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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Lgr5+
wild type
MGI:2437965
Summary 31 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
ht1
Lgr5em1(IMPC)Kmpc/Lgr5+ C57BL/6NTac-Lgr5em1(IMPC)Kmpc/Kmpc MGI:7472084
ht2
Lgr5tm1(cre/ERT2)Cle/Lgr5+ involves: 129P2/OlaHsd * C57BL/6 MGI:5559881
ht3
Lgr5tm2(Hbegf/EGFP)Fjs/Lgr5+ involves: C57BL/6N MGI:5298068
cn4
Rnf43tm1Cle/Rnf43tm1Cle
Znrf3tm1Cle/Znrf3tm1Cle
Lgr5tm1(cre/ERT2)Cle/Lgr5+
involves: 129P2/OlaHsd MGI:5439368
cn5
Slc39a7tm1.1Tfk/Slc39a7tm1.1Tfk
Lgr5tm1(cre/ERT2)Cle/Lgr5+
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 MGI:5902448
cn6
Rab11atm1.1Ngao/Rab11atm1.1Ngao
Lgr5tm1(cre/ERT2)Cle/Lgr5+
involves: 129P2/OlaHsd * 129S4/SvJae MGI:5608789
cn7
TigarGt(EUCE0047g05)Hmgu/TigarGt(EUCE0047g05)Hmgu
Apctm1Tno/Apctm1Tno
Lgr5tm1(cre/ERT2)Cle/Lgr5+
involves: 129P2/OlaHsd * 129S4/SvJae MGI:5522716
cn8
Apctm1Tno/Apctm1Tno
Lgr5tm1(cre/ERT2)Cle/Lgr5+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:5898006
cn9
Apctm1Tno/Apctm1Tno
Elp3tm1.1Tac/Elp3tm1.1Tac
Lgr5tm1(cre/ERT2)Cle/Lgr5+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * C57BL/6NTac MGI:5898005
cn10
Col1a1tm2(tetO-Pou5f1)Jae/Col1a1+
Gt(ROSA)26Sortm1(tTA)Roos/Gt(ROSA)26Sor+
Lgr5tm1(cre/ERT2)Cle/Lgr5+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA/2J MGI:5508640
cn11
Col1a1tm1(tetO-SOX2)Mjm/Col1a1+
Gt(ROSA)26Sortm1(tTA)Roos/Gt(ROSA)26Sor+
Lgr5tm1(cre/ERT2)Cle/Lgr5+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA/2J MGI:5508638
cn12
Gata6osem3Zfa/Gata6osem3Zfa
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sor+
Lgr5tm1(cre/ERT2)Cle/Lgr5+
involves: 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6 MGI:6367573
cn13
Gata6osem1Zfa/Gata6osem1Zfa
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sor+
Lgr5tm1(cre/ERT2)Cle/Lgr5+
involves: 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6 MGI:6367570
cn14
Nrbp1tm1.1Dja/Nrbp1tm1.2Dja
Lgr5tm1(cre/ERT2)Cle/Lgr5+
involves: 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6J MGI:5427571
cn15
Ctnnb1tm1Mmt/Ctnnb1+
Lgr5tm1(cre/ERT2)Cle/Lgr5+
involves: 129P2/OlaHsd * 129X1/SvJ MGI:5475209
cn16
Cdc42tm1Brak/Cdc42tm1Brak
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Lgr5tm1(cre/ERT2)Cle/Lgr5+
involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6 MGI:5427870
cn17
Hmgcs2tm1.1Yil/Hmgcs2tm1.1Yil
Lgr5tm1(cre/ERT2)Cle/Lgr5+
involves: 129P2/OlaHsd * C3H * C57BL/6 * C57BL/6J MGI:8159407
cn18
Cdx2tm2Fbe/Cdx2tm2Fbe
Lgr5tm1(cre/ERT2)Cle/Lgr5+
involves: 129P2/OlaHsd * C57BL/6 MGI:5308972
cn19
Bptfem1Zfa/Bptfem1Zfa
Lgr5tm1(cre/ERT2)Cle/Lgr5+
involves: 129P2/OlaHsd * C57BL/6 MGI:6367576
cn20
Bptfem1Zfa/Bptfem1Zfa
Ehfem1Zfa/Ehfem1Zfa
Lgr5tm1(cre/ERT2)Cle/Lgr5+
involves: 129P2/OlaHsd * C57BL/6 MGI:6367579
cn21
Gata6osem1Zfa/Gata6osem1Zfa
Lgr5tm1(cre/ERT2)Cle/Lgr5+
involves: 129P2/OlaHsd * C57BL/6 MGI:6367565
cn22
Lgr5tm1(cre/ERT2)Cle/Lgr5+
Stk26tm2.1Zzh/Stk26tm2.1Zzh
involves: 129P2/OlaHsd * C57BL/6 MGI:7491700
cn23
Apctm2.1Cip/Apc+
Lgr5tm1(cre/ERT2)Cle/Lgr5+
involves: 129P2/OlaHsd * C57BL/6 MGI:5432137
cn24
Cdc42tm1Brak/Cdc42tm1Brak
Lgr5tm1(cre/ERT2)Cle/Lgr5+
involves: 129P2/OlaHsd * C57BL/6 MGI:5427869
cn25
Elp3tm1.1Tac/Elp3tm1.1Tac
Lgr5tm1(cre/ERT2)Cle/Lgr5+
involves: 129P2/OlaHsd * C57BL/6 * C57BL/6NTac MGI:5898004
cn26
Rprd1btm1Tshu/Rprd1btm1Tshu
Lgr5tm1(cre/ERT2)Cle/Lgr5+
Tg(Vil1-cre)20Syr/0
involves: 129P2/OlaHsd * C57BL/6 * DBA/2 MGI:6822318
cn27
Rpap3tm1c(KOMP)Wtsi/Rpap3tm1c(KOMP)Wtsi
Lgr5tm1(cre/ERT2)Cle/Lgr5+
involves: 129P2/OlaHsd * C57BL/6N MGI:7310428
cn28
Hmgcs2tm1.1Yil/Hmgcs2tm1.1Yil
Lgr5tm3(cre/ERT2)Cle/Lgr5+
Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/Gt(ROSA)26Sor+
involves: 129S6/SvEvTac * C3H * C57BL/6J * C57BL/6NCrl MGI:8159410
cn29
Lgr5tm3(cre/ERT2)Cle/Lgr5+
Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/Gt(ROSA)26Sor+
involves: 129S6/SvEvTac * C57BL/6J * C57BL/6NCrl MGI:8159416
cx30
Lgr5tm1(cre/ERT2)Cle/Lgr5+
Lrig1tm1.1(cre/ERT2)Rjc/Lrig1tm1.1(cre/ERT2)Rjc
involves: 129 * 129P2/OlaHsd * C57BL/6 MGI:5432135
cx31
Lgr5tm1(cre/ERT2)Cle/Lgr5+
Mex3atm1.1(KOMP)Vlcg/Mex3a+
involves: 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6J * C57BL/6NTac MGI:6430341


Genotype
MGI:7472084
ht1
Allelic
Composition
Lgr5em1(IMPC)Kmpc/Lgr5+
Genetic
Background
C57BL/6NTac-Lgr5em1(IMPC)Kmpc/Kmpc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lgr5em1(IMPC)Kmpc mutation (0 available); any Lgr5 mutation (58 available)
Data Sources
phenotype observed in females
phenotype observed in males
N normal phenotype



Genotype
MGI:5559881
ht2
Allelic
Composition
Lgr5tm1(cre/ERT2)Cle/Lgr5+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lgr5tm1(cre/ERT2)Cle mutation (1 available); any Lgr5 mutation (58 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
N
• mice exhibit normal intestinal morphology and physiology under basal conditions and normal response to irradiation
• intestinal stem cells treated with tamoxifen exhibit impaired organoid formation compared with control cells




Genotype
MGI:5298068
ht3
Allelic
Composition
Lgr5tm2(Hbegf/EGFP)Fjs/Lgr5+
Genetic
Background
involves: C57BL/6N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lgr5tm2(Hbegf/EGFP)Fjs mutation (1 available); any Lgr5 mutation (58 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
N
• diphtheria-treated mice exhibit normal intestinal epithelial migration




Genotype
MGI:5439368
cn4
Allelic
Composition
Rnf43tm1Cle/Rnf43tm1Cle
Znrf3tm1Cle/Znrf3tm1Cle
Lgr5tm1(cre/ERT2)Cle/Lgr5+
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lgr5tm1(cre/ERT2)Cle mutation (1 available); any Lgr5 mutation (58 available)
Rnf43tm1Cle mutation (0 available); any Rnf43 mutation (36 available)
Znrf3tm1Cle mutation (0 available); any Znrf3 mutation (37 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• form after tamoxifen treatment and contain Olfm4+ stem cells and Paneth cells

digestive/alimentary system
• form after tamoxifen treatment and contain Olfm4+ stem cells and Paneth cells




Genotype
MGI:5902448
cn5
Allelic
Composition
Slc39a7tm1.1Tfk/Slc39a7tm1.1Tfk
Lgr5tm1(cre/ERT2)Cle/Lgr5+
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lgr5tm1(cre/ERT2)Cle mutation (1 available); any Lgr5 mutation (58 available)
Slc39a7tm1.1Tfk mutation (0 available); any Slc39a7 mutation (28 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• all tamoxifen-treated mice die within 4 days of gamma irradiation

digestive/alimentary system
N
• tamoxifen-treated mice exhibit normal epithelial organoid and crypt-derived epithelial organoid formation
• tamoxifen-treated mice exhibit massive apoptosis of transit-amplifying cells due to increased ER stress
• degeneration of Paneth cells in tamoxifen-treated mice

homeostasis/metabolism
• all tamoxifen-treated mice die within 4 days of gamma irradiation

endocrine/exocrine glands
• degeneration of Paneth cells in tamoxifen-treated mice




Genotype
MGI:5608789
cn6
Allelic
Composition
Rab11atm1.1Ngao/Rab11atm1.1Ngao
Lgr5tm1(cre/ERT2)Cle/Lgr5+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lgr5tm1(cre/ERT2)Cle mutation (1 available); any Lgr5 mutation (58 available)
Rab11atm1.1Ngao mutation (1 available); any Rab11a mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• increase in proliferation of intestinal epithelial stem cells and the transit-amplifying cells following tamoxifen induction




Genotype
MGI:5522716
cn7
Allelic
Composition
TigarGt(EUCE0047g05)Hmgu/TigarGt(EUCE0047g05)Hmgu
Apctm1Tno/Apctm1Tno
Lgr5tm1(cre/ERT2)Cle/Lgr5+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Tno mutation (5 available); any Apc mutation (156 available)
Lgr5tm1(cre/ERT2)Cle mutation (1 available); any Lgr5 mutation (58 available)
TigarGt(EUCE0047g05)Hmgu mutation (0 available); any Tigar mutation (58 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• in tamoxifen-treated mice compared with Apctm1Tno/Apctm1Tno Lgr5tm1(cre/ERT2)Cle/Lgr5+ mice

neoplasm
• tamoxifen-treated mice exhibit a reduced total tumor burden and average tumor size of abnormally proliferating adenomas in the small intestine and reduced size, but not number, of colon adenomas due to reduced proliferation and increased reactive oxygen species damage compared with Apctm1Tno/Apctm1Tno Lgr5tm1(cre/ERT2)Cle/Lgr5+ mice




Genotype
MGI:5898006
cn8
Allelic
Composition
Apctm1Tno/Apctm1Tno
Lgr5tm1(cre/ERT2)Cle/Lgr5+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Tno mutation (5 available); any Apc mutation (156 available)
Lgr5tm1(cre/ERT2)Cle mutation (1 available); any Lgr5 mutation (58 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• tamoxifen treated mice develop numerous hyperplasias in the intestine

neoplasm
• tamoxifen treated mice develop numerous hyperplasias in the intestine




Genotype
MGI:5898005
cn9
Allelic
Composition
Apctm1Tno/Apctm1Tno
Elp3tm1.1Tac/Elp3tm1.1Tac
Lgr5tm1(cre/ERT2)Cle/Lgr5+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * C57BL/6NTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Tno mutation (5 available); any Apc mutation (156 available)
Elp3tm1.1Tac mutation (0 available); any Elp3 mutation (40 available)
Lgr5tm1(cre/ERT2)Cle mutation (1 available); any Lgr5 mutation (58 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• the amount of Dclk1+/Sox9+ cells in the Lgr5+ population is decreased in ex vivo organoids
• intestinal crypts fail to efficiently generate spheroid structures ex vivo

neoplasm
• tamoxifen treated mice exhibit decreased numbers of hyperplastic foci/polyps in the intestine indicating impaired tumor initiation




Genotype
MGI:5508640
cn10
Allelic
Composition
Col1a1tm2(tetO-Pou5f1)Jae/Col1a1+
Gt(ROSA)26Sortm1(tTA)Roos/Gt(ROSA)26Sor+
Lgr5tm1(cre/ERT2)Cle/Lgr5+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA/2J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm2(tetO-Pou5f1)Jae mutation (1 available); any Col1a1 mutation (166 available)
Gt(ROSA)26Sortm1(tTA)Roos mutation (3 available); any Gt(ROSA)26Sor mutation (1095 available)
Lgr5tm1(cre/ERT2)Cle mutation (1 available); any Lgr5 mutation (58 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• expanded crypts in the ileum of doxycycline-treated mice
• increased cell proliferation in the intestine of doxycycline-treated mice without an increase in Lgr5+ cells

cellular
• in the intestine of doxycycline-treated mice without an increase in Lgr5+ cells

endocrine/exocrine glands
• expanded crypts in the ileum of doxycycline-treated mice




Genotype
MGI:5508638
cn11
Allelic
Composition
Col1a1tm1(tetO-SOX2)Mjm/Col1a1+
Gt(ROSA)26Sortm1(tTA)Roos/Gt(ROSA)26Sor+
Lgr5tm1(cre/ERT2)Cle/Lgr5+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA/2J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm1(tetO-SOX2)Mjm mutation (0 available); any Col1a1 mutation (166 available)
Gt(ROSA)26Sortm1(tTA)Roos mutation (3 available); any Gt(ROSA)26Sor mutation (1095 available)
Lgr5tm1(cre/ERT2)Cle mutation (1 available); any Lgr5 mutation (58 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• lyzsozyme+ Paneth cells in doxycycline-treated mice are not restricted to the base of the crypt unlike in control cells
• expanded crypts in the ileum of doxycycline-treated mice
• increased cell proliferation in the intestine of doxycycline-treated mice with an increase in intestinal stem Lgr5+ cells
• increased proliferation of intestinal stem cells in the intestine of doxycycline-treated mice
• expansion of intestinal stem cells is cell autonomous in doxycycline treated mice

cellular
• in the intestine of doxycycline-treated mice with an increase in Lgr5+ intestinal stem cells
• increased proliferation of intestinal stem cells in the intestine of doxycycline-treated mice
• expansion of intestinal stem cells is cell autonomous in doxycycline treated mice

endocrine/exocrine glands
• lyzsozyme+ Paneth cells in doxycycline-treated mice are not restricted to the base of the crypt unlike in control cells
• expanded crypts in the ileum of doxycycline-treated mice




Genotype
MGI:6367573
cn12
Allelic
Composition
Gata6osem3Zfa/Gata6osem3Zfa
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sor+
Lgr5tm1(cre/ERT2)Cle/Lgr5+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gata6osem3Zfa mutation (0 available); any Gata6os mutation (0 available)
Gt(ROSA)26Sortm1Sor mutation (10 available); any Gt(ROSA)26Sor mutation (1095 available)
Lgr5tm1(cre/ERT2)Cle mutation (1 available); any Lgr5 mutation (58 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• reduced cycling and proliferation of intestinal stem cells
• however, proliferation rates are normal

digestive/alimentary system
• reduced cycling and proliferation of intestinal stem cells
• however, proliferation rates are normal




Genotype
MGI:6367570
cn13
Allelic
Composition
Gata6osem1Zfa/Gata6osem1Zfa
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sor+
Lgr5tm1(cre/ERT2)Cle/Lgr5+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gata6osem1Zfa mutation (0 available); any Gata6os mutation (0 available)
Gt(ROSA)26Sortm1Sor mutation (10 available); any Gt(ROSA)26Sor mutation (1095 available)
Lgr5tm1(cre/ERT2)Cle mutation (1 available); any Lgr5 mutation (58 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• impaired intestinal epithelial renewal in tamoxifen treated mice




Genotype
MGI:5427571
cn14
Allelic
Composition
Nrbp1tm1.1Dja/Nrbp1tm1.2Dja
Lgr5tm1(cre/ERT2)Cle/Lgr5+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lgr5tm1(cre/ERT2)Cle mutation (1 available); any Lgr5 mutation (58 available)
Nrbp1tm1.1Dja mutation (0 available); any Nrbp1 mutation (46 available)
Nrbp1tm1.2Dja mutation (0 available); any Nrbp1 mutation (46 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• authors state that tamoxifen-treated mice exhibit similar phenotype as Nrbp1tm1.1Dja/Nrbp1tm1.1Dja Gt(ROSA)26Sortm1(cre/ERT)Brn/ Gt(ROSA)26Sor+ mice
• abnormal goblet cell production in tamoxifen-treated mice
• abnormal granularization of Paneth cells in tamoxifen-treated mice
• abnormal localization of Paneth cells in tamoxifen-treated mice

endocrine/exocrine glands
• abnormal granularization of Paneth cells in tamoxifen-treated mice
• abnormal localization of Paneth cells in tamoxifen-treated mice

cellular
• abnormal goblet cell production in tamoxifen-treated mice




Genotype
MGI:5475209
cn15
Allelic
Composition
Ctnnb1tm1Mmt/Ctnnb1+
Lgr5tm1(cre/ERT2)Cle/Lgr5+
Genetic
Background
involves: 129P2/OlaHsd * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ctnnb1tm1Mmt mutation (0 available); any Ctnnb1 mutation (47 available)
Lgr5tm1(cre/ERT2)Cle mutation (1 available); any Lgr5 mutation (58 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• 40 days after tamoxifen treatment, mice have developed numerous polyps




Genotype
MGI:5427870
cn16
Allelic
Composition
Cdc42tm1Brak/Cdc42tm1Brak
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Lgr5tm1(cre/ERT2)Cle/Lgr5+
Genetic
Background
involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdc42tm1Brak mutation (0 available); any Cdc42 mutation (44 available)
Gt(ROSA)26Sortm1(EYFP)Cos mutation (23 available); any Gt(ROSA)26Sor mutation (1095 available)
Lgr5tm1(cre/ERT2)Cle mutation (1 available); any Lgr5 mutation (58 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• intestinal crypt stem cells show increased cell death following tamoxifen administration
• 3 weeks after tamoxifen administration, mutant villus epithelial cells show disrupted cell polarity, as indicated by disorganized nuclear alignment
• stem cells contribute less to the villus epithelial compartments than in controls following tamoxifen administration
• 3 weeks after tamoxifen administration, more mutant stem cells in intestinal crypts undergo mitosis compared to control stem cells
• stem cells contribute less to the villus epithelial compartments than in controls following tamoxifen administration, indicating reduced clonal expansion of mutant stem cells
• 2 weeks after tamoxifen administration, mutant stem cells in intestinal crypts fail to give rise to Paneth cells
• 3 weeks after tamoxifen administration, mutant villus epithelial cells show disrupted cell polarity, as indicated by disorganized nuclear alignment

endocrine/exocrine glands
• 3 weeks after tamoxifen administration, more mutant stem cells in intestinal crypts undergo mitosis compared to control stem cells
• stem cells contribute less to the villus epithelial compartments than in controls following tamoxifen administration, indicating reduced clonal expansion of mutant stem cells
• 2 weeks after tamoxifen administration, mutant stem cells in intestinal crypts fail to give rise to Paneth cells

cellular
• intestinal crypt stem cells show increased cell death following tamoxifen administration




Genotype
MGI:8159407
cn17
Allelic
Composition
Hmgcs2tm1.1Yil/Hmgcs2tm1.1Yil
Lgr5tm1(cre/ERT2)Cle/Lgr5+
Genetic
Background
involves: 129P2/OlaHsd * C3H * C57BL/6 * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hmgcs2tm1.1Yil mutation (1 available); any Hmgcs2 mutation (33 available)
Lgr5tm1(cre/ERT2)Cle mutation (1 available); any Lgr5 mutation (58 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• when co-cultured with wild-type Paneth cells, flow-sorted GFPhi intestinal stem cells (ISCs) from tamoxifen (TAM)-treated mice form 42.9% fewer and 34.6% smaller organoids than wild-type ISCs, indicating reduced organoid-initiating capacity
• when adult mice are treated with TAM for 20 days, the % of Lgr5-GFPhi ISCs in small intestinal crypts is reduced by 50% at 1 day after the last TAM injection
• when adult mice are treated with TAM for 20 days, the frequencies of Lgr5-GFPhi ISCs and Lgr5-GFPlow progenitors in small intestinal crypts are reduced by 50% at 1 day after the last TAM injection

endocrine/exocrine glands
• when adult mice are treated with TAM for 20 days, the % of Lgr5-GFPhi ISCs in small intestinal crypts is reduced by 50% at 1 day after the last TAM injection
• when adult mice are treated with TAM for 20 days, the frequencies of Lgr5-GFPhi ISCs and Lgr5-GFPlow progenitors in small intestinal crypts are reduced by 50% at 1 day after the last TAM injection

cellular
• when co-cultured with wild-type Paneth cells, flow-sorted GFPhi intestinal stem cells (ISCs) from tamoxifen (TAM)-treated mice form 42.9% fewer and 34.6% smaller organoids than wild-type ISCs, indicating reduced organoid-initiating capacity




Genotype
MGI:5308972
cn18
Allelic
Composition
Cdx2tm2Fbe/Cdx2tm2Fbe
Lgr5tm1(cre/ERT2)Cle/Lgr5+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdx2tm2Fbe mutation (0 available); any Cdx2 mutation (21 available)
Lgr5tm1(cre/ERT2)Cle mutation (1 available); any Lgr5 mutation (58 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• by 6 weeks after treatment cystic vesicles persist and are often filled with mucous and detritus
• an excess of Paneth cells are found by 19-62 weeks after treatment and these cells contain an abnormally abundant number of normal looking secretory granules
• 4 weeks after treatment with tamoxifen a low level of excess mucous secretion is seen
• by 6 weeks after treatment dying Paneth cells are commonly seen

cellular
• recombined cells fail to migrate out of the crypts and up the villi in the intestine

endocrine/exocrine glands
• by 6 weeks after treatment cystic vesicles persist and are often filled with mucous and detritus
• an excess of Paneth cells are found by 19-62 weeks after treatment and these cells contain an abnormally abundant number of normal looking secretory granules




Genotype
MGI:6367576
cn19
Allelic
Composition
Bptfem1Zfa/Bptfem1Zfa
Lgr5tm1(cre/ERT2)Cle/Lgr5+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bptfem1Zfa mutation (0 available); any Bptf mutation (157 available)
Lgr5tm1(cre/ERT2)Cle mutation (1 available); any Lgr5 mutation (58 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• reduced intestinal stem cells with impaired organoid formation capacity




Genotype
MGI:6367579
cn20
Allelic
Composition
Bptfem1Zfa/Bptfem1Zfa
Ehfem1Zfa/Ehfem1Zfa
Lgr5tm1(cre/ERT2)Cle/Lgr5+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bptfem1Zfa mutation (0 available); any Bptf mutation (157 available)
Ehfem1Zfa mutation (0 available); any Ehf mutation (26 available)
Lgr5tm1(cre/ERT2)Cle mutation (1 available); any Lgr5 mutation (58 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• almost blocked organoid formation from intestinal stem cells

homeostasis/metabolism
• severely impaired intestinal epithelium regeneration after radiation injury compared with wild-type mice




Genotype
MGI:6367565
cn21
Allelic
Composition
Gata6osem1Zfa/Gata6osem1Zfa
Lgr5tm1(cre/ERT2)Cle/Lgr5+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gata6osem1Zfa mutation (0 available); any Gata6os mutation (0 available)
Lgr5tm1(cre/ERT2)Cle mutation (1 available); any Lgr5 mutation (58 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• reduced intestinal stem cells with impaired organoid formation capacity
• however, overexpression of Ehf rescues this phenotype
• short with fewer cells than in wild-type mice
• short with fewer cells than in wild-type mice
• impaired intestinal epithelium regeneration after radiation injury compared with wild-type mice

endocrine/exocrine glands
• short with fewer cells than in wild-type mice

homeostasis/metabolism
• impaired intestinal epithelium regeneration after radiation injury compared with wild-type mice




Genotype
MGI:7491700
cn22
Allelic
Composition
Lgr5tm1(cre/ERT2)Cle/Lgr5+
Stk26tm2.1Zzh/Stk26tm2.1Zzh
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lgr5tm1(cre/ERT2)Cle mutation (1 available); any Lgr5 mutation (58 available)
Stk26tm2.1Zzh mutation (0 available); any Stk26 mutation (11 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• reduced proliferation of intestinal stem cells after 5-fluoruracil (5-FU)-induced killing of proliferating intestinal cells

digestive/alimentary system
• reduced proliferation of intestinal stem cells after 5-fluoruracil (5-FU)-induced killing of proliferating intestinal cells




Genotype
MGI:5432137
cn23
Allelic
Composition
Apctm2.1Cip/Apc+
Lgr5tm1(cre/ERT2)Cle/Lgr5+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm2.1Cip mutation (2 available); any Apc mutation (156 available)
Lgr5tm1(cre/ERT2)Cle mutation (1 available); any Lgr5 mutation (58 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
N
• following tamoxifen treatment, no intestinal tumors are observed




Genotype
MGI:5427869
cn24
Allelic
Composition
Cdc42tm1Brak/Cdc42tm1Brak
Lgr5tm1(cre/ERT2)Cle/Lgr5+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdc42tm1Brak mutation (0 available); any Cdc42 mutation (44 available)
Lgr5tm1(cre/ERT2)Cle mutation (1 available); any Lgr5 mutation (58 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• one week after tamoxifen administration, 56% of mutant crypts show stem cells forming a clustering pattern lacking clear demarcation between each other, while at 3 weeks after tamoxifen administration, 85% do so
• stem cells in mutant crypts 3 weeks after tamoxifen treatment lose the typical triangle shapes and marker analysis indicates disrupted crypt cell polarity
• loss of stem cells
• intestinal crypt cells, most likely Paneth cells, contain large vacuoles
• reduction or absence of Paneth cell granules, indicating loss of Paneth cells

endocrine/exocrine glands
• one week after tamoxifen administration, 56% of mutant crypts show stem cells forming a clustering pattern lacking clear demarcation between each other, while at 3 weeks after tamoxifen administration, 85% do so
• stem cells in mutant crypts 3 weeks after tamoxifen treatment lose the typical triangle shapes and marker analysis indicates disrupted crypt cell polarity
• loss of stem cells
• intestinal crypt cells, most likely Paneth cells, contain large vacuoles
• reduction or absence of Paneth cell granules, indicating loss of Paneth cells




Genotype
MGI:5898004
cn25
Allelic
Composition
Elp3tm1.1Tac/Elp3tm1.1Tac
Lgr5tm1(cre/ERT2)Cle/Lgr5+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * C57BL/6NTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Elp3tm1.1Tac mutation (0 available); any Elp3 mutation (40 available)
Lgr5tm1(cre/ERT2)Cle mutation (1 available); any Lgr5 mutation (58 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
N
• tamoxifen treated mice show normal numbers of Lgr5+ cells in intestinal crypts




Genotype
MGI:6822318
cn26
Allelic
Composition
Rprd1btm1Tshu/Rprd1btm1Tshu
Lgr5tm1(cre/ERT2)Cle/Lgr5+
Tg(Vil1-cre)20Syr/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lgr5tm1(cre/ERT2)Cle mutation (1 available); any Lgr5 mutation (58 available)
Rprd1btm1Tshu mutation (0 available); any Rprd1b mutation (14 available)
Tg(Vil1-cre)20Syr mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• decreased Lgr5-GFP+ cells pre and post tamoxifen treatment
• tamoxifen-treated cultured intestinal crypt organoids exhibit fewer outgrowths and fail to reform after disaggregation unlike control cultures




Genotype
MGI:7310428
cn27
Allelic
Composition
Rpap3tm1c(KOMP)Wtsi/Rpap3tm1c(KOMP)Wtsi
Lgr5tm1(cre/ERT2)Cle/Lgr5+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lgr5tm1(cre/ERT2)Cle mutation (1 available); any Lgr5 mutation (58 available)
Rpap3tm1c(KOMP)Wtsi mutation (0 available); any Rpap3 mutation (34 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype
• tamoxifen-treated mice are normal and survive for 3 weeks at least




Genotype
MGI:8159410
cn28
Allelic
Composition
Hmgcs2tm1.1Yil/Hmgcs2tm1.1Yil
Lgr5tm3(cre/ERT2)Cle/Lgr5+
Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S6/SvEvTac * C3H * C57BL/6J * C57BL/6NCrl
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm9(CAG-tdTomato)Hze mutation (7 available); any Gt(ROSA)26Sor mutation (1095 available)
Hmgcs2tm1.1Yil mutation (1 available); any Hmgcs2 mutation (33 available)
Lgr5tm3(cre/ERT2)Cle mutation (0 available); any Lgr5 mutation (58 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• 12 days after a single TAM injection, mice show a significant increase in the number of mucin+ goblet cells in proximal jejunal crypts
• TAM treatment followed administration of the HDAC inhibitor quisinostat (JNJ, 1 mg/kg, 5 i.p. injections) restores the number of AB/PAS+ goblet cells in proximal jejunal crypts
• when mice are treated with TAM 24 h prior to crypt isolation, ISCs cultured in standard medium are 34.4% less capable of forming organoids, with resulting organoids showing a 40.5% increase in goblet cells and a 64.3% decrease in tdTomato+ cells per organoid relative to controls
• exogenous beta-hydroxybutyrate (beta-OHB), but not lactate (a Paneth niche-derived metabolite that sustains ISC function), restores the organoid-forming capacity and generation of tdTomato + clones and rescues the secretory lineage bias
• 12 and >22 days after a single TAM injection, mice show a significant increase in the number of LYZ1+ Paneth cells in proximal jejunal crypts
• 5 days after a single TAM injection, flow-sorted Lgr5+ ISC-derived tdTomato+ progeny show a 5.8-fold increase in Paneth cells (7.88% vs 1.36% in controls)
• as early 24 h after TAM injection, ISCs generate significantly greater numbers of tdTomato+ Paneth cells in jejunal sections
• TAM treatment followed administration of the HDAC inhibitor quisinostat (JNJ, 1 mg/kg, 5 i.p. injections) restores the number of LYZ+ Paneth cells in proximal jejunal crypts
• TAM-treated mice show a progressive loss of OLFM4+ intestinal stem cells (ISCs) and early progenitors (seen both at 10-12 days and at 17+ days but not at 5-7 days after a single TAM injection), along with an increase in the numbers of Paneth cells and goblet cells in proximal jejunal crypts
• 5 days after a single TAM injection, flow-sorted Lgr5+ ISC-derived tdTomato+ progeny show a modest increase in the fraction stem cells (35.34% vs 22.96% in controls), fewer transit-amplifying progenitors (18.40% vs 25.73% in controls) and a 5.8-fold increase in Paneth cells (7.88% vs 1.36% in controls), along with a weakened Lgr5+ stemness signature in ISCs but only minor effects on proliferation and apoptosis
• 12 days after a single TAM injection, crypt cells show induction of Atoh1 mRNA transcripts and reduction of Hes1 mRNA transcripts by ISH
• 17 days after a single TAM injection, no change in the proliferation or apoptosis of ISCs and progenitors is observed, and small intestine length, crypt depth, and numbers of chromogranin A+ enteroendocrine cells in jejunal crypts are normal
• TAM-treated mice show reduced numbers of H3K27ac-positive and Notch intracellular domain (NICD)-positive crypt cell nuclei, indicating increased class I histone deacetylase (HDAC) activity and less Notch signaling
• TAM treatment followed by administration of the HDAC inhibitor quisinostat (JNJ, 1 mg/kg, 5 i.p. injections) restores the number of H3K27ac-positive and NICD-positive crypt cell nuclei to wild-type numbers
• when mice are fed a ketogenic diet (KTD) for 4 weeks, TAM-treated and then irradiated, the number of tdTomato+ crypts per mm jejunum is significantly higher than in chow-fed control mice, indicating enhanced regenerative output of tdTomato-labeled ISCs after injury
• when mice are treated with TAM 1 day prior to radiation-induced intestinal epithelial injury, ISCs generate 5-fold less labeled tdTomato+ crypts with fewer Lgr5+ ISC-derived labeled progeny extending up crypt-villous units at 5 days post-radiation, and the overall number of surviving intact jejunal crypts is reduced by 2-fold
• oral administration of poly(lactic-co-glycolic acid) (PLGA) encapsulated beta-hydroxybutyrate (beta-OHB) nanoparticles or betaOHB oligomers partially rescues intestinal regeneration after radiation-induced damage
• TAM treatment followed administration of the HDAC inhibitor quisinostat (JNJ, 1 mg/kg, 5 i.p. injections) rescues the decline in ISC numbers and ISC function after radiation-induced injury

endocrine/exocrine glands
• 12 and >22 days after a single TAM injection, mice show a significant increase in the number of LYZ1+ Paneth cells in proximal jejunal crypts
• 5 days after a single TAM injection, flow-sorted Lgr5+ ISC-derived tdTomato+ progeny show a 5.8-fold increase in Paneth cells (7.88% vs 1.36% in controls)
• as early 24 h after TAM injection, ISCs generate significantly greater numbers of tdTomato+ Paneth cells in jejunal sections
• TAM treatment followed administration of the HDAC inhibitor quisinostat (JNJ, 1 mg/kg, 5 i.p. injections) restores the number of LYZ+ Paneth cells in proximal jejunal crypts
• TAM-treated mice show a progressive loss of OLFM4+ intestinal stem cells (ISCs) and early progenitors (seen both at 10-12 days and at 17+ days but not at 5-7 days after a single TAM injection), along with an increase in the numbers of Paneth cells and goblet cells in proximal jejunal crypts
• 5 days after a single TAM injection, flow-sorted Lgr5+ ISC-derived tdTomato+ progeny show a modest increase in the fraction stem cells (35.34% vs 22.96% in controls), fewer transit-amplifying progenitors (18.40% vs 25.73% in controls) and a 5.8-fold increase in Paneth cells (7.88% vs 1.36% in controls), along with a weakened Lgr5+ stemness signature in ISCs but only minor effects on proliferation and apoptosis
• 12 days after a single TAM injection, crypt cells show induction of Atoh1 mRNA transcripts and reduction of Hes1 mRNA transcripts by ISH
• 17 days after a single TAM injection, no change in the proliferation or apoptosis of ISCs and progenitors is observed, and small intestine length, crypt depth, and numbers of chromogranin A+ enteroendocrine cells in jejunal crypts are normal
• TAM-treated mice show reduced numbers of H3K27ac-positive and Notch intracellular domain (NICD)-positive crypt cell nuclei, indicating increased class I histone deacetylase (HDAC) activity and less Notch signaling
• TAM treatment followed by administration of the HDAC inhibitor quisinostat (JNJ, 1 mg/kg, 5 i.p. injections) restores the number of H3K27ac-positive and NICD-positive crypt cell nuclei to wild-type numbers

homeostasis/metabolism
• mice treated with TAM 1 day prior to radiation-induced intestinal epithelial injury show impaired Lgr5+ ISC-mediated repair in jejunal crypts relative to controls
• oral administration of nanoparticle PLGA-encapsulated beta-OHB or betaOHB oligomers partially rescues intestinal regeneration after radiation-induced damage
• when mice are fed a ketogenic diet (KTD) for 4 weeks, TAM-treated and then irradiated, the number of tdTomato+ crypts per mm jejunum is significantly higher than in chow-fed controls, indicating enhanced regenerative output of tdTomato-labeled ISCs after injury
• TAM treatment followed administration of the HDAC inhibitor quisinostat (JNJ, 1 mg/kg, 5 i.p. injections) rescues the decline in ISC numbers and ISC function after radiation-induced injury

cellular
• 12 days after a single TAM injection, mice show a significant increase in the number of mucin+ goblet cells in proximal jejunal crypts
• TAM treatment followed administration of the HDAC inhibitor quisinostat (JNJ, 1 mg/kg, 5 i.p. injections) restores the number of AB/PAS+ goblet cells in proximal jejunal crypts
• when mice are treated with TAM 24 h prior to crypt isolation, ISCs cultured in standard medium are 34.4% less capable of forming organoids, with resulting organoids showing a 40.5% increase in goblet cells and a 64.3% decrease in tdTomato+ cells per organoid relative to controls
• exogenous beta-hydroxybutyrate (beta-OHB), but not lactate (a Paneth niche-derived metabolite that sustains ISC function), restores the organoid-forming capacity and generation of tdTomato + clones and rescues the secretory lineage bias




Genotype
MGI:8159416
cn29
Allelic
Composition
Lgr5tm3(cre/ERT2)Cle/Lgr5+
Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6J * C57BL/6NCrl
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm9(CAG-tdTomato)Hze mutation (7 available); any Gt(ROSA)26Sor mutation (1095 available)
Lgr5tm3(cre/ERT2)Cle mutation (0 available); any Lgr5 mutation (58 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• when mice are fed with a glucose-supplemented chow diet for 2 weeks and treated with TAM prior to radiation-induced intestinal injury, the ability of ISCs to generate tdTomato+ labeled progeny is reduced by 2-fold while the overall number of surviving intact jejunal crypts is significantly decreased at 3 days post-radiation
• a single oral bolus of beta-hydroxybutyrate (beta-OHB) 16 h prior to irradiation rescues these functional deficits

homeostasis/metabolism
• when mice are fed with a glucose-supplemented chow diet for 2 weeks and treated with TAM prior to radiation-induced intestinal injury, the ability of intestinal stem cells (ISCs) to generate tdTomato+ labeled progeny is reduced by 2-fold while the overall number of surviving intact jejunal crypts is significantly decreased at 3 days post-radiation
• a single oral bolus of beta-hydroxybutyrate (beta-OHB) 16 h prior to irradiation rescues these functional deficits




Genotype
MGI:5432135
cx30
Allelic
Composition
Lgr5tm1(cre/ERT2)Cle/Lgr5+
Lrig1tm1.1(cre/ERT2)Rjc/Lrig1tm1.1(cre/ERT2)Rjc
Genetic
Background
involves: 129 * 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lgr5tm1(cre/ERT2)Cle mutation (1 available); any Lgr5 mutation (58 available)
Lrig1tm1.1(cre/ERT2)Rjc mutation (1 available); any Lrig1 mutation (49 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• at 5-6 months, nearly 90% of mice develop duodenal tumors (usually low grade adenomas)
• in one instance, a 13-month old mouse had a tumor with areas showing high grade dysplasia, and focal extension of neoplastic glands into deeper layers of the bowel wall; tumor showed intact Apc however

digestive/alimentary system
• number of crypts showing Lgr5-EGFP fluorescence is doubled in absence of Lrig1 protein, compared to mice with one or two copies of Lrig1
• at 5-6 months, nearly 90% of mice develop duodenal tumors (usually low grade adenomas)
• in one instance, a 13-month old mouse had a tumor with areas showing high grade dysplasia, and focal extension of neoplastic glands into deeper layers of the bowel wall; tumor showed intact Apc however

endocrine/exocrine glands
• number of crypts showing Lgr5-EGFP fluorescence is doubled in absence of Lrig1 protein, compared to mice with one or two copies of Lrig1




Genotype
MGI:6430341
cx31
Allelic
Composition
Lgr5tm1(cre/ERT2)Cle/Lgr5+
Mex3atm1.1(KOMP)Vlcg/Mex3a+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6J * C57BL/6NTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lgr5tm1(cre/ERT2)Cle mutation (1 available); any Lgr5 mutation (58 available)
Mex3atm1.1(KOMP)Vlcg mutation (0 available); any Mex3a mutation (27 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 16% of mice exhibit postnatal lethality associated with disturbances in the intestinal epithelium

digestive/alimentary system
• disturbances in the intestinal epithelium
• loss of Lgr5+ intestinal stem cells in the intestine

endocrine/exocrine glands
• loss of Lgr5+ intestinal stem cells in the intestine





Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
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last database update
03/18/2025
MGI 6.24
The Jackson Laboratory