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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(Tyr-cre)1Lru
transgene insertion 1, Lionel Larue
MGI:3573939
Summary 19 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Ctnnb1tm2Kem/Ctnnb1tm2Kem
Tg(Tyr-cre)1Lru/0
B6.Cg-Ctnnb1tm2Kem Tg(Tyr-cre)1Lru MGI:6272341
cn2
Ctnnb1tm2Kem/Ctnnb1tm2Kem
Tg(Dct-lacZ)A12Jkn/0
Tg(Tyr-cre)1Lru/0
B6.Cg-Ctnnb1tm2Kem Tg(Tyr-cre)1Lru Tg(Dct-lacZ)A12Jkn MGI:6272344
cn3
Ptentm1Hwu/Ptentm1Hwu
Tg(Tyr-cre)1Lru/0
B6.Cg-Ptentm1Hwu Tg(Tyr-cre)1Lru MGI:4882033
cn4
Ppargc1atm2Brsp/Ppargc1atm2Brsp
Ppargc1btm1Dpk/Ppargc1btm1Dpk
Tg(Tyr-cre)1Lru/0
involves: 129 * 129X1/SvJ * C57BL/6 MGI:6272349
cn5
Acvr2atm1Hsch/Acvr2atm1Hsch
Bmpr2tm1.1Enl/Bmpr2tm1.1Enl
Tg(Tyr-cre)1Lru/Y
involves: 129S1/Sv * 129S4/SvJae * C57BL/6 * DBA/2 MGI:6258677
cn6
Acvr2atm1Hsch/Acvr2atm1Hsch
Bmpr2tm1.1Enl/Bmpr2tm1.1Enl
Tg(Tyr-cre)1Lru/0
involves: 129S1/Sv * 129S4/SvJae * C57BL/6 * DBA/2 MGI:6258685
cn7
Zeb2tm1.1Yhi/Zeb2tm1.1Yhi
Tg(Dct-lacZ)A12Jkn/0
Tg(Tyr-cre)1Lru/Y
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA * DBA/2 MGI:6220636
cn8
Fscn1Gt(OST124903)Lex/Fscn1Gt(OST124903)Lex
Tg(CAG-Bgeo/GFP)21Lbe/0
Tg(Tyr-cre)1Lru/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA/2 MGI:6209605
cn9
Zeb2tm1.1Yhi/Zeb2tm1.1Yhi
Tg(Tyr-cre)1Lru/Y
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA/2 MGI:6220632
cn10
Yy1tm2.1Yshi/Yy1tm2.1Yshi
Tg(Dct-lacZ)A12Jkn/0
Tg(Tyr-cre)1Lru/Y
involves: 129S4/SvJae * C57BL/6 * CBA * DBA/2 MGI:6226060
cn11
Resttm1.1Yasu/Rest+
Tg(Tyr-cre)1Lru/Y
involves: 129S4/SvJae * C57BL/6 * DBA/2 MGI:6241517
cn12
Yy1tm2.1Yshi/Yy1tm2.1Yshi
Tg(Tyr-cre)1Lru/Y
involves: 129S4/SvJae * C57BL/6 * DBA/2 MGI:6226058
cn13
Resttm1.1Yasu/Resttm1.1Yasu
Tg(Tyr-cre)1Lru/Y
involves: 129S4/SvJae * C57BL/6 * DBA/2 MGI:6241524
cn14
Atg7tm1Tchi/Atg7tm1Tchi
Tg(Tyr-cre)1Lru/Y
involves: C57BL/6 * C57BL/6NCrlj * CBA/JNCrlj * DBA/2 MGI:6209426
cn15
Chek1tm1Jmr/Chek1+
Tg(Dct-lacZ)A12Jkn/0
Tg(Tyr-cre)1Lru/Y
involves: C57BL/6 * CBA * DBA/2 MGI:6220869
cn16
Chek1tm1Jmr/Chek1tm1Jmr
Tg(Dct-lacZ)A12Jkn/0
Tg(Tyr-cre)1Lru/Y
involves: C57BL/6 * CBA * DBA/2 MGI:6220868
cn17
Nrastm1Tyj/Nras+
Tg(Tyr-cre)1Lru/0
involves: C57BL/6 * DBA/2 MGI:5755101
cn18
Nrastm1Tyj/Nrastm1Tyj
Tg(Tyr-cre)1Lru/0
involves: C57BL/6 * DBA/2 MGI:5755097
cn19
Chek1tm1Jmr/Chek1tm1Jmr
Tg(Tyr-cre)1Lru/Y
involves: C57BL/6 * DBA/2 MGI:6220867


Genotype
MGI:6272341
cn1
Allelic
Composition
Ctnnb1tm2Kem/Ctnnb1tm2Kem
Tg(Tyr-cre)1Lru/0
Genetic
Background
B6.Cg-Ctnnb1tm2Kem Tg(Tyr-cre)1Lru
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ctnnb1tm2Kem mutation (1 available); any Ctnnb1 mutation (49 available)
Tg(Tyr-cre)1Lru mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
pigmentation
• at 7 days of age, mice show absence of pigmentation in the hair follicle bulbs, unlike wild-type controls
• spectrophotometry revealed absence of melanin in hairs, unlike in wild-type controls
• mice exhibit white ears, similar to their coat pigmentation
• mice exhibit white tails, similar to their coat pigmentation
• mice exhibit a white coat color, unlike the black coat color of wild-type controls

integument
• at 7 days of age, mice show absence of pigmentation in the hair follicle bulbs, unlike wild-type controls
• spectrophotometry revealed absence of melanin in hairs, unlike in wild-type controls
• mice exhibit white ears, similar to their coat pigmentation
• mice exhibit white tails, similar to their coat pigmentation
• mice exhibit a white coat color, unlike the black coat color of wild-type controls




Genotype
MGI:6272344
cn2
Allelic
Composition
Ctnnb1tm2Kem/Ctnnb1tm2Kem
Tg(Dct-lacZ)A12Jkn/0
Tg(Tyr-cre)1Lru/0
Genetic
Background
B6.Cg-Ctnnb1tm2Kem Tg(Tyr-cre)1Lru Tg(Dct-lacZ)A12Jkn
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ctnnb1tm2Kem mutation (1 available); any Ctnnb1 mutation (49 available)
Tg(Dct-lacZ)A12Jkn mutation (4 available)
Tg(Tyr-cre)1Lru mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
embryo
• overall, melanoblasts exhibit a much lower level of BrdU incorporation in the epidermis (E12.5 to E14.5) and dermis (E14.5) relative to wild-type controls
• however, no differences in apoptosis, cell differentiation or fate are observed
• in the trunk region, melanoblast number is normal at E10.5 but significantly lower than that in wild-type controls at each developmental stage from E12.5 to E15.5; this difference increases with time
• at E14.5, melanoblasts are less abundant than in mice hemizygous for the Tg(Tyr-Ctnnb1/EGFP)#Lru transgene, reflecting the differences in coat color observed after birth
• although melanoblast numbers are reduced in both the epidermis and dermis, the reduction is far greater in the epidermis than in the dermis

cellular
• overall, melanoblasts exhibit a much lower level of BrdU incorporation in the epidermis (E12.5 to E14.5) and dermis (E14.5) relative to wild-type controls
• however, no differences in apoptosis, cell differentiation or fate are observed

nervous system
• in the trunk region, melanoblast number is normal at E10.5 but significantly lower than that in wild-type controls at each developmental stage from E12.5 to E15.5; this difference increases with time
• at E14.5, melanoblasts are less abundant than in mice hemizygous for the Tg(Tyr-Ctnnb1/EGFP)#Lru transgene, reflecting the differences in coat color observed after birth
• although melanoblast numbers are reduced in both the epidermis and dermis, the reduction is far greater in the epidermis than in the dermis




Genotype
MGI:4882033
cn3
Allelic
Composition
Ptentm1Hwu/Ptentm1Hwu
Tg(Tyr-cre)1Lru/0
Genetic
Background
B6.Cg-Ptentm1Hwu Tg(Tyr-cre)1Lru
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm1Hwu mutation (16 available); any Pten mutation (81 available)
Tg(Tyr-cre)1Lru mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Smaller body size of Ptentm1Hwu/Ptentm1Hwu Tg(Tyr-cre)1Lru/0 (HM) mice at P20

mortality/aging
• die between 13 and 20 days after birth

growth/size/body
• although mutants are similar in weight and size as wild-type mice on P2, they fail to gain as much weight over the next 20 days as controls

digestive/alimentary system
• mutants exhibit some intraluminal bubbles along the gastrointestinal tract
• mutants exhibit intestinal pseudoobstruction
• dilatation of the cecum
• mutants exhibit intestinal pseudoobstruction

nervous system
• hypertrophy and hyperplasia of the myenteric and submucosal plexus in the enteric nervous system by 2 weeks of age resulting in ganglioneuromatosis
• enteric ganglia are bigger than in wild-type at P15
• hyperplasia is observed in enteric neuronal cells at E17.5 while hypertrophy of enteric neuronal cells is only seen after birth and not during embryonic development

pigmentation
• hyperpigmentation in the tail, pinna, paws, skin, and olfactory bulb

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
intestinal pseudo-obstruction DOID:0080072 J:155110




Genotype
MGI:6272349
cn4
Allelic
Composition
Ppargc1atm2Brsp/Ppargc1atm2Brsp
Ppargc1btm1Dpk/Ppargc1btm1Dpk
Tg(Tyr-cre)1Lru/0
Genetic
Background
involves: 129 * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ppargc1atm2Brsp mutation (0 available); any Ppargc1a mutation (47 available)
Ppargc1btm1Dpk mutation (1 available); any Ppargc1b mutation (56 available)
Tg(Tyr-cre)1Lru mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
pigmentation
N
• on a C57BL/6 background, mice show no change in baseline coat color relative to control mice




Genotype
MGI:6258677
cn5
Allelic
Composition
Acvr2atm1Hsch/Acvr2atm1Hsch
Bmpr2tm1.1Enl/Bmpr2tm1.1Enl
Tg(Tyr-cre)1Lru/Y
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Acvr2atm1Hsch mutation (0 available); any Acvr2a mutation (38 available)
Bmpr2tm1.1Enl mutation (1 available); any Bmpr2 mutation (45 available)
Tg(Tyr-cre)1Lru mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
pigmentation
• male pups show a dramatic hypopigmentation of the hair coat
• gray-haired skin shows normal melanocyte distribution but substantially less melanin in the hair follicles than control skin
• a reduction in melanin is noted in the hair bulb, where melanocytes form a conical cluster
• a reduction in melanin is noted in the hair shaft
• male pups develop uniformly gray coats; gray hair develops during the first period of hair production
• melanocytes of gray-haired skin produce numerous, dakly-pigmented miniaturized melanosomes, indicating impaired melanosome growth with no significant reduction in melanosome number or pigment-making ability
• failure of melanosomes to grow leads to less production/accumulation of melanin per melanosome
• miniaturized melanosomes are still transferred to epithelial cells of the hair shaft but hair shafts receive less pigment in total, resulting in hypopigmentation and gray color

integument
• male pups show a dramatic hypopigmentation of the hair coat
• gray-haired skin shows normal melanocyte distribution but substantially less melanin in the hair follicles than control skin
• a reduction in melanin is noted in the hair bulb, where melanocytes form a conical cluster
• a reduction in melanin is noted in the hair shaft
• male pups develop uniformly gray coats; gray hair develops during the first period of hair production




Genotype
MGI:6258685
cn6
Allelic
Composition
Acvr2atm1Hsch/Acvr2atm1Hsch
Bmpr2tm1.1Enl/Bmpr2tm1.1Enl
Tg(Tyr-cre)1Lru/0
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Acvr2atm1Hsch mutation (0 available); any Acvr2a mutation (38 available)
Bmpr2tm1.1Enl mutation (1 available); any Bmpr2 mutation (45 available)
Tg(Tyr-cre)1Lru mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
pigmentation
• female pups develop gray hair mosaically, consistent with the mosaic inactivation of the transgene-carrying X chromosome

integument
• female pups develop gray hair mosaically, consistent with the mosaic inactivation of the transgene-carrying X chromosome




Genotype
MGI:6220636
cn7
Allelic
Composition
Zeb2tm1.1Yhi/Zeb2tm1.1Yhi
Tg(Dct-lacZ)A12Jkn/0
Tg(Tyr-cre)1Lru/Y
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Dct-lacZ)A12Jkn mutation (4 available)
Tg(Tyr-cre)1Lru mutation (1 available)
Zeb2tm1.1Yhi mutation (1 available); any Zeb2 mutation (76 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
pigmentation
• at P5.5, mice show significantly fewer pigmented or LacZ+ hair follicles than control mice; also, completely undifferentiated hair follicles that are neither pigmented nor LacZ+ are observed, unlike in control mice
• at P5.5, the total number of melanocytes (S100b+) per hair follicle is reduced by 40% relative to that in control mice
• at P5.5, mice exhibit formation of undifferentiated melanocytes in the bulge area of hair follicles, along with loss of MITF (the master regulator of melanocyte development) and upregulation of ZEB1 expression
• the number of MITF+ melanocytes is strongly reduced relative to the total number of melanocytes per hair follicle (S100b+ melanocytes), whereas the number of PAX3+ melanocytes is normal; also, MITF protein levels are reduced in MITF+ cells
• most hair follicles are negative for terminal melanocyte differentiation markers, such as TYRP1 and tyrosinase enzymatic activity
• mRNA expression of several melanocyte differentiation markers (Tyrp1,Tyr, Dct, Pmel, Mc1R and Mitf) is significantly down-regulated in skin at E15.5
• at P5.5, a few remaining melanosomes are visible in some hair follicles; however, these melanosomes are spherical with irregular borders, unlike the rod-shaped melanosomes of control hair follicles
• at P5.5, ZEB2-stained sections revealed absence of melanin in most melanocytes of the bulb area
• at P5.5, ZEB2-stained sections revealed absence of melanin in the hair shafts

integument
• at P5.5, mice show significantly fewer pigmented or LacZ+ hair follicles than control mice; also, completely undifferentiated hair follicles that are neither pigmented nor LacZ+ are observed, unlike in control mice
• at P5.5, the total number of melanocytes (S100b+) per hair follicle is reduced by 40% relative to that in control mice
• at P5.5, mice exhibit formation of undifferentiated melanocytes in the bulge area of hair follicles, along with loss of MITF (the master regulator of melanocyte development) and upregulation of ZEB1 expression
• the number of MITF+ melanocytes is strongly reduced relative to the total number of melanocytes per hair follicle (S100b+ melanocytes), whereas the number of PAX3+ melanocytes is normal; also, MITF protein levels are reduced in MITF+ cells
• most hair follicles are negative for terminal melanocyte differentiation markers, such as TYRP1 and tyrosinase enzymatic activity
• mRNA expression of several melanocyte differentiation markers (Tyrp1,Tyr, Dct, Pmel, Mc1R and Mitf) is significantly down-regulated in skin at E15.5
• at P5.5, ZEB2-stained sections revealed absence of melanin in most melanocytes of the bulb area
• at P5.5, ZEB2-stained sections revealed absence of melanin in the hair shafts
• mice show a reduction in LacZ+ melanocyte stem cells in the bulge area relative to control mice, consistent with fewer melanoblasts found in the epidermis

embryo
• at E15.5, the number of LacZ+ melanoblasts in the epidermis of both the belly and the back is significantly lower than that in control embryos; however, 30% of them reach the dorsal area (back) at E15.5
• at P5.5, some hair follicles are still LacZ+ and/or (hypo-)pigmented, indicating that melanoblasts can migrate and populate the bulb area of the hair follicles
• the number of melanoblasts present in the dermis at E15.5 is normal
• at E15.5, the number of LacZ+ melanoblasts is significantly reduced in both dorsal and ventral areas relative to control embryos; melanoblast numbers are reduced more on the belly (95%) than on the back (70%), consistent with a migration defect
• at E15.5, melanoblasts exhibit less cell protrusions than control cells

nervous system
• at E15.5, the number of LacZ+ melanoblasts is significantly reduced in both dorsal and ventral areas relative to control embryos; melanoblast numbers are reduced more on the belly (95%) than on the back (70%), consistent with a migration defect
• at E15.5, melanoblasts exhibit less cell protrusions than control cells

cellular
• at E15.5, the number of LacZ+ melanoblasts in the epidermis of both the belly and the back is significantly lower than that in control embryos; however, 30% of them reach the dorsal area (back) at E15.5
• at P5.5, some hair follicles are still LacZ+ and/or (hypo-)pigmented, indicating that melanoblasts can migrate and populate the bulb area of the hair follicles
• the number of melanoblasts present in the dermis at E15.5 is normal




Genotype
MGI:6209605
cn8
Allelic
Composition
Fscn1Gt(OST124903)Lex/Fscn1Gt(OST124903)Lex
Tg(CAG-Bgeo/GFP)21Lbe/0
Tg(Tyr-cre)1Lru/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fscn1Gt(OST124903)Lex mutation (1 available); any Fscn1 mutation (42 available)
Tg(CAG-Bgeo/GFP)21Lbe mutation (2 available)
Tg(Tyr-cre)1Lru mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
embryo
• melanoblasts in E14.5 skin explants show significantly reduced cell migration speed and euclidean distance travelled relative to wild-type controls
• ~30% of melanoblasts migrate with a speed slower than 0.5 um/minute versus fewer than 10% of melanoblasts in wild-type explants
• however, directionality (the ratio between the euclidean distance and total distance travelled) is normal
• melanoblasts in E14.5 live skin explants are slightly smaller than wild type
• the rate of pseudopod generation in melanoblasts is modestly reduced but the lifetime of pseudopods is increased
• melanoblasts extend thinner protrusions with a smaller cross-sectional width than wild type controls
• thinner pseudopodia are less dynamic (longer-lived) leading to slower melanoblast migration

cellular
• melanoblasts in E14.5 skin explants show significantly reduced cell migration speed and euclidean distance travelled relative to wild-type controls
• ~30% of melanoblasts migrate with a speed slower than 0.5 um/minute versus fewer than 10% of melanoblasts in wild-type explants
• however, directionality (the ratio between the euclidean distance and total distance travelled) is normal

nervous system
• melanoblasts in E14.5 live skin explants are slightly smaller than wild type
• the rate of pseudopod generation in melanoblasts is modestly reduced but the lifetime of pseudopods is increased
• melanoblasts extend thinner protrusions with a smaller cross-sectional width than wild type controls
• thinner pseudopodia are less dynamic (longer-lived) leading to slower melanoblast migration




Genotype
MGI:6220632
cn9
Allelic
Composition
Zeb2tm1.1Yhi/Zeb2tm1.1Yhi
Tg(Tyr-cre)1Lru/Y
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Tyr-cre)1Lru mutation (1 available)
Zeb2tm1.1Yhi mutation (1 available); any Zeb2 mutation (76 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
pigmentation
• at 4-6 months of age, the melanin content of the dorsal and ventral hair shafts is reduced by 93% and 91%, respectively
• light microscopy confirmed the loss of melanin pigment from the hair shafts; however, hair with mixed pigmentation are also observed
• mice show severe congenital loss of hair pigmentation relative to control mice
• loss of hair pigmentation is evident from the first hair cycle and continues through adulthood
• however, eyes remain pigmented

integument
• at 4-6 months of age, the melanin content of the dorsal and ventral hair shafts is reduced by 93% and 91%, respectively
• light microscopy confirmed the loss of melanin pigment from the hair shafts; however, hair with mixed pigmentation are also observed




Genotype
MGI:6226060
cn10
Allelic
Composition
Yy1tm2.1Yshi/Yy1tm2.1Yshi
Tg(Dct-lacZ)A12Jkn/0
Tg(Tyr-cre)1Lru/Y
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * CBA * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Dct-lacZ)A12Jkn mutation (4 available)
Tg(Tyr-cre)1Lru mutation (1 available)
Yy1tm2.1Yshi mutation (0 available); any Yy1 mutation (34 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Absence of melanocytes or pigment in hair follicles of Yy1tm2.1Yshi/Yy1tm2.1Yshi Tg(Tyr-cre)1Lru/Y Tg(Dct-lacZ)A12Jkn/0 mice at the anagen phase of the second hair cycle

pigmentation
• mice show absence of differentiated melanocytes in hair follicles at the anagen phase of the second hair cycle (P38)
• mice show absence of pigment in hair follicles at the anagen phase of the second hair cycle (P38)
• absence of differentiated melanocytes in hair follicles at P38

integument
• mice show absence of differentiated melanocytes in hair follicles at the anagen phase of the second hair cycle (P38)
• mice show absence of pigment in hair follicles at the anagen phase of the second hair cycle (P38)

embryo
• absence of Dct-LacZ+ melanocyte stem cells (melanoblasts) in hair follicles at P38

nervous system
• absence of Dct-LacZ+ melanocyte stem cells (melanoblasts) in hair follicles at P38




Genotype
MGI:6241517
cn11
Allelic
Composition
Resttm1.1Yasu/Rest+
Tg(Tyr-cre)1Lru/Y
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Resttm1.1Yasu mutation (1 available); any Rest mutation (95 available)
Tg(Tyr-cre)1Lru mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
pigmentation
N
• mice never form white spots including on the belly region




Genotype
MGI:6226058
cn12
Allelic
Composition
Yy1tm2.1Yshi/Yy1tm2.1Yshi
Tg(Tyr-cre)1Lru/Y
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Tyr-cre)1Lru mutation (1 available)
Yy1tm2.1Yshi mutation (0 available); any Yy1 mutation (34 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Skin and hair pigmentation phenotype of Yy1tm2.1Yshi/Yy1tm2.1Yshi Tg(Tyr-cre)1Lru/Y mice

pigmentation
• mice exhibit premature gray hair after the first hair cycle
• during the first hair cycle (P0-P28), P10 ventral hairs are essentially devoid of pigment, whereas hairs from dorsal skin are much less pigmented than those in control mice; however, white dorsal fur is observed by P45
• in the second hair cycle anagen phase (P28-P42), new dorsal hair follicles completely lack DCT+ melanocytes, corresponding to subsequent white dorsal fur seen at P45
• at P4, dorsal skin shows small amounts of residual hair follicle melanin; residual dorsal melanocytes (DCT+) continue to express YY1, indicating incomplete Cre-mediated deletion
• in the second hair cycle anagen phase (P28-P42), new dorsal hair follicles completely lack melanin pigment
• at P4, mice show profoundly lighter skin pigmentation relative to control mice
• mice exhibit complete loss of hair follicle melanocytes after the first hair cycle

integument
• mice exhibit premature gray hair after the first hair cycle
• during the first hair cycle (P0-P28), P10 ventral hairs are essentially devoid of pigment, whereas hairs from dorsal skin are much less pigmented than those in control mice; however, white dorsal fur is observed by P45
• in the second hair cycle anagen phase (P28-P42), new dorsal hair follicles completely lack DCT+ melanocytes, corresponding to subsequent white dorsal fur seen at P45
• at P4, dorsal skin shows small amounts of residual hair follicle melanin; residual dorsal melanocytes (DCT+) continue to express YY1, indicating incomplete Cre-mediated deletion
• in the second hair cycle anagen phase (P28-P42), new dorsal hair follicles completely lack melanin pigment
• at P4, mice show profoundly lighter skin pigmentation relative to control mice




Genotype
MGI:6241524
cn13
Allelic
Composition
Resttm1.1Yasu/Resttm1.1Yasu
Tg(Tyr-cre)1Lru/Y
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Resttm1.1Yasu mutation (1 available); any Rest mutation (95 available)
Tg(Tyr-cre)1Lru mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
pigmentation
N
• mice never form white spots including on the belly region




Genotype
MGI:6209426
cn14
Allelic
Composition
Atg7tm1Tchi/Atg7tm1Tchi
Tg(Tyr-cre)1Lru/Y
Genetic
Background
involves: C57BL/6 * C57BL/6NCrlj * CBA/JNCrlj * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg7tm1Tchi mutation (3 available); any Atg7 mutation (51 available)
Tg(Tyr-cre)1Lru mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
pigmentation
• cultured primary autophagy-deficient melanocytes stop proliferating after the third passage, unlike autophagy-competent melanocytes which can be maintained up to passage 5
• mice show decreased pigmentation of dorsal hair; melanin content of dorsal hair is reduced by 10-15% relative to that in control mice
• mice exhibit slight hypopigmentation of the tail epidermis
• some melanocytes of tail skin contain misshapen, swollen, and possibly disintegrating mitochondria, not observed in control melanocytes
• however, when cultured in vitro, primary autophagy-deficient melanocytes isolated from body skin of newborn mice show no significant change of melanin content relative to autophagy-competent melanocytes
• pigmentation of the feet is decreased but to a lesser extent than in tail epidermis
• at 9 months of age, pigmentation of tail skin is consistently lower than that of control mice
• melanocyte counts are consistently lower but not significantly decreased in the tail epidermis
• when cultured in vitro, primary autophagy-deficient melanocytes isolated from body skin of newborn mice show increased melanosome-associated vacuolation, unlike autophagy-competent melanocytes
• however, in vivo, both melanocytes and keratinocytes of tail skin contain mature melanosomes, suggesting normal melanosome formation, maturation, and transfer in the absence of an intact autophagy system

integument
• mice show decreased pigmentation of dorsal hair; melanin content of dorsal hair is reduced by 10-15% relative to that in control mice
• mice exhibit slight hypopigmentation of the tail epidermis
• some melanocytes of tail skin contain misshapen, swollen, and possibly disintegrating mitochondria, not observed in control melanocytes
• however, when cultured in vitro, primary autophagy-deficient melanocytes isolated from body skin of newborn mice show no significant change of melanin content relative to autophagy-competent melanocytes
• pigmentation of the feet is decreased but to a lesser extent than in tail epidermis
• at 9 months of age, pigmentation of tail skin is consistently lower than that of control mice
• melanocyte counts are consistently lower but not significantly decreased in the tail epidermis

cellular
• swollen mitochondria are observed in some melanocytes of tail skin, unlike in control mice
• lipidation of microtubule-associated protein 1 light chain 3 beta (LC3), i.e. conversion of LC3-I to LC3-II, is completely blocked, indicating efficient disruption of autophagy in isolated melanocytes; in contrast, both LC3-I and LC3-II are detected in melanocytes of control mice
• cultured primary autophagy-deficient melanocytes stop proliferating after the third passage, unlike autophagy-competent melanocytes which can be maintained up to passage 5
• in culture, primary autophagy-deficient melanocytes show a strong reduction in proliferative capacity and start acquiring senescent morphotypes with distended cytoplasms early in the second passage
• the premature senescent phenotype becomes even more prominent at the end of passage 2 and beginning of passage 3
• autophagy-deficient melanocytes accumulate reactive oxygen species damage, ubiquitinated proteins, and the multi-functional adapter protein SQSTM1/p62

homeostasis/metabolism
• lipidation of microtubule-associated protein 1 light chain 3 beta (LC3), i.e. conversion of LC3-I to LC3-II, is completely blocked, indicating efficient disruption of autophagy in isolated melanocytes; in contrast, both LC3-I and LC3-II are detected in melanocytes of control mice

limbs/digits/tail
• at 9 months of age, pigmentation of tail skin is consistently lower than that of control mice
• melanocyte counts are consistently lower but not significantly decreased in the tail epidermis




Genotype
MGI:6220869
cn15
Allelic
Composition
Chek1tm1Jmr/Chek1+
Tg(Dct-lacZ)A12Jkn/0
Tg(Tyr-cre)1Lru/Y
Genetic
Background
involves: C57BL/6 * CBA * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Chek1tm1Jmr mutation (1 available); any Chek1 mutation (41 available)
Tg(Dct-lacZ)A12Jkn mutation (4 available)
Tg(Tyr-cre)1Lru mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
pigmentation
N
• despite a slight reduction of melanoblast numbers at E13.5, adult mice exhibit normal coat pigmentation relative to control mice

embryo
• at E13.5, a slight but significant reduction of melanoblast numbers is noted in the head, dorsal, and ventral regions relative to control embryos

nervous system
• at E13.5, a slight but significant reduction of melanoblast numbers is noted in the head, dorsal, and ventral regions relative to control embryos




Genotype
MGI:6220868
cn16
Allelic
Composition
Chek1tm1Jmr/Chek1tm1Jmr
Tg(Dct-lacZ)A12Jkn/0
Tg(Tyr-cre)1Lru/Y
Genetic
Background
involves: C57BL/6 * CBA * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Chek1tm1Jmr mutation (1 available); any Chek1 mutation (41 available)
Tg(Dct-lacZ)A12Jkn mutation (4 available)
Tg(Tyr-cre)1Lru mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
embryo
• significantly fewer beta-gal+ melanoblasts are noted in the head and trunk regions at E12.5, and by E13.5, melanoblasts are completely lost even from the pinna, vibrissae, and around the eyes
• many cleaved caspase 3+ melanoblasts are observed in the head and trunk regions, unlike in control embryos, suggesting increased melanoblast apoptosis
• however, the number and distribution of beta-gal+ melanoblasts is normal at E10.5 and E11.5

nervous system
• significantly fewer beta-gal+ melanoblasts are noted in the head and trunk regions at E12.5, and by E13.5, melanoblasts are completely lost even from the pinna, vibrissae, and around the eyes
• many cleaved caspase 3+ melanoblasts are observed in the head and trunk regions, unlike in control embryos, suggesting increased melanoblast apoptosis
• however, the number and distribution of beta-gal+ melanoblasts is normal at E10.5 and E11.5

cellular
• many gamma-H2AX+ melanoblasts are noted in the head and trunk regions, unlike in control embryos, suggesting that aberrant DNA replication leads to spontaneous DNA damage and ultimately cell death

homeostasis/metabolism
• many gamma-H2AX+ melanoblasts are noted in the head and trunk regions, unlike in control embryos, suggesting that aberrant DNA replication leads to spontaneous DNA damage and ultimately cell death




Genotype
MGI:5755101
cn17
Allelic
Composition
Nrastm1Tyj/Nras+
Tg(Tyr-cre)1Lru/0
Genetic
Background
involves: C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nrastm1Tyj mutation (1 available); any Nras mutation (44 available)
Tg(Tyr-cre)1Lru mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• progress to akathisia and general malaise
• at a median age of 12.5 months
• seen at a median age of 12.5 months
• mice exhibit incoordination at a median age of 12.5 months
• mice show impaired gait at a median age of 12.5 months

skeleton
• most mice develop increasing cranial perimeter or cranial deformity symptoms

mortality/aging
• mice begin to die around 6 months of age with about 25% surviving past 18 months of age

craniofacial
• most mice develop increasing cranial perimeter or cranial deformity symptoms

pigmentation
• darkening of the skin, tails, paws, and snouts that is evident from day 1 and persists throughout life, that is less pronounced than that in homozygotes




Genotype
MGI:5755097
cn18
Allelic
Composition
Nrastm1Tyj/Nrastm1Tyj
Tg(Tyr-cre)1Lru/0
Genetic
Background
involves: C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nrastm1Tyj mutation (1 available); any Nras mutation (44 available)
Tg(Tyr-cre)1Lru mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
skeleton
• most mice develop increasing cranial perimeter or cranial deformity

cellular
• increase in proliferation of leptomeningeal pigmented melanocytes

behavior/neurological
• symptoms progress rapidly to akathisia and general malaise
• at a median age of 4 months
• seen at a median age of 4 months
• mice exhibit incoordination at a median age of 4 months
• mice show impaired gait at a median age of 4 months

mortality/aging
• mice die before 12 months of age

craniofacial
• most mice develop increasing cranial perimeter or cranial deformity

integument
• mice develop benign paucicellular dermal melanocytic lesions resembling human blue nevi

pigmentation
• increase in proliferation of leptomeningeal pigmented melanocytes
• brains show darkening of the leptomeninges that follows the sulci and fissures, and is more prominent in the frontoparietal region
• increase in the number of pigmented melanocytes that follow the gyri and sulci and envelop the ventricles (melanocytosis)
• hyperpigmented dendritic melanocytes are seen in 3 week old and adult mice, particularly between the collagen bundles of the reticular dermis and along the adnexae of the deep dermal layers
• darkening of the skin, tails, paws, and snouts that is evident from day 1 and persists throughout life

neoplasm
• darkly pigmented areas in the brain are composed of large melanocytic lesions comprising pleomorphic cells that invade the brain parenchyma with tumor cells rapidly dividing, indicating primary melanoma of the central nervous system
• however, mice do not develop cutaneous melanoma or tumors in the uvea, hearts, or oral and genital mucosa
• tumor cells frequently present intracytoplasmic melanin




Genotype
MGI:6220867
cn19
Allelic
Composition
Chek1tm1Jmr/Chek1tm1Jmr
Tg(Tyr-cre)1Lru/Y
Genetic
Background
involves: C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Chek1tm1Jmr mutation (1 available); any Chek1 mutation (41 available)
Tg(Tyr-cre)1Lru mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
pigmentation
• no DCT-expressing melanocytes are observed in the hair follicles, unlike in control mice
• adult male mice are completely devoid of coat pigmentation, unlike control mice
• male mice show complete lack of epidermal melanocytes
• adult males show a marked reduction or absence of neural crest-derived melanocytes in the eyes, unlike control mice
• however, males retain normal eye pigmentation in the retinal pigmented epithelium (RPE) due to inefficient transgene expression in the RPE

integument
• no DCT-expressing melanocytes are observed in the hair follicles, unlike in control mice
• adult male mice are completely devoid of coat pigmentation, unlike control mice
• male mice show complete lack of epidermal melanocytes





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last database update
04/23/2024
MGI 6.23
The Jackson Laboratory