gt(ROSA)26Sor+
Tg(Wnt1-cre)11Rth/0
involves: 129S1/Sv * 129S6/SvEvTac * 129X1/SvJ * C57BL/6J * CBA/J MGI:5440183
cn45
Ctnnb1tm2Kem/Ctnnb1tm2.1Kem
Gt(ROSA)26Sortm1(Ctnnb1)Kem/Gt(ROSA)26Sortm1(Ctnnb1)Kem
Tg(Wnt1-cre)11Rth/0
involves: 129S1/Sv * 129S6/SvEvTac * 129X1/SvJ * C57BL/6J * CBA/J MGI:5440182
cn46
Hand2tm1Cse/Hand2tm1Dsr
Tg(Wnt1-cre)11Rth/0
involves: 129S1/Sv * 129S7/SvEvBrd * C57BL/6 * CBA MGI:3848967
cn47
Hand2tm1Cse/Hand2tm1Cse
Tg(Wnt1-cre)11Rth/0
involves: 129S1/Sv * 129S7/SvEvBrd * C57BL/6 * CBA MGI:3715254
cn48
Mapk1tm1Gela/Mapk1tm1Gela
Tg(Wnt1-cre)11Rth/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * C57BL/6J * CBA/J MGI:5902457
cn49
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sor+
Isl1tm2Sev/Isl1tm2Sev
Tg(Wnt1-cre)11Rth/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA MGI:3817490
cn50
Pygo2tm1.1Ssp/Pygo2tm1.2Ssp
Tg(Wnt1-cre)11Rth/?
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA MGI:3711498
cn51
Tgfbr2tm1Karl/Tgfbr2tm1Karl
Tg(Wnt1-cre)11Rth/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA MGI:3623411
cn52
Fgfr1tm1Jpa/Fgfr1tm1Jpa
Tg(Wnt1-cre)11Rth/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA MGI:3702775
cn53
Gata6tm2Msp/Gata6tm2Msp
Tg(Wnt1-cre)11Rth/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA MGI:3623951
cn54
Acvr1tm1Vk/Acvr1tm1.1Vk
Tg(Wnt1-cre)11Rth/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA MGI:3697607
cn55
Gt(ROSA)26Sortm2(Pax3)Joe/Gt(ROSA)26Sor+
Tg(Wnt1-cre)11Rth/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA MGI:3804321
cn56
Gt(ROSA)26Sortm2(Pax3)Joe/Gt(ROSA)26Sortm2(Pax3)Joe
Tg(Wnt1-cre)11Rth/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA MGI:3804318
cn57
Nf1tm1Par/Nf1tm1Par
Tg(Wnt1-cre)11Rth/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA MGI:3710237
cn58
Pygo2tm1.1Ssp/Pygo2tm1.2Ssp
Tg(Pax6-cre,GFP)1Pgr/?
Tg(Wnt1-cre)11Rth/?
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA * FVB MGI:3711516
cn59
Fgfr1tm1Jpa/Fgfr1tm1.1Jpa
Tg(Wnt1-cre)11Rth/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA * ICR MGI:3703447
cn60
Fgfr1tm2Jrt/Fgfr1tm2Jrt
Tg(Wnt1-cre)11Rth/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA * ICR MGI:3703441
cn61
Fgfr1tm1Jpa/Fgfr1tm1Jpa
Tg(Wnt1-cre)11Rth/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA * ICR MGI:3703442
cn62
Ednrbtm1Nrd/Ednrbtm1Nrd
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Tg(Wnt1-cre)11Rth/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA/J MGI:3814191
cn63
Mapk1tm1Gela/Mapk1tm1Gela
Mapk3tm1Gela/Mapk3tm1Gela
Tg(Wnt1-cre)11Rth/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * CBA/J MGI:5660197
cn64
Pax3tm2Joe/Pax3tm2Joe
Tg(Wnt1-cre)11Rth/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * CBA/J MGI:4442469
cn65
Kif3atm2Gsn/Kif3atm2Gsn
Tg(Wnt1-cre)11Rth/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * CBA/J MGI:4443124
cn66
Ndst1tm1Grob/Ndst1tm1Grob
Tg(Wnt1-cre)11Rth/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * CBA/J MGI:4943277
cn67
Ndst1tm1Grob/Ndst1tm1Grob
Ndst2tm1Lkj/Ndst2tm1Lkj
Tg(Wnt1-cre)11Rth/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * CBA/J MGI:5430386
cn68
Dph1tm1.1Cmch/Dph1tm1.1Cmch
Tg(Wnt1-cre)11Rth/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * CBA/J MGI:5659973
cn69
Dph1tm1.1Cmch/Dph1tm1.1Cmch
Gt(ROSA)26Sortm4(ACTB-tdTomato,-EGFP)Luo/Gt(ROSA)26Sor+
Tg(Wnt1-cre)11Rth/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * CBA/J MGI:5659974
cn70
Mapk1tm1Gela/Mapk1tm1Gela
Tg(Wnt1-cre)11Rth/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * CBA/J MGI:5660194
cn71
Mapk1tm1Gela/Mapk1tm1Gela
Mapk3tm1Gela/Mapk3+
Tg(Wnt1-cre)11Rth/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * CBA/J MGI:5660196
cn72
Snai1tm1Grid/Snai1tm2Grid
Tg(Wnt1-cre)11Rth/0
involves: 129S1/Sv * C57BL/6 * CBA MGI:3715215
cn73
Zfpm2tm1Sho/Zfpm2tm2Sho
Tg(Wnt1-cre)11Rth/0
involves: 129S1/Sv * C57BL/6 * CBA MGI:3851405
cn74
Jag1tm2Grid/Jag1tm2Grid
Tg(Wnt1-cre)11Rth/0
involves: 129S1/Sv * C57BL/6 * CBA MGI:5318528
cn75
Snai1tm1Grid/Snai1tm2Grid
Snai2tm2Grid/Snai2tm2Grid
Tg(Wnt1-cre)11Rth/0
involves: 129S1/Sv * C57BL/6 * CBA MGI:3715216
cn76
Hand2tm1Cse/Hand2+
Tg(Wnt1-cre)11Rth/0
involves: 129S1/Sv * C57BL/6J * CBA/J MGI:4417976
cn77
Hand2tm1.1Majh/Hand2tm1.1Majh
Tg(Wnt1-cre)11Rth/0
involves: 129S1/SvImJ * C57BL/6 * CBA * DBA/2 MGI:3804452
cn78
Nfatc1tm1Glm/Nfatc1tm1Glm
Tg(Wnt1-cre)11Rth/0
Gt(ROSA)26Sortm1Sho/Gt(ROSA)26Sor+
involves: 129S2/SvPas * 129S4/SvJaeSor * C57BL/6 * CBA MGI:5432553
cn79
Mau2tm1.1Hpt/Mau2tm1.1Hpt
Nipbltm1.1Hpt/Nipbl+
Tg(Wnt1-cre)11Rth/0
involves: 129S2/SvPas * C57BL/6 * C57BL/6J * CBA/J * SJL MGI:5698689
cn80
Mau2tm1.1Hpt/Mau2tm1.1Hpt
Tg(Wnt1-cre)11Rth/0
involves: 129S2/SvPas * C57BL/6 * C57BL/6J * CBA/J * SJL MGI:5698674
cn81
Mau2tm1.1Hpt/Mau2tm1.1Hpt
Nipbltm1.1Hpt/Nipbltm1.1Hpt
Tg(Wnt1-cre)11Rth/0
involves: 129S2/SvPas * C57BL/6 * C57BL/6J * CBA/J * SJL MGI:5698685
cn82
Nipbltm1.1Hpt/Nipbltm1.1Hpt
Tg(Wnt1-cre)11Rth/0
involves: 129S2/SvPas * C57BL/6 * C57BL/6J * CBA/J * SJL MGI:5698653
cn83
Bdnftm1Krj/Bdnftm1Lfr
Tg(Wnt1-cre)11Rth/0
involves: 129S2/SvPas * C57BL/6 * CBA MGI:3584263
cn84
Pax9tm1.1Hpt/Pax9tm1.1Hpt
Tg(Wnt1-cre)11Rth/?
involves: 129S2/SvPas * C57BL/6 * CBA * SJL MGI:3723641
cn85
Phox2btm3Jbr/Phox2btm3Jbr
Tg(Wnt1-cre)11Rth/0
involves: 129S2/SvPas * C57BL/6J * CBA/J MGI:4438210
cn86
Phox2atm2Jbr/Phox2atm2Jbr
Tg(Wnt1-cre)11Rth/0
involves: 129S2/SvPas * C57BL/6J * CBA/J MGI:4438209
cn87
Ngfrtm1.1Vk/Ngfrtm1.1Vk
Tg(Wnt1-cre)11Rth/0
involves: 129S2/SvPas * C57BL/6J * CBA/J * FVB/N MGI:5301302
cn88
Hoxa2tm1.1Fmr/Hoxa2tm1.1Fmr
Tg(Wnt1-cre)11Rth/0
involves: 129S2/SvPas * C57BL/6 * SJL MGI:5491198
cn89
Gt(ROSA)26Sortm7(SMO*/YFP)Amc/Gt(ROSA)26Sor+
Tg(Wnt1-cre)11Rth/0
involves: 129S4/SvJae *129X1/SvJ * C57BL/6 * CBA * Swiss Webster MGI:4839958
cn90
Flnatm1.1Caw/Y
Tg(Wnt1-cre)11Rth/0
involves: 129S4/SvJae * C57BL/6 * CBA MGI:3699953
cn91
Col1a1tm1(tetO-EWSR1/ATF1)Yasu/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Tg(CAG-cat-lacZ)11Miya/0
Tg(Wnt1-cre)11Rth/0
involves: 129S4/SvJae * C57BL/6 * CBA/J * DBA/2 MGI:5485200
cn92
Bmpr2tm1.1Enl/Bmpr2tm1.2Enl
Tg(Wnt1-cre)11Rth/0
involves: 129S4/SvJae * C57BL/6J * CBA/J MGI:5558941
cn93
Ror1tm1.1Meg/Ror1tm1.1Meg
Ror2tm1.1Meg/Ror2tm1.1Meg
Tg(Wnt1-cre)11Rth/0
involves: 129S4/SvJae * C57BL/6J * CBA/J MGI:5315491
cn94
Gt(ROSA)26Sortm1Sor/?
Myctm2Fwa/Myctm2Fwa
Tg(Wnt1-cre)11Rth/0
involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6 * CBA MGI:3720325
cn95
Krastm4Tyj/Krastm4Tyj
Ugdhtm1.1Xzh/Ugdhtm1.1Xzh
Tg(Wnt1-cre)11Rth/0
involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6 * CBA/J MGI:5430385
cn96
Ugdhtm1.1Xzh/Ugdhtm1.1Xzh
Tg(Wnt1-cre)11Rth/0
involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6 * CBA/J MGI:5430383
cn97
Ugdhtm1.1Xzh/Ugdhtm1.1Xzh
Tg(Pax6-HRAS*G12V)2044Ove/0
Tg(Wnt1-cre)11Rth/0
involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6 * CBA/J * FVB/N MGI:5430384
cn98
Pomt2tm1.1Hhu/Pomt2tm1.1Hhu
Tg(Wnt1-cre)11Rth/0
involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6J * CBA/J MGI:5302859
cn99
Zic3tm2.1Jwb/Y
Tg(Wnt1-cre)11Rth/0
involves: 129S4/SvJaeSor * 129S7/SvSvBrd * C57BL/6J * CBA/J MGI:5470170
cn100
Smotm2Amc/Smotm2.1Amc
Tg(Wnt1-cre)11Rth/0
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sor+
involves: 129S4/SvJaeSor * 129X1/SvJ * C57BL/6J * CBA/J MGI:4843924
cn101
Efnb1tm1Sor/Efnb1+
Tg(Wnt1-cre)11Rth/?
involves: 129S4/SvJaeSor * C57BL/6 * CBA MGI:3719104
cn102
Bmp2tm1Jfm/Bmp2+
Bmp4tm1Jfm/Bmp4tm1Jfm
Tg(Wnt1-cre)11Rth/0
involves: 129S4/SvJaeSor * C57BL/6J * CBA/J MGI:5312866
cn103
Bmp4tm1Jfm/Bmp4tm1Jfm
Bmp7tm1Jfm/Bmp7tm1Jfm
Tg(Wnt1-cre)11Rth/0
involves: 129S4/SvJaeSor * C57BL/6J * CBA/J MGI:5312867
cn104
Bmp2tm1Jfm/Bmp2tm1Jfm
Bmp4tm1Jfm/Bmp4tm1Jfm
Bmp7tm1Jfm/Bmp7tm1Jfm
Tg(Wnt1-cre)11Rth/0
involves: 129S4/SvJaeSor * C57BL/6J * CBA/J MGI:5312868
cn105
Bmp2tm1Jfm/Bmp2+
Bmp4tm1Jfm/Bmp4+
Bmp7tm1Jfm/Bmp7tm1Jfm
Tg(Wnt1-cre)11Rth/0
involves: 129S4/SvJaeSor * C57BL/6J * CBA/J MGI:5312869
cn106
Bmp2tm1Jfm/Bmp2tm1Jfm
Bmp4tm1Jfm/Bmp4+
Bmp7tm1Jfm/Bmp7+
Tg(Wnt1-cre)11Rth/0
involves: 129S4/SvJaeSor * C57BL/6J * CBA/J MGI:5312870
cn107
Bmp2tm1Jfm/Bmp2+
Bmp4tm1Jfm/Bmp4tm1Jfm
Bmp7tm1Jfm/Bmp7+
Tg(Wnt1-cre)11Rth/0
involves: 129S4/SvJaeSor * C57BL/6J * CBA/J MGI:5312871
cn108
Bmp2tm1Jfm/Bmp2tm1Jfm
Bmp4tm1Jfm/Bmp4+
Bmp7tm1Jfm/Bmp7tm1Jfm
Tg(Wnt1-cre)11Rth/0
involves: 129S4/SvJaeSor * C57BL/6J * CBA/J MGI:5312873
cn109
Bmp2tm1Jfm/Bmp2+
Bmp4tm1Jfm/Bmp4tm1Jfm
Bmp7tm1Jfm/Bmp7tm1Jfm
Tg(Wnt1-cre)11Rth/0
involves: 129S4/SvJaeSor * C57BL/6J * CBA/J MGI:5312874
cn110
Bmp2tm1Jfm/Bmp2tm1Jfm
Bmp4tm1Jfm/Bmp4tm1Jfm
Bmp7tm1Jfm/Bmp7+
Tg(Wnt1-cre)11Rth/0
involves: 129S4/SvJaeSor * C57BL/6J * CBA/J MGI:5312875
cn111
Lgi4tm1.1Jrb/Lgi4tm1.1Jrb
Tg(Wnt1-cre)11Rth/0
involves: 129S4/SvJaeSor * C57BL/6J * CBA/J MGI:4441318
cn112
Arid1atm1.1Mag/Arid1atm1.1Mag
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sor+
Tg(Wnt1-cre)11Rth/0
involves: 129S4/SvJaeSor * C57BL/6J * CBA/J MGI:5784731
cn113
Adam22tm1.1Mejr/Adam22tm1.1Mejr
Tg(Wnt1-cre)11Rth/0
involves: 129S4/SvJaeSor * C57BL/6J * CBA/J MGI:4441314
cn114
Bmp4tm1Jfm/Bmp4tm1Jfm
Tg(Wnt1-cre)11Rth/0
involves: 129S4/SvJaeSor * C57BL/6J * CBA/J MGI:5312863
cn115
Bmp2tm1Jfm/Bmp2tm1Jfm
Bmp4tm1Jfm/Bmp4tm1Jfm
Tg(Wnt1-cre)11Rth/0
involves: 129S4/SvJaeSor * C57BL/6J * CBA/J MGI:5312864
cn116
Bmp2tm1Jfm/Bmp2tm1Jfm
Bmp4tm1Jfm/Bmp4+
Tg(Wnt1-cre)11Rth/0
involves: 129S4/SvJaeSor * C57BL/6J * CBA/J MGI:5312865
cn117
Tg(Wnt1-cre)11Rth/0
Wnt5atm1Amc/Wnt5atm1.1Krvl
involves: 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6 * CBA/J MGI:5605991
cn118
Tgfbr2tm1.2Hlm/Tgfbr2tm1.2Hlm
Tg(Wnt1-cre)11Rth/0
involves: 129S6/SvEvTac * C57BL/6 * CBA MGI:3623395
cn119
Foxd3tm2Lby/Foxd3tm3Lby
Tg(Wnt1-cre)11Rth/0
involves: 129S6/SvEvTac * C57BL/6 * CBA MGI:3806465
cn120
Myctm2Fwa/Myc+
Tg(Wnt1-cre)11Rth/0
involves: 129S6/SvEvTac * C57BL/6 * CBA MGI:3720194
cn121
Myctm2Fwa/Myctm2Fwa
Tg(Wnt1-cre)11Rth/0
involves: 129S6/SvEvTac * C57BL/6 * CBA MGI:3720189
cn122
Zfpm1tm4Sho/Zfpm1tm4Sho
Tg(Wnt1-cre)11Rth/0
involves: 129S6/SvEvTac * C57BL/6 * CBA MGI:3586444
cn123
Ptpn11tm6Bgn/Ptpn11+
Tg(Wnt1-cre)11Rth/0
involves: 129S6/SvEvTac * C57BL/6 * CBA/J MGI:3840256
cn124
Megf8tm1.2Ddg/Megf8tm1.2Ddg
Tg(Wnt1-cre)11Rth/0
involves: 129S6/SvEvTac * C57BL/6J * CBA/J MGI:5558940
cn125
Wlstm1.1Whsu/Wlstm1.1Whsu
Tg(Wnt1-cre)11Rth/0
involves: 129S6/SvEvTac * C57BL/6J * CBA/J MGI:4881721
cn126
Srftm1Rmn/Srftm1Rmn
Tg(Wnt1-cre)11Rth/0
involves: 129S6/SvEvTac * C57BL/6J * CBA/J MGI:5659953
cn127
Cbfbtm2.1Ddg/Cbfbtm2.1Ddg
Tg(Wnt1-cre)11Rth/?
involves: 129S6/SvEvTac * C57BL/6J * CBA/J MGI:5702482
cn128
Hprttm2(Pgk1-Pac/TK)Brd/Y
Tg(Wnt1-cre)11Rth/0
involves: 129S7/SvEvBrd * C57BL/6 * CBA MGI:3772558
cn129
Hprttm2(Pgk1-Pac/TK)Brd/Hprt+
Tg(Wnt1-cre)11Rth/0
involves: 129S7/SvEvBrd * C57BL/6 * CBA MGI:3772559
cn130
Lmx1btm1Rjo/Lmx1btm1Zfc
Tg(Wnt1-cre)11Rth/0
involves: 129S7/SvEvBrd * C57BL/6 * CBA MGI:3697386
cn131
Fkbp1atm1.1Shou/Fkbp1atm1Zuk
Tg(Wnt1-cre)11Rth/0
involves: 129S7/SvEvBrd * C57BL/6J * CBA/J MGI:5490240
cn132
Lmx1btm1Rjo/Lmx1btm4Rjo
Tg(Wnt1-cre)11Rth/0
involves: 129S7/SvEvBrd * C57BL/6J * CBA/J MGI:4818571
cn133
Hoxa3tm1Mrc/Hoxa3tm3.1Nrm
Tg(Wnt1-cre)11Rth/0
involves: 129S7/SvEvBrd * C57BL/6J * CBA/J MGI:4461312
cn134
Dvl3tm1Awb/Dvl3tm1Awb
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sor+
Tg(Wnt1-cre)11Rth/0
involves: 129S/Sv * Black Swiss * C57BL/6J * CBA/J MGI:3831922
cn135
Dph1tm2Bhr/Dph1+
Gt(ROSA)26Sortm1(DTA)Jpmb/Gt(ROSA)26Sor+
Tg(Wnt1-cre)11Rth/0
involves: 129S/SvEv * 129S4/SvJae * C57BL/6J * CBA/J MGI:5659976
cn136
Dph1tm2Bhr/Dph1tm2Bhr
Gt(ROSA)26Sortm1(DTA)Jpmb/Gt(ROSA)26Sor+
Tg(Wnt1-cre)11Rth/0
involves: 129S/SvEv * 129S4/SvJae * C57BL/6J * CBA/J MGI:5659977
cn137
Plxnd1tm1.1Tmj/Plxnd1tm1.1Tmj
Tg(Wnt1-cre)11Rth/0
involves: 129S/SvEv * 129S4/SvJaeSor * C57BL/6 * CBA/J MGI:3848822
cn138
Plxnd1tm1Ddg/Plxnd1tm1.1Tmj
Tg(Wnt1-cre)11Rth/0
involves: 129S/SvEv * C57BL/6 * C57BL/6J * CBA/J MGI:3848832
cn139
Sox9tm2Crm/Sox9tm2Crm
Tg(Wnt1-cre)11Rth/0
involves: 129S/SvEv * C57BL/6 * CBA MGI:3718120
cn140
Sox9tm2Crm/Sox9+
Tg(Wnt1-cre)11Rth/0
involves: 129S/SvEv * C57BL/6 * CBA MGI:3718125
cn141
Wlstm1.1Lan/Wlstm1.1Lan
Tg(Wnt1-cre)11Rth/0
involves: 129S/SvEv * C57BL/6J * CBA/J * SJL MGI:4838405
cn142
Myocdtm1Msp/Myocdtm1Msp
Tg(Wnt1-cre)11Rth/0
involves: 129/Sv * C57BL/6 * CBA MGI:3797650
cn143
Ctnnb1tm2Kem/Ctnnb1tm2.1Kem
Tg(Wnt1-cre)11Rth/?
involves: 129/Sv * C57BL/6 * CBA MGI:2674120
cn144
Nf1tm1Par/Nf1tm1Tyj
Tg(Wnt1-cre)11Rth/0
involves: 129/Sv * C57BL/6 * CBA MGI:3776056
cn145
Gt(ROSA)26Sortm1(PDGFRA*)Hsc/Gt(ROSA)26Sor+
Tg(Wnt1-cre)11Rth/0
involves: 129/Sv * C57BL/6 * CBA MGI:3835760
cn146
Hoxa2tm1.1Fmr/Hoxa2tm1.1Fmr
Tg(Wnt1-cre)11Rth/0
involves: 129/Sv * C57BL/6J * CBA/J MGI:4415143
cn147
Bmp4tm2(tetO-Bmp4,lacZ)Jfm/Bmp4+
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Tg(Wnt1-cre)11Rth/0
involves: 129/Sv * C57BL/6J * CBA/J MGI:5312862
cn148
Bhlhe22tm2.1Meg/Bhlhe22tm2.1Meg
Tg(Wnt1-cre)11Rth/0
involves: 129/Sv * C57BL/6J * CBA/J MGI:4440902
cn149
Gja1tm1Gfi/Gja1tm1Gfi
Tg(Wnt1-cre)11Rth/0
involves: 129/Sv * C57BL/6J * CBA/J * FVB/N MGI:3652904
cn150
Map2k1tm1Chrn/Map2k1tm1Chrn
Map2k2tm1Chrn/Map2k2tm1Chrn
Tg(Wnt1-cre)11Rth/0
involves: 129/Sv * C57BL/6J * CBA/J * SJL MGI:5659952
cn151
Rarbtm2Ipc/Rarbtm2Ipc
Rargtm3Ipc/Rargtm3Ipc
Tg(Wnt1-cre)11Rth/?
involves: 129/Sv * C57BL/6 * SJL MGI:3620540
cn152
Notch1tm2Rko/Notch1tm2Rko
Tg(Wnt1-cre)11Rth/0
involves: 129X1/SvJ * C57BL/6 * CBA MGI:5318530
cn153
Ctnnb1tm1Mmt/Ctnnb1tm1Mmt
Tg(Wnt1-cre)11Rth/0
involves: 129X1/SvJ * C57BL/6 * CBA MGI:3773283
cn154
Gt(ROSA)26Sortm1(Smo/EYFP)Amc/?
Tg(Wnt1-cre)11Rth/?
involves: 129X1/SvJ * C57BL/6J * CBA/J MGI:3716199
cn155
Smotm2Amc/Smotm2.1Amc
Tg(Wnt1-cre)11Rth/0
involves: 129X1/SvJ * C57BL/6J * CBA/J MGI:4843923
cn156
Gt(ROSA)26Sortm1(Smo/EYFP)Amc/Gt(ROSA)26Sor+
Tg(Wnt1-cre)11Rth/0
involves: 129X1/SvJ * C57BL/6J * CBA/J MGI:4843925
cn157
Fgfr2tm1Dor/Fgfr2tm1Dor
Tg(Wnt1-cre)11Rth/0
involves: 129X1/SvJ * C57BL/6J * CBA/J MGI:4943276
cn158
Hmx1tm1.1Arte/Hmx1tm1.1Arte
Tg(Wnt1-cre)11Rth/0
involves: BALB/c * C57BL/6J * CBA/J MGI:5515738
cn159
Tg(CAG-Otx2,-EGFP)1Eno/?
Tg(Wnt1-cre)11Rth/?
involves: C3H * C57BL/6 MGI:3851922
cn160
Tg(Wnt1-cre)11Rth/?
Tg(CAG-Lhx,-EGFP)1Eno/?
involves: C3H * C57BL/6 MGI:3851921
cn161
Hoxa3tm2Nrm/Hoxa3tm3.1Nrm
Tg(Wnt1-cre)11Rth/0
involves: C3H * C57BL/6 * CBA/J MGI:4461313
cn162
Pdgfratm8Sor/Pdgfratm8Sor
Tg(Wnt1-cre)11Rth/?
involves: C57BL/6 * CBA MGI:3715094
cn163
Pdgfratm8Sor/Pdgfratm8Sor
Pdgfrbtm1Mdt/Pdgfrbtm1Mdt
Tg(Wnt1-cre)11Rth/?
involves: C57BL/6 * CBA MGI:3715096
cn164
Pdgfrbtm1Mdt/Pdgfrbtm1Mdt
Tg(Wnt1-cre)11Rth/?
involves: C57BL/6 * CBA MGI:3715095
cn165
Ikbkaptm1c(KOMP)Wtsi/Ikbkaptm1c(KOMP)Wtsi
Tg(Wnt1-cre)11Rth/0
involves: C57BL/6J * C57BL/6N * CBA/J MGI:5558037
cn166
Gt(ROSA)26Sortm4(EWSR1/ATF1)Mrc/Gt(ROSA)26Sor+
Tg(Wnt1-cre)11Rth/?
involves: C57BL/6J * CBA/J MGI:5495316
cn167
Gt(ROSA)26Sortm5(Wnt5a)Flng/?
Tg(Wnt1-cre)11Rth/0
involves: C57BL/6J * CBA/J MGI:5613589
cn168
Arid1atm1.1Mag/Arid1a+
Tg(Wnt1-cre)11Rth/0
involves: C57BL/6J * CBA/J MGI:5784729
cn169
Arid1atm1.1Mag/Arid1atm1.1Mag
Tg(Wnt1-cre)11Rth/0
involves: C57BL/6J * CBA/J MGI:5784730
cn170
Map3k7tm1Mis/Map3k7tm1Mis
Tg(Wnt1-cre)11Rth/0
involves: C57BL/6J * CBA/J MGI:5514176
cn171
Zic3tm1.1Smwa/Y
Tg(Wnt1-cre)11Rth/0
involves: C57BL/6J * CBA/J MGI:5476842
cn172
Smotm1Amc/Smotm2Amc
Tg(Wnt1-cre)11Rth/?
involves: C57BL/6J * CBA/J MGI:3716198
cn173
Irx3tm3Hui/Irx3tm3Hui
Irx5tm3Hui/Irx5tm3Hui
Tg(Wnt1-cre)11Rth/0
involves: C57BL/6J * CBA/J MGI:5444486
cn174
Ednratm2Ywa/Ednratm2Ywa
Tg(Wnt1-cre)11Rth/0
involves: C57BL/6J * CBA/J MGI:3849287
cn175
Rhoatm1Yuyo/Rhoatm1Yuyo
Tg(Wnt1-cre)11Rth/0
involves: C57BL/6J * CBA/J MGI:5004977
cn176
Tg(CAG-cat,-Ptpn11*Q97R)1Rbns/0
Tg(Wnt1-cre)11Rth/0
involves: C57BL/6J * CBA/J * FVB/N MGI:4361520
cn177
Hoxb1tm5Mrc/Hoxb1tm7Mrc
Tg(Wnt1-cre)11Rth/0
Not Specified MGI:3050407
cn178
Tfap2atm1Hsv/Tfap2atm2Will
Tg(Wnt1-cre)11Rth/0
Not Specified MGI:3038354
cn179
Pdgfratm8Sor/Pdgfratm8Sor
Tg(Wnt1-cre)11Rth/0
Not Specified MGI:2450742
cx180
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sor+
Msx2tm1Rilm/Msx2tm1Rilm
Tg(Wnt1-cre)11Rth/0
involves: 129S4/SvJae * C57BL/6J * CBA/J MGI:5427701
cx181
Plxnd1tm1.1Tmj/Plxnd1+
Plxnd1tm1Ddg/Plxnd1+
Tg(Wnt1-cre)11Rth/0
involves: 129S/SvEv * C57BL/6J * CBA/J MGI:5550533
cx182
Tg(Wnt1-cre)11Rth/0
Tg(Wnt1-GAL4)11Rth/0
involves: C57BL/6J * CBA/J * Swiss albino MGI:5551395


Genotype
MGI:5882546
cn1
Allelic
Composition
Fgfr1tm5.1Sor/Fgfr1tm10.1Sor
Tg(Wnt1-cre)11Rth/0
Genetic
Background
129S4.Cg-Fgfr1tm5.1Sor Fgfr1tm10.1Sor Tg(Wnt1-cre)11Rth
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fgfr1tm10.1Sor mutation (0 available); any Fgfr1 mutation (206 available)
Fgfr1tm5.1Sor mutation (0 available); any Fgfr1 mutation (206 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
craniofacial
• at P0, 2 of 13 mice exhibit clefting of the palatine and palatal process of the maxilla

growth/size/body
• at P0, 2 of 13 mice exhibit clefting of the palatine and palatal process of the maxilla

digestive/alimentary system
• at P0, 2 of 13 mice exhibit clefting of the palatine and palatal process of the maxilla




Genotype
MGI:5882544
cn2
Allelic
Composition
Fgfr1tm5.1Sor/Fgfr1tm9.1Sor
Tg(Wnt1-cre)11Rth/0
Genetic
Background
129S4.Cg-Fgfr1tm5.1Sor Fgfr1tm9.1Sor Tg(Wnt1-cre)11Rth
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fgfr1tm5.1Sor mutation (0 available); any Fgfr1 mutation (206 available)
Fgfr1tm9.1Sor mutation (1 available); any Fgfr1 mutation (206 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
craniofacial
• at P0, 1 of 7 mice exhibit clefting of the palatine and palatal process of the maxilla

growth/size/body
• at P0, 1 of 7 mice exhibit clefting of the palatine and palatal process of the maxilla

digestive/alimentary system
• at P0, 1 of 7 mice exhibit clefting of the palatine and palatal process of the maxilla




Genotype
MGI:5882528
cn3
Allelic
Composition
Fgfr1tm5.1Sor/Fgfr1tm5.1Sor
Tg(Wnt1-cre)11Rth/0
Genetic
Background
129S4.Cg-Fgfr1tm5.1Sor Tg(Wnt1-cre)11Rth
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fgfr1tm5.1Sor mutation (0 available); any Fgfr1 mutation (206 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
craniofacial
• at P0, all (16 of 16) mice exhibit midline facial clefting

growth/size/body
• at P0, all (16 of 16) mice exhibit midline facial clefting




Genotype
MGI:4360747
cn4
Allelic
Composition
Ext1tm1Yama/Ext1tm1Yama
Tg(Wnt1-cre)11Rth/0
Genetic
Background
B6.Cg-Ext1tm1Yama Tg(Wnt1-cre)11Rth
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ext1tm1Yama mutation (0 available); any Ext1 mutation (43 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Craniofacial malformation in Ext1tm1Yama/Ext1tm1YamaTg(Wnt1-cre)11Rth/0 mice

mortality/aging
• all mice die within the first day of birth

vision/eye
• mice exhibit eye morphology defects
• however, lens thickness is normal
• 58% of mutant mice exhibit ciliary body coloboma
• at E18.5, 99% of mutant mice exhibit ventral iris coloboma
• the corneal stroma lacks collagen staining unlike in wild-type mice

craniofacial

hearing/vestibular/ear

embryo
• at E15.5, neural crest cell proliferation is reduced compared to in wild-type mice
• however, neural crest cell migration into the periocular mesenchyme at E11.5 and levels of apoptosis are normal

digestive/alimentary system

cellular
• at E15.5, neural crest cell proliferation is reduced compared to in wild-type mice
• however, neural crest cell migration into the periocular mesenchyme at E11.5 and levels of apoptosis are normal

growth/size/body




Genotype
MGI:3852467
cn5
Allelic
Composition
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sor+
Ptpn11tm1.1Rbns/Ptpn11tm1.1Rbns
Tg(Wnt1-cre)11Rth/0
Genetic
Background
B6.Cg-Ptpn11tm1.1Rbns Gt(ROSA)26Sortm1Sor Tg(Wnt1-cre)11Rth
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1Sor mutation (7 available); any Gt(ROSA)26Sor mutation (393 available)
Ptpn11tm1.1Rbns mutation (0 available); any Ptpn11 mutation (30 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
embryo
• at E12.5, the number of neural crest cells in the outflow tract cushions are less than in wild-type mice
• at E17.5, the number of neural crest cells in the proximal outflow tract is less than in wild-type mice
• however, initial proliferation and migration are normal
• cranial neural crest cells fail to differentiate into osteoblasts unlike in wild-type mice

nervous system
• at E12.5, the number of neural crest cells in the outflow tract cushions are less than in wild-type mice
• at E17.5, the number of neural crest cells in the proximal outflow tract is less than in wild-type mice
• however, initial proliferation and migration are normal
• cranial neural crest cells fail to differentiate into osteoblasts unlike in wild-type mice

cardiovascular system
• at E12.5, the number of neural crest cells in the outflow tract cushions are less than in wild-type mice
• at E17.5, the number of neural crest cells in the proximal outflow tract is less than in wild-type mice
• however, initial proliferation and migration are normal




Genotype
MGI:3852466
cn6
Allelic
Composition
Ptpn11tm1.1Rbns/Ptpn11tm1.1Rbns
Tg(Wnt1-cre)11Rth/0
Genetic
Background
B6.Cg-Ptpn11tm1.1Rbns Tg(Wnt1-cre)11Rth
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptpn11tm1.1Rbns mutation (0 available); any Ptpn11 mutation (30 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• embryo survival drops after E15.5 and no mice are born alive

craniofacial
• neural crest cell-derived mandible is dramatically ablated or completely absent
• neural crest cell-derived craniofacial bones are dramatically ablated or completely absent
• neural crest cell-derived nasal cartilage is dramatically ablated or completely absent
• small nose

cardiovascular system
• abnormal arch arteries are observed in 32% with 5 of 19 mice exhibiting malpositioning of the left carotid artery and 1 of 19 exhibiting defective left carotid artery
• mice exhibit a truncal valve containing 3 leaflets (in 90% of mice) or 4 leaflets (in 10% of mice) unlike in wild-type mice
• the truncal valve is longer and thicker than the aortic valves of wild-type mice
• however, the atrioventricular valves are normal
• all mice exhibit persistent truncus arteriosus
• 84% of heart have type II and 16% type I persistent truncus arteriosus

growth/size/body
• neural crest cell-derived nasal cartilage is dramatically ablated or completely absent
• small nose

hearing/vestibular/ear

respiratory system
• neural crest cell-derived nasal cartilage is dramatically ablated or completely absent

skeleton
• neural crest cell-derived mandible is dramatically ablated or completely absent
• neural crest cell-derived craniofacial bones are dramatically ablated or completely absent
• neural crest cell-derived nasal cartilage is dramatically ablated or completely absent

vision/eye
• eye placement anomalies

digestive/alimentary system




Genotype
MGI:4360749
cn7
Allelic
Composition
Ext1tm1Yama/Ext1+
Tg(Wnt1-cre)11Rth/0
Tgfb2tm1Doe/Tgfb2+
Genetic
Background
B6.Cg-Tgfb2tm1Doe Ext1tm1Yama Tg(Wnt1-cre)11Rth
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ext1tm1Yama mutation (0 available); any Ext1 mutation (43 available)
Tgfb2tm1Doe mutation (1 available); any Tgfb2 mutation (17 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Thin cornea and iridocorneal dysgenesis in Ext1tm1Yama/Ext1+ Tg(Wnt1-cre)11Rth/0 Tgfb2tm1Doe/Tgfb2+ mice

mortality/aging
N
• mice survive into adulthood

vision/eye
• mice exhibit defects in components of the aqueous drainage system
• however, the iridocorneal angle is normal
• the trabecular beam contains fewer cells than in wild-type mice
• mice exhibit ocular hypertension unlike single heterozygotes




Genotype
MGI:4410359
cn8
Allelic
Composition
Chd7Gt(XK403)Byg/Chd7+
Tg(Wnt1-cre)11Rth/0
Genetic
Background
either: (involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J * CBA/J) or (involves: 129P2/OlaHsd * C57BL/6J * CBA/J * CD-1)
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Chd7Gt(XK403)Byg mutation (0 available); any Chd7 mutation (87 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Effects of Cre-mediated rescue of Chd7Gt(XK403)Byg mutation on the arch artery phenotype at E10.5

cardiovascular system

craniofacial

embryo




Genotype
MGI:3611573
cn9
Allelic
Composition
Gt(ROSA)26Sortm1(DTA)Jpmb/Gt(ROSA)26Sor+
Tg(Wnt1-cre)11Rth/0
Genetic
Background
either: (involves: 129S/SvEv * C57BL/6 * CBA) or (involves: 129S/SvEv * C57BL/6 * CBA * CD-1)
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(DTA)Jpmb mutation (2 available); any Gt(ROSA)26Sor mutation (393 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• at E9.5 and E10.5, the cranial neural tube is open dorsally
• at E9.5 and E10.5, the isthmus (the constriction of the neural tube at the midbrain hindbrain boundary) is absent
• at E9.5 and E10.5 the brain rostral to the otic vesicle is significantly smaller

embryo
• at E9.5 and E10.5, the cranial neural tube is open dorsally




Genotype
MGI:4410368
cn10
Allelic
Composition
Tbx1tm2.1Bem/Tbx1tm2.1Bem
Tg(Wnt1-cre)11Rth/0
Genetic
Background
either: (involves: 129/Sv * C57BL/6 * C57BL/6J * CBA/J * SJL) or (involves: 129/Sv * C57BL/6J * CBA/J * CD-1 * SJL)
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tbx1tm2.1Bem mutation (0 available); any Tbx1 mutation (17 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype
• mice exhibit no abnormalities




Genotype
MGI:3035941
cn11
Allelic
Composition
Lmo4tm1Sho/Lmo4tm1Sho
Tg(Wnt1-cre)11Rth/0
Genetic
Background
either: (involves: 129/Sv * CD-1) or (involves: 129/Sv * C57BL/6)
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lmo4tm1Sho mutation (0 available); any Lmo4 mutation (7 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
craniofacial
N
• presphenoid bone formed properly




Genotype
MGI:4413446
cn12
Allelic
Composition
Mrgprdtm1Mjz/?
Rettm1Ddg/Rettm1Ddg
Tg(Wnt1-cre)11Rth/0
Genetic
Background
involves: 129 * 129S1/Sv * C57BL/6 * C57BL/6J * CBA/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mrgprdtm1Mjz mutation (2 available); any Mrgprd mutation (9 available)
Rettm1Ddg mutation (0 available); any Ret mutation (30 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• at P14, GFP+ skin neuron projections are reduced and punctate unlike in control Mrgprdtm1Mjz Rettm1Ddg homozygotes
• however, central axonal projections in the thoracic spinal cord exhibit normal lamina specific innervation of peptidergic and nonpectidergic projections




Genotype
MGI:3779094
cn13
Allelic
Composition
Mfn2tm1Dcc/Mfn2tm3Dcc
Tg(Wnt1-cre)11Rth/0
Genetic
Background
involves: 129 * 129S4/SvJaeSor * Black Swiss
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mfn2tm1Dcc mutation (0 available); any Mfn2 mutation (20 available)
Mfn2tm3Dcc mutation (2 available); any Mfn2 mutation (20 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mutant pups are born at appropriate Mendelian ratio
• after birth, about one third of mutant mice die on postnatal day 1
• all remaining mutant mice die by P17

behavior/neurological
• mice surviving beyond P1 cannot easily regain posture when placed on their backs
• mice surviving beyond P1 display uncoordinated limb movements, and move primarily by writhing on their abdomen

growth/size/body
• mice surviving beyond P1 are severely runted, likely due to feeding problems secondary to their movement disorder

nervous system
• severe defect in postnatal cerebellar growth




Genotype
MGI:5285375
cn14
Allelic
Composition
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sor+
Sox11tm2.1Weg/Sox11tm2.1Weg
Sox4tm1Vlf/Sox4tm1Vlf
Tg(Wnt1-cre)11Rth/0
Genetic
Background
involves: 129 * C57BL/6 * C57BL/6J * CBA/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1Sor mutation (7 available); any Gt(ROSA)26Sor mutation (393 available)
Sox11tm2.1Weg mutation (0 available); any Sox11 mutation (7 available)
Sox4tm1Vlf mutation (0 available); any Sox4 mutation (11 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
embryo
• massive cell death in the branchial arches without a decrease in cell proliferation




Genotype
MGI:4413445
cn15
Allelic
Composition
Rettm1Ddg/Rettm1Ddg
Tg(Wnt1-cre)11Rth/0
Genetic
Background
involves: 129 * C57BL/6 * C57BL/6J * CBA/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rettm1Ddg mutation (0 available); any Ret mutation (30 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• few mice survive beyond 3 weeks

digestive/alimentary system
• at P14
• enlarged at P14

nervous system
• at P14, non-peptidergic neurons are hypotrophic unlike in control Rettm1Ddg homozygotes
• in the small intestine and colon
• at P14, the dorsal root ganglia is 30% smaller than in control Rettm1Ddg homozygotes

behavior/neurological
• beginning at P3 mice develop progressive weakness

growth/size/body




Genotype
MGI:3851919
cn16
Allelic
Composition
Hdac2tm1.1Eno/Hdac2tm1.1Eno
Tg(Wnt1-cre)11Rth/?
Genetic
Background
involves: 129 * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hdac2tm1.1Eno mutation (0 available); any Hdac2 mutation (24 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype
• no abnormal phenotype is detected in skull development




Genotype
MGI:3851918
cn17
Allelic
Composition
Hdac1tm1.1Eno/Hdac1tm1.1Eno
Tg(Wnt1-cre)11Rth/?
Genetic
Background
involves: 129 * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hdac1tm1.1Eno mutation (0 available); any Hdac1 mutation (25 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype
• no abnormal phenotype is detected in skull development




Genotype
MGI:3851920
cn18
Allelic
Composition
Hdac8tm1.1Eno/Y
Tg(Wnt1-cre)11Rth/0
Genetic
Background
involves: 129 * C57BL/6 * CBA * CD-1
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hdac8tm1.1Eno mutation (0 available); any Hdac8 mutation (12 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• some mice die within 4-6 hours after birth from brain hemorrhaging

cardiovascular system
• some mice die within 4-6 hours after birth from brain hemorrhaging
• hemorrhaging results from ossification defects in the skull

craniofacial
• ossification defects lead to the presence of soft tissues in the frontal and interparietal bone

nervous system
• some mice die within 4-6 hours after birth from brain hemorrhaging
• hemorrhaging results from ossification defects in the skull

skeleton
• ossification defects lead to the presence of soft tissues in the frontal and interparietal bone
• ossification defects lead to the presence of soft tissues in the frontal and interparietal bone and incomplete skull closure




Genotype
MGI:5308958
cn19
Allelic
Composition
Ctnnb1tm2Kem/Ctnnb1tm2Kem
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sor+
Tg(Wnt1-cre)11Rth/0
Genetic
Background
involves: 129 * C57BL/6 * CBA/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ctnnb1tm2Kem mutation (1 available); any Ctnnb1 mutation (32 available)
Gt(ROSA)26Sortm1Sor mutation (7 available); any Gt(ROSA)26Sor mutation (393 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
craniofacial
• at E12.5
• at E12.5
• rudimentary at E12.5

nervous system
• absence of midbrain structures at E10.5
• absence of hindbrain structures at E10.5

embryo
• rudimentary at E12.5

skeleton
• at E12.5
• at E12.5




Genotype
MGI:4868120
cn20
Allelic
Composition
Dicer1tm1Bdh/Dicer1tm1Bdh
Tg(Wnt1-cre)11Rth/0
Genetic
Background
involves: 129 * C57BL/6 * CBA/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Dicer1tm1Bdh mutation (2 available); any Dicer1 mutation (59 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

cardiovascular system
• discontinuance of the ascending aortic arch with the descending aorta, indicating improper pattering of the aortic arch due to a left fourth aortic arch defect
• the outflow tract does not fully septate into a pulmonary artery and aorta in some cases, resulting in the persistence of a common outflow vessel

craniofacial
• severe craniofacial defects are seen by E14.5
• although pharyngeal arches appear similar to wild-type in emergence, size and shape, expression of Dlx2 and Fgf8 are downregulated in pharyngeal arch 1
• apoptosis is increased in the first pharyngeal arch at E11.5

embryo
• although pharyngeal arches appear similar to wild-type in emergence, size and shape, expression of Dlx2 and Fgf8 are downregulated in pharyngeal arch 1
• apoptosis is increased in the first pharyngeal arch at E11.5

hematopoietic system
• thymus development is absent

immune system
• thymus development is absent

nervous system
• loss of neural crest cell derived neuronal tissue from the thoracic sympathetic ganglia
• loss of neural crest cell derived neuronal tissue from the dorsal root ganglia

skeleton
• neural crest cell derived maxillary and mandibular regions of the face and frontonasal process lack cartilaginous tissue, however mesodermally derived cartilage near the base of the skull is present

endocrine/exocrine glands
• thymus development is absent

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
DiGeorge syndrome DOID:11198 OMIM:188400
J:166758




Genotype
MGI:4868201
cn21
Allelic
Composition
Dicer1tm1Bdh/Dicer1+
Tg(Wnt1-cre)11Rth/0
Genetic
Background
involves: 129 * C57BL/6 * CBA/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Dicer1tm1Bdh mutation (2 available); any Dicer1 mutation (59 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
• thymus development is delayed at E14.5, but by E16.5, the thymus is indistinguishable from wild-type

immune system
• thymus development is delayed at E14.5, but by E16.5, the thymus is indistinguishable from wild-type

endocrine/exocrine glands
• thymus development is delayed at E14.5, but by E16.5, the thymus is indistinguishable from wild-type




Genotype
MGI:5308953
cn22
Allelic
Composition
Ctnnb1tm2Kem/Ctnnb1tm3Kba
Tg(Wnt1-cre)11Rth/0
Genetic
Background
involves: 129 * C57BL/6 * CBA/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ctnnb1tm2Kem mutation (1 available); any Ctnnb1 mutation (32 available)
Ctnnb1tm3Kba mutation (0 available); any Ctnnb1 mutation (32 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• differentiation of sensory neurons in the neural tube is defective
• milder defects than in conditional mutant mice homozygous for Ctnnb1tm2Kem at E12.5

craniofacial
• milder defects than in conditional mutant mice homozygous for Ctnnb1tm2Kem at E12.5

embryo
N
• apical neural tube morphology is not disrupted at E12.5

cellular
• differentiation of sensory neurons in the neural tube is defective




Genotype
MGI:5308955
cn23
Allelic
Composition
Ctnnb1tm2Kem/Ctnnb1tm2Kem
Tg(Wnt1-cre)11Rth/0
Genetic
Background
involves: 129 * C57BL/6 * CBA/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ctnnb1tm2Kem mutation (1 available); any Ctnnb1 mutation (32 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• disruption of apical neural tube morphology leading to migration of cells into the neural canal
• malformed telencephalic lobes at E12.5

craniofacial

embryo
• disruption of apical neural tube morphology leading to migration of cells into the neural canal

cellular




Genotype
MGI:5308956
cn24
Allelic
Composition
Ctnnb1tm2Kem/Ctnnb1tm3Kba
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sor+
Tg(Wnt1-cre)11Rth/0
Genetic
Background
involves: 129 * C57BL/6 * CBA/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ctnnb1tm2Kem mutation (1 available); any Ctnnb1 mutation (32 available)
Ctnnb1tm3Kba mutation (0 available); any Ctnnb1 mutation (32 available)
Gt(ROSA)26Sortm1Sor mutation (7 available); any Gt(ROSA)26Sor mutation (393 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• not developed at E10.5

craniofacial
• hypoplastic and malformed

skeleton
• hypoplastic and malformed




Genotype
MGI:3804086
cn25
Allelic
Composition
Cited2tm1Bha/Cited2tm2Bha
Tg(Wnt1-cre)11Rth/0
Genetic
Background
involves: 129 * C57BL/6 * CBA * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cited2tm1Bha mutation (4 available); any Cited2 mutation (15 available)
Cited2tm2Bha mutation (2 available); any Cited2 mutation (15 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• despite present in Mendelian ratios at E18.5, fewer than expected survive to weaning
• despite present in Mendelian ratios at E18.5, fewer than expected survive to weaning

nervous system
• in one mouse
• 11 of 14 mice exhibit fusion of ganglia IX and X
• 11 of 14 mice exhibit fusion of ganglia IX and X




Genotype
MGI:5430387
cn26
Allelic
Composition
Hs2st1tm1.1Je/Hs2st1tm1.1Je
Hs6st1tm1Wvc/Hs6st1tm1Wvc
Hs6st2tm1Lex/Hs6st2tm1Lex
Tg(Wnt1-cre)11Rth/0
Genetic
Background
involves: 129 * C57BL/6J * CBA/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hs2st1tm1.1Je mutation (0 available); any Hs2st1 mutation (21 available)
Hs6st1tm1Wvc mutation (0 available); any Hs6st1 mutation (16 available)
Hs6st2tm1Lex mutation (2 available); any Hs6st2 mutation (8 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
N
• lacrimal gland budding is preserved




Genotype
MGI:5702481
cn27
Allelic
Composition
Mapttm2Arbr/?
Runx1tm3Spe/Runx1tm3Spe
Tg(Wnt1-cre)11Rth/?
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6J * CBA/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mapttm2Arbr mutation (1 available); any Mapt mutation (408 available)
Runx1tm3Spe mutation (0 available); any Runx1 mutation (19 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• reduction of sensory innervtion of the epidermic at P0
• reduction in epidermal nerve fiber density




Genotype
MGI:5882547
cn28
Allelic
Composition
Fgfr1tm5.1Sor/Fgfr1tm10.1Sor
Stat3tm2Aki/Stat3tm2Aki
Tg(Wnt1-cre)11Rth/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJaeSor
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fgfr1tm10.1Sor mutation (0 available); any Fgfr1 mutation (206 available)
Fgfr1tm5.1Sor mutation (0 available); any Fgfr1 mutation (206 available)
Stat3tm2Aki mutation (0 available); any Stat3 mutation (46 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
craniofacial
N
• none of the 4 mice examined exhibit cleft palate, likely due to the low penetrance of cleft palate found in Fgfr1tm5.1Sor/Fgfr1tm10.1Sor mice (2 of 13)




Genotype
MGI:5882548
cn29
Allelic
Composition
Stat3tm2Aki/Stat3tm2Aki
Tg(Wnt1-cre)11Rth/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJaeSor
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Stat3tm2Aki mutation (0 available); any Stat3 mutation (46 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype
N
• mice are viable and developmentally normal with no detectable craniofacial abnormalities




Genotype
MGI:5702479
cn30
Allelic
Composition
Cbfbtm2.1Ddg/Cbfbtm2.1Ddg
Mapttm2Arbr/?
Tg(Wnt1-cre)11Rth/?
Genetic
Background
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6J * CBA/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cbfbtm2.1Ddg mutation (1 available); any Cbfb mutation (29 available)
Mapttm2Arbr mutation (1 available); any Mapt mutation (408 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• reduction of sensory innervation of the epidermis at P0
• reduction in epidermal nerve fiber density
• deficiency of peripheral projections of nonpeptidergic (mechanical) nociceptors

craniofacial

mortality/aging
• mice die perinatally due to craniofacial defects




Genotype
MGI:5305927
cn31
Allelic
Composition
Pbx1tm1Koss/Pbx1tm1Koss
Pbx2tm1Mlc/Pbx2+
Tg(Wnt1-cre)11Rth/0
Genetic
Background
involves: 129P2/OlaHsd * 129S/Sv * C57BL/6J * CBA/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pbx1tm1Koss mutation (0 available); any Pbx1 mutation (27 available)
Pbx2tm1Mlc mutation (0 available); any Pbx2 mutation (8 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

craniofacial

nervous system
N
• cranial neural crest cell migration and olfactory placodes are normal

digestive/alimentary system

growth/size/body




Genotype
MGI:5524256
cn32
Allelic
Composition
Nrg1tm4Cbm/Nrg1tm4.1Cbm
Tg(Wnt1-cre)11Rth/0
Genetic
Background
involves: 129P2/OlaHsd * BALB/cJ * C57BL/6J * CBA/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nrg1tm4.1Cbm mutation (0 available); any Nrg1 mutation (20 available)
Nrg1tm4Cbm mutation (0 available); any Nrg1 mutation (20 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
N
• mice exhibit normal myelination
• small diameter and few intrafusal fibers

behavior/neurological
• on an inverted grid, mice loss their grip 5 times faster than control mice
• impaired left/right coordination with frequent hopping

muscle
• small diameter and few intrafusal fibers




Genotype
MGI:4365544
cn33
Allelic
Composition
Ptpn11tm1.1Wbm/Ptpn11tm1.1Wbm
Tg(Wnt1-cre)11Rth/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J * SJL * SJL/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptpn11tm1.1Wbm mutation (1 available); any Ptpn11 mutation (30 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

nervous system
• at E11.5, cutaneous, intercostal, and limb sensory neuron projections exhibit reduced axonal arborization compared to in wild-type mice
• however, incubation with wild-type Schwann cells restores axon outgrowth
• at E11.5, cutaneous, intercostal, and limb sensory neuron projections exhibit defasciculation unlike in wild-type mice
• Ret+ enteric neural crest cells are reduced compared to in wild-type mice
• at E11.5, BFABP+ Schwann cell precursors are reduced compared to in wild-type mice
• at E12.5, Sox10+ Schwann cell precursors are not detected in peripheral nerves unlike in wild-type mice
• at E13.5, Schwann cell nuclei in peripheral nerves are virtually absent unlike in wild-type mice
• at E11.5, cutaneous, intercostal, and limb sensory neuron projections exhibit defasciculation and reduced axonal arborization compared to in wild-type mice
• at E12.5, lumbar dorsal root ganglia sensory neurons exhibit increased cell death compared to in wild-type mice
• numbers of sensory neurons in the dorsal root ganglia are strongly reduced compared to in wild-type mice

craniofacial

pigmentation
• melanocytes are reduced in number compared to in wild-type mice

embryo
• Ret+ enteric neural crest cells are reduced compared to in wild-type mice

cellular
• at E11.5, cutaneous, intercostal, and limb sensory neuron projections exhibit reduced axonal arborization compared to in wild-type mice
• however, incubation with wild-type Schwann cells restores axon outgrowth
• at E11.5, cutaneous, intercostal, and limb sensory neuron projections exhibit defasciculation unlike in wild-type mice




Genotype
MGI:3811608
cn34
Allelic
Composition
Pkd1tm3Jzh/Pkd1tm3Jzh
Tg(Wnt1-cre)11Rth/?
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pkd1tm3Jzh mutation (0 available); any Pkd1 mutation (88 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
craniofacial
• the sphenoid bones are much smaller
• early postnatal obliteration of the presphenoid synchondrosis results in the shortening of the presphenoid bone
• the growth of the upper jaw is profoundly retarded where the nasal, premaxillary and maxillary bones are severely reduced in length by three weeks of age
• mineralization of the caudal nasal bone is markedly reduced
• noticeable by three weeks after birth
• maxilla hypoplasia leads to an abnormal apposition of the incisors (class III malocclusion)
• shortened and bent snouts are obvious three weeks after birth resulting from abnormal nasal bone growth in the rostral direction

skeleton
• the sphenoid bones are much smaller
• early postnatal obliteration of the presphenoid synchondrosis results in the shortening of the presphenoid bone
• the growth of the upper jaw is profoundly retarded where the nasal, premaxillary and maxillary bones are severely reduced in length by three weeks of age
• mineralization of the caudal nasal bone is markedly reduced
• noticeable by three weeks after birth
• maxilla hypoplasia leads to an abnormal apposition of the incisors (class III malocclusion)
• early postnatal obliteration of the presphenoid synchondrosis results in the shortening of the sphenoid bones
• there is a population of apoptotic cells in the perichondrium of the presphenoid synchondrosis prior to its closure
• synchondrosal chondrocytes have reduced proliferative activity
• there is a population of apoptotic cells in the perichondrium of the presphenoid synchondrosis prior to its closure
• there is a delay in the intramembranous ossification of the facial and calvarial bones noted at 5 days after birth

growth/size/body
• shortened and bent snouts are obvious three weeks after birth resulting from abnormal nasal bone growth in the rostral direction




Genotype
MGI:3653215
cn35
Allelic
Composition
Gja1tm1Kwi/Gja1tm1Kwi
Tg(Wnt1-cre)11Rth/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gja1tm1Kwi mutation (1 available); any Gja1 mutation (43 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype
• normal embryonic development and cardiac morphogenesis is observed




Genotype
MGI:3697616
cn36
Allelic
Composition
Mkl2Gt(RRJ478)Byg/Mkl2Gt(RRJ478)Byg
Tg(Wnt1-cre)11Rth/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J * CBA/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mkl2Gt(RRJ478)Byg mutation (1 available); any Mkl2 mutation (53 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• fewer than expected numbers of newborns are seen (11.5% instead of the expected 25%), indicating partial lethality, however lethality is lower than in single Mkl2 homozygotes




Genotype
MGI:5659950
cn37
Allelic
Composition
Braftm1Wds/Braftm1Wds
Raf1tm2Bacc/Raf1tm2Bacc
Tg(Wnt1-cre)11Rth/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J * CBA/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Braftm1Wds mutation (0 available); any Braf mutation (38 available)
Raf1tm2Bacc mutation (0 available); any Raf1 mutation (102 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

cardiovascular system
• in 4 of 6 mice at E17.5
• mild conotruncal defects at E16.5
• in 4 of 6 mice at E17.5 with 1 mouse also exhibiting double outlet right ventricle

endocrine/exocrine glands
• in 5 of 8 mice at E16.5 and E17.5
• hypoplastic or malpositioned in 2 of 3 mice at E16.5
• hypoplastic or malpositioned in 2 of 3 mice at E16.5

craniofacial

growth/size/body
N
• mice exhibit normal embryonic crown-rump length

hearing/vestibular/ear
N
• mice exhibit normal external ear

skeleton

immune system
• in 5 of 8 mice at E16.5 and E17.5

hematopoietic system
• in 5 of 8 mice at E16.5 and E17.5

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
cardiofaciocutaneous syndrome DOID:0060233 OMIM:115150
OMIM:615278
OMIM:615279
OMIM:615280
J:144862




Genotype
MGI:5707466
cn38
Allelic
Composition
Hic2Gt(E225A08)1.1Wrst/Hic2Gt(E225A08)1.1Wrst
Tg(Wnt1-cre)11Rth/?
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J * CBA/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hic2Gt(E225A08)1.1Wrst mutation (0 available); any Hic2 mutation (252 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• no embryonic or perinatal lethality




Genotype
MGI:4438212
cn39
Allelic
Composition
Gt(ROSA)26Sortm2(DTA)Riet/Gt(ROSA)26Sor+
Tg(Wnt1-cre)11Rth/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J * CBA/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm2(DTA)Riet mutation (0 available); any Gt(ROSA)26Sor mutation (393 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• numerous anomalies are evident in the branching pattern of the facial nerve




Genotype
MGI:5298219
cn40
Allelic
Composition
Pitx2tm1.1Sac/Pitx2tm2Sac
Tg(Wnt1-cre)11Rth/?
Gt(ROSA)26Sortm1Sor/?
Genetic
Background
involves: 129S1/Sv * 129S4/SvJaeSor * 129X1/SvJ * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1Sor mutation (7 available); any Gt(ROSA)26Sor mutation (393 available)
Pitx2tm1.1Sac mutation (1 available); any Pitx2 mutation (18 available)
Pitx2tm2Sac mutation (0 available); any Pitx2 mutation (18 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
vision/eye
• devoid of pigment except for a cone shaped region in the anterior segment
• retinal pigment layer is normal at E10.5 but pigment loss begins at E12.5
• corneal stroma and epithelium are absent
• hypomorphic hyaloid blood vessels
• muscle bundles present adjacent to the anterior segment
• eye stalk fails to extend at E12.5
• eyes directly attached to ventral diencephalon by E14.5
• retinal ganglion cell axons enter ventral thalamus and form an optic chiasma-like structure
• eyes are not visible externally at E16.5
• eyes present but buried within the skull near the midline directly beneath the brain
• lens and retina present

pigmentation
• devoid of pigment except for a cone shaped region in the anterior segment
• retinal pigment layer is normal at E10.5 but pigment loss begins at E12.5

nervous system

muscle
• muscle bundles present adjacent to the anterior segment




Genotype
MGI:5447985
cn41
Allelic
Composition
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sor+
HhatTg(TFAP2A-cre)1Will/HhatTg(TFAP2A-cre)1Will
Tg(Wnt1-cre)11Rth/0
Genetic
Background
involves: 129S1/Sv * 129S4/SvJaeSor * 129X1/SvJ * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1Sor mutation (7 available); any Gt(ROSA)26Sor mutation (393 available)
HhatTg(TFAP2A-cre)1Will mutation (1 available); any Hhat mutation (18 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• hypoplastic, particularly the trigeminal ganglion
• maxillary branch is consistently narrower than in controls




Genotype
MGI:3639491
cn42
Allelic
Composition
Fgf15tm1Sms/Fgf15tm1Sms
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sor+
Tg(Wnt1-cre)11Rth/0
Genetic
Background
involves: 129S1/Sv * 129S4/SvJaeSor * 129X1/SvJ * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fgf15tm1Sms mutation (1 available); any Fgf15 mutation (8 available)
Gt(ROSA)26Sortm1Sor mutation (7 available); any Gt(ROSA)26Sor mutation (393 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
embryo
• at E12.5, homozygotes exhibit successful septation of the distal outflow tract; however, the number of NCCs contributing to the proximal outflow tract is significantly reduced
• at E9.5, cardiac NCCs migrate to the developing caudal pharyngeal arches of mutant embryos in numbers comparable to those of wild-type embryos; however, at E11.5, NCCs fail to invaginate on the right side of the proximal aortic sac at the level of its connection with the 6th aortic arch arteries
• as a result, the conotruncal cushions remain oriented laterally relative to one another

cardiovascular system
• at E12.5, homozygotes exhibit successful septation of the distal outflow tract; however, the number of NCCs contributing to the proximal outflow tract is significantly reduced
• homozygotes exhibit abnormal NCC behavior during outflow tract remodeling

nervous system
• at E12.5, homozygotes exhibit successful septation of the distal outflow tract; however, the number of NCCs contributing to the proximal outflow tract is significantly reduced

cellular
• at E9.5, cardiac NCCs migrate to the developing caudal pharyngeal arches of mutant embryos in numbers comparable to those of wild-type embryos; however, at E11.5, NCCs fail to invaginate on the right side of the proximal aortic sac at the level of its connection with the 6th aortic arch arteries
• as a result, the conotruncal cushions remain oriented laterally relative to one another




Genotype
MGI:5896991
cn43
Allelic
Composition
Ednrbtm1Nrd/Ednrbtm1Nrd
Gt(ROSA)26Sortm14(CAG-tdTomato)Hze/Gt(ROSA)26Sor+
Tg(Wnt1-cre)11Rth/0
Genetic
Background
involves: 129S1/Sv * 129S6/SvEvTac * 129X1/SvJ * C57BL/6 * CBA/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ednrbtm1Nrd mutation (1 available); any Ednrb mutation (74 available)
Gt(ROSA)26Sortm14(CAG-tdTomato)Hze mutation (2 available); any Gt(ROSA)26Sor mutation (393 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• mice develop intestinal inflammation in both the proximal and mid-colon by P26-29
• however, no inflammation is seen at earlier time points on in the small intestine

hematopoietic system
• mature B-lymphocytes are reduced in Peyers patches and are enriched in the spleen
• the proportion of total B-lymphocytes in Peyers patches is decreased to about 80% of levels seen in controls, indicating a 3.6-fold reduction in the number of B cells
• mice show a decrease of B-lymphocytes in the germinal centers of spleens and a decrease of B-lymphocytes within the marginal zones
• however, no differences in pre/pro-B lymphocyte and mature B lymphocyte populations at P21 in the bone marrow
• mice show a decrease of B-lymphocytes in the germinal centers of spleens
• mice exhibit splenic lymphopenia
• mice show a decrease of B-lymphocytes within the marginal zones
• spleens in P21-P24 mice are smaller in size
• spleens weigh less than those of controls as a proportion of the total body weight
• decrease in the proportion of total (B220+) B-lymphocytes and in the numbers of total B lymphocytes in spleens
• increase in the proportion of mature B-lymphocytes in the spleen, although numbers are decreased
• secretory IgA is decreased in the small intestine
• however, no differences in secretory IgA are seen in the nasal airway lavage or bronchoalveolar lavage and no differences in small bowel luminal IgM levels are seen

immune system
• mice develop intestinal inflammation in both the proximal and mid-colon by P26-29
• however, no inflammation is seen at earlier time points on in the small intestine
• mature B-lymphocytes are reduced in Peyers patches and are enriched in the spleen
• the proportion of total B-lymphocytes in Peyers patches is decreased to about 80% of levels seen in controls, indicating a 3.6-fold reduction in the number of B cells
• mice show a decrease of B-lymphocytes in the germinal centers of spleens and a decrease of B-lymphocytes within the marginal zones
• however, no differences in pre/pro-B lymphocyte and mature B lymphocyte populations at P21 in the bone marrow
• mice show a decrease of B-lymphocytes in the germinal centers of spleens
• mice exhibit splenic lymphopenia
• mice show a decrease of B-lymphocytes within the marginal zones
• spleens in P21-P24 mice are smaller in size
• spleens weigh less than those of controls as a proportion of the total body weight
• decrease in the proportion of total (B220+) B-lymphocytes and in the numbers of total B lymphocytes in spleens
• increase in the proportion of mature B-lymphocytes in the spleen, although numbers are decreased
• secretory IgA is decreased in the small intestine
• however, no differences in secretory IgA are seen in the nasal airway lavage or bronchoalveolar lavage and no differences in small bowel luminal IgM levels are seen
• Peyers patches are hypocellular and exhibit B-cell lymphopenia
• Peyers patches are small in size in P21-P24 mice but have normal architecture




Genotype
MGI:5440183
cn44
Allelic
Composition
Ctnnb1tm2Kem/Ctnnb1tm2.1Kem
Gt(ROSA)26Sortm1(Ctnnb1)Kem/Gt(ROSA)26Sor+
Tg(Wnt1-cre)11Rth/0
Genetic
Background
involves: 129S1/Sv * 129S6/SvEvTac * 129X1/SvJ * C57BL/6J * CBA/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ctnnb1tm2.1Kem mutation (0 available); any Ctnnb1 mutation (32 available)
Ctnnb1tm2Kem mutation (1 available); any Ctnnb1 mutation (32 available)
Gt(ROSA)26Sortm1(Ctnnb1)Kem mutation (0 available); any Gt(ROSA)26Sor mutation (393 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

nervous system
• brain defects

craniofacial
• impaired morphogenesis of craniofacial structures




Genotype
MGI:5440182
cn45
Allelic
Composition
Ctnnb1tm2Kem/Ctnnb1tm2.1Kem
Gt(ROSA)26Sortm1(Ctnnb1)Kem/Gt(ROSA)26Sortm1(Ctnnb1)Kem
Tg(Wnt1-cre)11Rth/0
Genetic
Background
involves: 129S1/Sv * 129S6/SvEvTac * 129X1/SvJ * C57BL/6J * CBA/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ctnnb1tm2.1Kem mutation (0 available); any Ctnnb1 mutation (32 available)
Ctnnb1tm2Kem mutation (1 available); any Ctnnb1 mutation (32 available)
Gt(ROSA)26Sortm1(Ctnnb1)Kem mutation (0 available); any Gt(ROSA)26Sor mutation (393 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• die within hours of birth probably because of an inability to feed




Genotype
MGI:3848967
cn46
Allelic
Composition
Hand2tm1Cse/Hand2tm1Dsr
Tg(Wnt1-cre)11Rth/0
Genetic
Background
involves: 129S1/Sv * 129S7/SvEvBrd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hand2tm1Cse mutation (0 available); any Hand2 mutation (3 available)
Hand2tm1Dsr mutation (0 available); any Hand2 mutation (3 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• embryos begin to die by 12 dpc and no live embryos are recovered at 13 dpc

cardiovascular system
• blood pools in major vessels, heart, liver, and coelom by 12 dpc
• circulatory defects develop by 12 dpc

homeostasis/metabolism
• number of neuronal cells in sympathetic nervous system expressing tyrosine hydroxylase or dopamine beta-hydroxylase is greatly reduced compared to controls at 12.5 dpc

nervous system
N
• neural crest cell colonization of the sympathetic nervous system is normal, and sympathetic nervous system differentiation is unaffected in mutant embryos
• catecholaminergic differentiation of the sympathetic nervous system is abnormal in mutants; fewer neurons produce enzymes needed for synthesis of noradrenaline than in wild-type controls




Genotype
MGI:3715254
cn47
Allelic
Composition
Hand2tm1Cse/Hand2tm1Cse
Tg(Wnt1-cre)11Rth/0
Genetic
Background
involves: 129S1/Sv * 129S7/SvEvBrd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hand2tm1Cse mutation (0 available); any Hand2 mutation (3 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
craniofacial
N
• palate is normal
• no changes in cell proliferation or apoptosis are observed in palatal shelves at E13.5




Genotype
MGI:5902457
cn48
Allelic
Composition
Mapk1tm1Gela/Mapk1tm1Gela
Tg(Wnt1-cre)11Rth/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * C57BL/6J * CBA/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mapk1tm1Gela mutation (1 available); any Mapk1 mutation (28 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

craniofacial
• mandibular asymmetry in newborns, with the proximal region severely affected and the distal region only mildly affected; this asymmetry is associated with the asymmetry of tongue and the elevation of a single palatal shelf
• in newborns, the more severely affected side of the mandible corresponds to the side lacking palatal shelf elevation
• marker analysis indicates an initial decrease in the pool of osteogenic progenitors in the mandible followed by a delay in the osteogenic process
• however, cell proliferation and survival in mandibles at E12.5-E15.5 is similar to controls
• the angle is severely disrupted or completely absent in some mice
• condyle is greatly reduced in size
• the coronoid process is severely disrupted or completely absent in some mice
• newborn mandibles show an approximate 50% reduction in mandibular volume
• micrognathia is detectable by E13.5 and mandibular defects are more severe at E14.5
• when micrognathia affects both sides equally, the tongue is symmetrically positioned in a high location and neither palatal shelf is elevated
• morphology of Meckel's cartilage is disrupted at E14.5, with a reduction in size and a complete discontinuity on one side
• small at E14.5
• complete cleft palate
• palatal shelf elevation is impaired; both anterior and posterior regions of the palate are affected
• elevation defect is seen along the AP axis at E14.5 and E15.5
• in a rotational culture system, palatal shelves (dissected away from the mandible and tongue) from E13.5 mutants are able to elevate but do not fuse, suggesting that palatal shelf elevation defect results from primary malformation in the tongue and/or mandible
• tongues exhibit malposition and disruption of muscle patterning
• typically, one side of the tongue descends whereas the other side remains high, blocking the elevation of one palatal shelf
• absence of tendons in tongues
• cell survival in the tongue and cell proliferation in muscular and neural crest-derived components of the tongue are not affected at E12.5-E14.5 and marker analysis indicates that muscle differentiation in the tongue is not affected
• the organization of fibers in both the intrinsic and extrinsic muscles of the tongue is altered, resulting in gross disruption of the muscle pattern and position
• at E15.5, the extrinsic muscles of the tongue are attached directly to the Meckel's cartilage and in close vicinity to the bone primordium compared to control muscles which are not in contact with the cartilage or the osteogenic progenitors
• approximate 45% reduction in tongue volume

digestive/alimentary system
• complete cleft palate
• palatal shelf elevation is impaired; both anterior and posterior regions of the palate are affected
• elevation defect is seen along the AP axis at E14.5 and E15.5
• in a rotational culture system, palatal shelves (dissected away from the mandible and tongue) from E13.5 mutants are able to elevate but do not fuse, suggesting that palatal shelf elevation defect results from primary malformation in the tongue and/or mandible
• tongues exhibit malposition and disruption of muscle patterning
• typically, one side of the tongue descends whereas the other side remains high, blocking the elevation of one palatal shelf
• absence of tendons in tongues
• cell survival in the tongue and cell proliferation in muscular and neural crest-derived components of the tongue are not affected at E12.5-E14.5 and marker analysis indicates that muscle differentiation in the tongue is not affected
• the organization of fibers in both the intrinsic and extrinsic muscles of the tongue is altered, resulting in gross disruption of the muscle pattern and position
• at E15.5, the extrinsic muscles of the tongue are attached directly to the Meckel's cartilage and in close vicinity to the bone primordium compared to control muscles which are not in contact with the cartilage or the osteogenic progenitors
• approximate 45% reduction in tongue volume

growth/size/body
• complete cleft palate
• palatal shelf elevation is impaired; both anterior and posterior regions of the palate are affected
• elevation defect is seen along the AP axis at E14.5 and E15.5
• in a rotational culture system, palatal shelves (dissected away from the mandible and tongue) from E13.5 mutants are able to elevate but do not fuse, suggesting that palatal shelf elevation defect results from primary malformation in the tongue and/or mandible
• tongues exhibit malposition and disruption of muscle patterning
• typically, one side of the tongue descends whereas the other side remains high, blocking the elevation of one palatal shelf
• absence of tendons in tongues
• cell survival in the tongue and cell proliferation in muscular and neural crest-derived components of the tongue are not affected at E12.5-E14.5 and marker analysis indicates that muscle differentiation in the tongue is not affected
• the organization of fibers in both the intrinsic and extrinsic muscles of the tongue is altered, resulting in gross disruption of the muscle pattern and position
• at E15.5, the extrinsic muscles of the tongue are attached directly to the Meckel's cartilage and in close vicinity to the bone primordium compared to control muscles which are not in contact with the cartilage or the osteogenic progenitors
• approximate 45% reduction in tongue volume

muscle
• the organization of fibers in both the intrinsic and extrinsic muscles of the tongue is altered, resulting in gross disruption of the muscle pattern and position
• at E15.5, the extrinsic muscles of the tongue are attached directly to the Meckel's cartilage and in close vicinity to the bone primordium compared to control muscles which are not in contact with the cartilage or the osteogenic progenitors

skeleton
• mandibular asymmetry in newborns, with the proximal region severely affected and the distal region only mildly affected; this asymmetry is associated with the asymmetry of tongue and the elevation of a single palatal shelf
• in newborns, the more severely affected side of the mandible corresponds to the side lacking palatal shelf elevation
• marker analysis indicates an initial decrease in the pool of osteogenic progenitors in the mandible followed by a delay in the osteogenic process
• however, cell proliferation and survival in mandibles at E12.5-E15.5 is similar to controls
• the angle is severely disrupted or completely absent in some mice
• condyle is greatly reduced in size
• the coronoid process is severely disrupted or completely absent in some mice
• newborn mandibles show an approximate 50% reduction in mandibular volume
• micrognathia is detectable by E13.5 and mandibular defects are more severe at E14.5
• when micrognathia affects both sides equally, the tongue is symmetrically positioned in a high location and neither palatal shelf is elevated
• morphology of Meckel's cartilage is disrupted at E14.5, with a reduction in size and a complete discontinuity on one side
• small at E14.5

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
Weissenbacher-Zweymuller syndrome DOID:4258 OMIM:261800
J:239772




Genotype
MGI:3817490
cn49
Allelic
Composition
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sor+
Isl1tm2Sev/Isl1tm2Sev
Tg(Wnt1-cre)11Rth/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1Sor mutation (7 available); any Gt(ROSA)26Sor mutation (393 available)
Isl1tm2Sev mutation (1 available); any Isl1 mutation (20 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice die within a few hours of birth

nervous system
• cutaneous branch of the ventral ramus is absent in E14.5 embryos
• innervation of the distal limbs at E14.5 confirmed a nearly complete loss of fine cutaneous sensory fibers with only a single sensory branch innervating one side of digits 1, 2 and 5 in both the forelimb and hindlimb
• there is an increased rate of apoptosis within the trigeminal ganglia of E11.5 and E12.5 embryos
• the dorsal root ganglion (DRG) of E12.5 embryos do not express Isl1 protein
• TrkA+ neurons are lower in number starting at E12.5 and by E14.5 are less than one-third of what is found in controls
• TrkB+ neurons are also lower in number starting at E12.5 and are markedly reduced at E14.5 and birth
• TrkC+ neurons do not appear until E12.5, a delay of two days compared to controls
• the DRG of E14.5 embryos is markedly smaller than controls with a smaller number neurons found within the ganglion
• an increased rate of apoptosis is noted in the E12.5 DRG

behavior/neurological
• mice have a reduced response to a mild noxious stimulus that was applied to the skin of the trunk or limbs

integument
• mice have a reduced response to a mild noxious stimulus that was applied to the skin of the trunk or limbs




Genotype
MGI:3711498
cn50
Allelic
Composition
Pygo2tm1.1Ssp/Pygo2tm1.2Ssp
Tg(Wnt1-cre)11Rth/?
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pygo2tm1.1Ssp mutation (1 available); any Pygo2 mutation (15 available)
Pygo2tm1.2Ssp mutation (0 available); any Pygo2 mutation (15 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
vision/eye
• at E12.5, lens size is reduced comparable to Pygo2tm1Lan/Pygo2tm1.1Lan mice




Genotype
MGI:3623411
cn51
Allelic
Composition
Tgfbr2tm1Karl/Tgfbr2tm1Karl
Tg(Wnt1-cre)11Rth/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tgfbr2tm1Karl mutation (1 available); any Tgfbr2 mutation (21 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

craniofacial
• malformations of cranial bones at E18

cardiovascular system
• abnormal branching of the left carotid artery from the brachiocephalic trunk in mutant mice
• venous congestion
• defective separation of the aorta from the pulmonary trunk, leading to persistent truncus arteriosis
• exhibit vasodilatation of the jugular veins
• heart defects lead to functional right-sided heart failure with venous congestion, resulting in a vasodilatation of the jugular veins

endocrine/exocrine glands
• 2 of 5 do not have parathyroid glands
• 3 of 5 exhibit hypoplastic parathyroid glands at E18
• thymus gland is 58% the size of wild-type at E18

immune system
• thymus gland is 58% the size of wild-type at E18

nervous system
• defect in neural crest cell differentiation in the pharyngeal apparatus but not in the migration or survival of neural crest cells
• absence of neural crest-derived smooth muscle cells
• midbrain abnormalities
• hindbrain abnormalities

skeleton
• malformations of cranial bones at E18
• malformation of cartilage at E18

hematopoietic system
• thymus gland is 58% the size of wild-type at E18

digestive/alimentary system

embryo
• defect in neural crest cell differentiation in the pharyngeal apparatus but not in the migration or survival of neural crest cells
• absence of neural crest-derived smooth muscle cells

muscle
• exhibit vasodilatation of the jugular veins

growth/size/body

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
DiGeorge syndrome DOID:11198 OMIM:188400
J:96359




Genotype
MGI:3702775
cn52
Allelic
Composition
Fgfr1tm1Jpa/Fgfr1tm1Jpa
Tg(Wnt1-cre)11Rth/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fgfr1tm1Jpa mutation (1 available); any Fgfr1 mutation (206 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

nervous system
• dorsal cerebellum development is abnormal
• inferior colliculus is deleted in the posterior midbrain
• the vermis is present but severely malformed




Genotype
MGI:3623951
cn53
Allelic
Composition
Gata6tm2Msp/Gata6tm2Msp
Tg(Wnt1-cre)11Rth/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gata6tm2Msp mutation (0 available); any Gata6 mutation (12 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• die between E18.5 and P1

cardiovascular system
• exhibit a spectrum of aortic arch patterning and cardiac outflow tract septation defects indistinguishable from those seen in mice homozygous for Gata6tm2Msp and hemizygous for Tg(Tagln-cre)1Jjl
• hypoplastic aortic arch
• seen as early as E9.5
• membranous ventricular septal defect




Genotype
MGI:3697607
cn54
Allelic
Composition
Acvr1tm1Vk/Acvr1tm1.1Vk
Tg(Wnt1-cre)11Rth/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Acvr1tm1.1Vk mutation (0 available); any Acvr1 mutation (28 available)
Acvr1tm1Vk mutation (0 available); any Acvr1 mutation (28 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mutants that are born alive die during the first postnatal day
• about 40% die in utero (J:90453)
• only 60% of expected numbers are recovered at birth, however the expected numbers are recovered at E14, indicating 40% lethality between E14 and birth (J:90988)

cardiovascular system
• display abnormal regression of the pharyngeal arch arteries
• at E11.5, the 6th arteries display bilaterally inappropriate regression
• at E11.5, the 3rd arteries display bilaterally inappropriate regression
• aortic arch defects
• 77% exhibit either a short or missing brachiocephalic artery so that the right common carotid artery directly branches from the truncus arteriosus
• 77% exhibit either a short or missing brachiocephalic artery
• the distal outflow tract has reduced numbers of neural crest cells
• the proximal outflow tract is essentially devoid of neural crest cells
• differentiation of neural crest cells to smooth muscle around aortic arch arteries is deficient
• the proximal outflow tract is essentially devoid of neural crest cells while the distal outflow tract has reduced numbers of neural crest cells
• outflow tract cushions are reduced in size
• 100% penentrance or persistent truncus arteriosus type A2 (complete failure of outflow tract septation)
• persistent truncus arteriosus is associated with a ventricular septation defect
• 100% penetrance
• 85% show hyperplastic right ventricle

nervous system
• the distal outflow tract has reduced numbers of neural crest cells
• the proximal outflow tract is essentially devoid of neural crest cells
• differentiation of neural crest cells to smooth muscle around aortic arch arteries is deficient

craniofacial
• display abnormal regression of the pharyngeal arch arteries
• at E11.5, the 6th arteries display bilaterally inappropriate regression
• at E11.5, the 3rd arteries display bilaterally inappropriate regression
• enlarged frontal fontanels in newborns
• squamous parts of the frontal bones lack ossification towards the metopic region, resulting in enlarged frontal fontanels in newborns
• squamal bones lack the retrotympanic process
• the temporal squama is smaller, lacking the lower portion with the mandibular fossa and its joint cartilage
• zygomatic arches are incomplete in newborns, with developed maxillary zygomatic process but completely absent jugal (zygomatic) bone and zygomatic process of the squamal bone
• the mandibular fossa and its joint cartilage are missing
• coronoid process of the mandible is rudimentary in size
• the mental symphysis is not formed resulting in persistently separate mandibular bones
• the temporomandibular articulation is undetectable
• hypotrophic mandible is apparent as early as E14
• mandible is about 40% shorter
• completely absent jugal (zygomatic) bone
• slightly shorter manubrium mallei
• the anterior cartilage derived from the distal extremity of Meckel's cartilage is absent
• anterior region of Meckel's cartilage displays retarded growth and also fails to fuse at E15
• display approximately a 3-fold reduction in proliferation of chondrocytes in the anterior and interior parts of Meckel's cartilage at E13
• complete cleft of the secondary palate
• palatal shelves fail to elevate, either bilaterally or unilaterally, at E14
• in newborns, the unfused palatal shelves are bilaterally elevated, indicating that cleft palate develops as a result of delayed, asynchronous elevation of palatal shelves
• newborns have a shorter head

embryo
• display abnormal regression of the pharyngeal arch arteries
• at E11.5, the 6th arteries display bilaterally inappropriate regression
• at E11.5, the 3rd arteries display bilaterally inappropriate regression
• the distal outflow tract has reduced numbers of neural crest cells
• the proximal outflow tract is essentially devoid of neural crest cells
• differentiation of neural crest cells to smooth muscle around aortic arch arteries is deficient
• migration of mutant neural crest cells to the outflow tract is impaired

behavior/neurological
• newborns lack milk in stomachs and fail to suckle

digestive/alimentary system
• complete cleft of the secondary palate
• palatal shelves fail to elevate, either bilaterally or unilaterally, at E14
• in newborns, the unfused palatal shelves are bilaterally elevated, indicating that cleft palate develops as a result of delayed, asynchronous elevation of palatal shelves

hearing/vestibular/ear
• slightly shorter manubrium mallei

skeleton
• enlarged frontal fontanels in newborns
• squamous parts of the frontal bones lack ossification towards the metopic region, resulting in enlarged frontal fontanels in newborns
• squamal bones lack the retrotympanic process
• the temporal squama is smaller, lacking the lower portion with the mandibular fossa and its joint cartilage
• zygomatic arches are incomplete in newborns, with developed maxillary zygomatic process but completely absent jugal (zygomatic) bone and zygomatic process of the squamal bone
• the mandibular fossa and its joint cartilage are missing
• coronoid process of the mandible is rudimentary in size
• the mental symphysis is not formed resulting in persistently separate mandibular bones
• the temporomandibular articulation is undetectable
• hypotrophic mandible is apparent as early as E14
• mandible is about 40% shorter
• completely absent jugal (zygomatic) bone
• slightly shorter manubrium mallei
• secondary cartilage of the mandibular condyle does not develop, making the temporomandibular articulation undetectable
• the secondary cartilage of the mandibular angular process is completely missing
• the anterior cartilage derived from the distal extremity of Meckel's cartilage is absent
• anterior region of Meckel's cartilage displays retarded growth and also fails to fuse at E15
• display approximately a 3-fold reduction in proliferation of chondrocytes in the anterior and interior parts of Meckel's cartilage at E13

cellular
• differentiation of neural crest cells to smooth muscle around aortic arch arteries is deficient
• migration of mutant neural crest cells to the outflow tract is impaired

growth/size/body
• complete cleft of the secondary palate
• palatal shelves fail to elevate, either bilaterally or unilaterally, at E14
• in newborns, the unfused palatal shelves are bilaterally elevated, indicating that cleft palate develops as a result of delayed, asynchronous elevation of palatal shelves
• newborns have a shorter head




Genotype
MGI:3804321
cn55
Allelic
Composition
Gt(ROSA)26Sortm2(Pax3)Joe/Gt(ROSA)26Sor+
Tg(Wnt1-cre)11Rth/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm2(Pax3)Joe mutation (0 available); any Gt(ROSA)26Sor mutation (393 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
craniofacial
• in one mouse

digestive/alimentary system
• in one mouse

growth/size/body
• in one mouse




Genotype
MGI:3804318
cn56
Allelic
Composition
Gt(ROSA)26Sortm2(Pax3)Joe/Gt(ROSA)26Sortm2(Pax3)Joe
Tg(Wnt1-cre)11Rth/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm2(Pax3)Joe mutation (0 available); any Gt(ROSA)26Sor mutation (393 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
craniofacial
• authors state that mice exhibit identical phenotypes as observed in Gt(ROSA)26Sortm2Joe/Gt(ROSA)26Sortm2Joe Pax3tm1(cre)Joe/Pax3+ mice
• authors state that mice exhibit identical phenotypes as observed in Gt(ROSA)26Sortm2Joe/Gt(ROSA)26Sortm2Joe Pax3tm1(cre)Joe/Pax3+ mice

vision/eye
• authors state that mice exhibit identical phenotypes as observed in Gt(ROSA)26Sortm2Joe/Gt(ROSA)26Sortm2Joe Pax3tm1(cre)Joe/Pax3+ mice

digestive/alimentary system
• authors state that mice exhibit identical phenotypes as observed in Gt(ROSA)26Sortm2Joe/Gt(ROSA)26Sortm2Joe Pax3tm1(cre)Joe/Pax3+ mice

growth/size/body
• authors state that mice exhibit identical phenotypes as observed in Gt(ROSA)26Sortm2Joe/Gt(ROSA)26Sortm2Joe Pax3tm1(cre)Joe/Pax3+ mice




Genotype
MGI:3710237
cn57
Allelic
Composition
Nf1tm1Par/Nf1tm1Par
Tg(Wnt1-cre)11Rth/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nf1tm1Par mutation (4 available); any Nf1 mutation (96 available)
Tg(Wnt1-cre)11Rth mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body

respiratory system
• pups do not initiate normal respiration

nervous system
• increase in the number of adrenal medullary cells, suggesting pheochromocytoma
• massively enlarged sympathetic ganglia that consist of axons that stain for neurofilament and small cell bodies with large nuclei that express tyrosine hydroxylase, a morphology consistent with ganglioneuroma or ganglioneurosarcoma

endocrine/exocrine glands
• a thinning and distortion of the adrenal cortex
• increase in the number of adrenal medullary cells, suggesting pheochromocytoma

neoplasm
• develop tumors of neural crest origin such as ganglioneuroma, ganglioneurosarcoma, and pheochromocytoma

cardiovascular system
N
• normal cardiac development