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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(Tyr-cre/ERT2)13Bos
transgene insertion 13, Marcus Bosenberg
MGI:3641203
Summary 33 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Hsp90b1tm1Zhli/Hsp90b1tm1Zhli
Tg(Tyr-cre/ERT2)13Bos/0
B6.Cg-Hsp90b1tm1Zhli Tg(Tyr-cre/ERT2)13Bos MGI:6220403
cn2
Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh
Krastm4Tyj/Kras+
Tg(Tyr-cre/ERT2)13Bos/0
B6J.Cg-Cdkn2atm2.1Nesh Krastm4Tyj Tg(Tyr-cre/ERT2)13Bos MGI:5752237
cn3
Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh
Nrastm1.1Nesh/Nrastm1.1Nesh
Stk11tm1.1Rdp/Stk11tm1.1Rdp
Tg(Tyr-cre/ERT2)13Bos/0
B6J.Cg-Nrastm1.1Nesh Cdkn2atm2.1Nesh Stk11tm1.1Rdp Tg(Tyr-cre/ERT2)13Bos MGI:5752239
cn4
Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh
Nrastm1.1Nesh/Nrastm1.1Nesh
Tg(Tyr-cre/ERT2)13Bos/0
B6J.Cg-Nrastm1.1Nesh Cdkn2atm2.1Nesh Tg(Tyr-cre/ERT2)13Bos MGI:5752235
cn5
Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh
Nrastm1Tyj/Nrastm1Tyj
Tg(Tyr-cre/ERT2)13Bos/0
B6J.Cg-Nrastm1Tyj Cdkn2atm2.1Nesh Tg(Tyr-cre/ERT2)13Bos MGI:5752233
cn6
Gt(ROSA)26Sortm1(GNAQ*)Cvr/Gt(ROSA)26Sor+
Tg(Tyr-cre/ERT2)13Bos/0
C3FeJ.Cg-Gt(ROSA)26Sortm1(GNAQ*)Cvr Tg(Tyr-cre/ERT2)13Bos MGI:5702889
cn7
Trp53tm1Brn/Trp53tm1Brn
Tg(Tyr-cre/ERT2)13Bos/0
Tg(Tyr-NRAS*Q61K)1Bee/0
FVB.Cg-Trp53tm1Brn Tg(Tyr-cre/ERT2)13Bos Tg(Tyr-NRAS*Q61K)1Bee MGI:5645995
cn8
Braftm1Mmcm/Braf+
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129P2/OlaHsd * 129S1/Sv * FVB MGI:5902129
cn9
Braftm1Mmcm/Braf+
Ptentm2.1Ppp/Pten+
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129P2/OlaHsd * 129S1/Sv * FVB MGI:5902136
cn10
Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB MGI:4835041
cn11
Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh
Trp53tm1Brn/Trp53tm1Brn
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB MGI:4835042
cn12
Cdkn2atm2.1Nesh/Cdkn2a+
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB MGI:4835045
cn13
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129P2/OlaHsd * 129S4/SvJae * FVB MGI:4835046
cn14
Braftm1Mmcm/Braf+
Ptentm1Rdp/Ptentm1Rdp
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 * FVB/N MGI:5902132
cn15
Sox10tm7.1(Sox10)Weg/Sox10+
Tg(Tyr-cre/ERT2)13Bos/0
Tg(Tyr-NRAS*Q61K)1Bee/0
involves: 129P2/OlaHsd * C57BL/6J * DBA/2 * FVB/N MGI:5515811
cn16
Braftm1Mmcm/Braf+
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129P2/OlaHsd * FVB MGI:5902125
cn17
Braftm1Mmcm/Braftm1Mmcm
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129P2/OlaHsd * FVB MGI:5902126
cn18
Ednrbtm1Nrd/Ednrbtm1Nrd
Gt(ROSA)26Sortm14(CAG-tdTomato)Hze/Gt(ROSA)26Sor+
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129S1/Sv * 129S6/SvEvTac * 129X1/SvJ * C57BL/6J MGI:6269398
cn19
Ednrbtm1Nrd/Ednrbtm1Nrd
Tg(Dct-lacZ)#Ove/0
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * FVB/N MGI:6269406
cn20
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129S1/Sv * FVB MGI:5902133
cn21
Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh
Krastm4Tyj/Kras+
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129S4/SvJae * C57BL/6 * FVB MGI:4835044
cn22
Krastm4Tyj/Kras+
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129S4/SvJae * FVB MGI:4835047
cn23
Ptentm1Rdp/Ptentm1Rdp
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129S6/SvEvTac * C57BL/6 * FVB/N MGI:5902135
cn24
Mc1rtm1.1Mymi/Mc1rtm1.1Mymi
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129S6/SvEvTac * C57BL/6J * C57BL/6NTac MGI:6269418
cn25
Mc1rtm1.1Mymi/Mc1rtm1.1Mymi
Tg(KRT14-rtTA)F42Efu/0
Tg(tetO-EDN1,-lacZ)9Mhus/0
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129S6/SvEvTac * C57BL/6J * C57BL/6NTac * FVB MGI:6269451
cn26
Mc1rtm1.1Mymi/Mc1rtm1.1Mymi
Tg(Dct-lacZ)#Ove/0
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129S6/SvEvTac * C57BL/6J * C57BL/6NTac * FVB/N MGI:6269447
cn27
Braftm1Tuv/Braftm1Tuv
Gt(ROSA)26Sortm1(sb13)Tuv/Gt(ROSA)26Sor+
Tg(Tyr-cre/ERT2)13Bos/0
TgTn(sb-T2/Onc)#Dla/0
involves: 129S6/SvEvTac * FVB/N MGI:5318067
cn28
Cdkn2atm1Rdp/Cdkn2atm1Rdp
Ptentm1Rps/Ptentm1Rps
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129/Sv * 129S1/Sv * C57BL/6J * FVB/N * SJL MGI:4418448
cn29
Cdkn2atm1Rdp/Cdkn2atm1Rdp
Ctnnb1tm1Mmt/Ctnnb1tm1Mmt
Ptentm1Rps/Ptentm1Rps
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129/Sv * C57BL/6J * FVB * SJL MGI:4418449
cn30
Cdkn2atm1Rdp/Cdkn2atm1Rdp
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Ptentm1Rdp/Ptentm1Rdp
Tg(tetO-BRAF*V600E)29Lc/0
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129/Sv * C57BL/6J * FVB * SJL MGI:5700641
cn31
Pikfyvetm2.1Tssk/Pikfyvetm2.1Tssk
Tg(Tyr-cre/ERT2)13Bos/0
involves: C57BL/6 * C57BL/6J MGI:6256964
cn32
Gt(ROSA)26Sortm4(ACTB-tdTomato,-EGFP)Luo/Gt(ROSA)26Sor+
Pikfyvetm2.1Tssk/Pikfyvetm2.1Tssk
Tg(Tyr-cre/ERT2)13Bos/0
involves: C57BL/6 * C57BL/6J MGI:6256968
cn33
Ctnnb1tm2Kem/Ctnnb1tm2Kem
Tg(KRT14-rtTA)F42Efu/0
Tg(tetO-EDN1,-lacZ)9Mhus/0
Tg(Tyr-cre/ERT2)13Bos/0
involves: C57BL/6J * FVB MGI:6269417


Genotype
MGI:6220403
cn1
Allelic
Composition
Hsp90b1tm1Zhli/Hsp90b1tm1Zhli
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
B6.Cg-Hsp90b1tm1Zhli Tg(Tyr-cre/ERT2)13Bos
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hsp90b1tm1Zhli mutation (0 available); any Hsp90b1 mutation (6 available)
Tg(Tyr-cre/ERT2)13Bos mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
pigmentation
• mice show decreased levels of melanin in hair bulbs in the 4-OHT-treated area relative to control mice
• mice show decreased levels of melanin in hair shafts plucked from the 4-OHT-treated area relative to control mice
• following 4 weeks of topical application of 4-hydroxytamoxifen (4-OHT) to shaved skin on the right flank, coat hair that re-grows in the 4-OHT-treated area is grey/white in color, whereas hair re-grown in the vehicle (ethanol)-treated left flank is black; control mice treated with either 4-OHT or vehicle show no change in hair color

integument
• mice show decreased levels of melanin in hair bulbs in the 4-OHT-treated area relative to control mice
• mice show decreased levels of melanin in hair shafts plucked from the 4-OHT-treated area relative to control mice
• following 4 weeks of topical application of 4-hydroxytamoxifen (4-OHT) to shaved skin on the right flank, coat hair that re-grows in the 4-OHT-treated area is grey/white in color, whereas hair re-grown in the vehicle (ethanol)-treated left flank is black; control mice treated with either 4-OHT or vehicle show no change in hair color




Genotype
MGI:5752237
cn2
Allelic
Composition
Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh
Krastm4Tyj/Kras+
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
B6J.Cg-Cdkn2atm2.1Nesh Krastm4Tyj Tg(Tyr-cre/ERT2)13Bos
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm2.1Nesh mutation (4 available); any Cdkn2a mutation (50 available)
Krastm4Tyj mutation (6 available); any Kras mutation (35 available)
Tg(Tyr-cre/ERT2)13Bos mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
pigmentation
• mice treated with 4-hydroxytamoxifen (4-OHT) neonatally exhibit the presence of nevi and hyperpigmented regions on the paws and tails

integument
• mice treated with 4-OHT neonatally develop melanoma with 76% penetrance and a median latency of 36.3 weeks
• melanomas contain both spindle-cell and desmoplastic cell types with no overt signs of macrometastatic spread

neoplasm
• mice treated with 4-OHT neonatally develop melanoma with 76% penetrance and a median latency of 36.3 weeks
• melanomas contain both spindle-cell and desmoplastic cell types with no overt signs of macrometastatic spread




Genotype
MGI:5752239
cn3
Allelic
Composition
Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh
Nrastm1.1Nesh/Nrastm1.1Nesh
Stk11tm1.1Rdp/Stk11tm1.1Rdp
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
B6J.Cg-Nrastm1.1Nesh Cdkn2atm2.1Nesh Stk11tm1.1Rdp Tg(Tyr-cre/ERT2)13Bos
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm2.1Nesh mutation (4 available); any Cdkn2a mutation (50 available)
Nrastm1.1Nesh mutation (2 available); any Nras mutation (22 available)
Stk11tm1.1Rdp mutation (0 available); any Stk11 mutation (7 available)
Tg(Tyr-cre/ERT2)13Bos mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
integument
• mice treated with 4-hydroxytamoxifen (4-OHT) neonatally or in adulthood exhibit enhanced nevus formation
• mice treated with 4-OHT neonatally develop melanoma with 85% penetrance and a median latency of 22.1 weeks

neoplasm
• mice treated with 4-hydroxytamoxifen (4-OHT) neonatally or in adulthood exhibit enhanced nevus formation
• mice treated with 4-OHT neonatally develop melanoma with 85% penetrance and a median latency of 22.1 weeks
• 36% of mice treated with 4-OHT neonatally that develop melanoma show macrometastatic spread to lymph nodes, lung, spleen and/or liver




Genotype
MGI:5752235
cn4
Allelic
Composition
Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh
Nrastm1.1Nesh/Nrastm1.1Nesh
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
B6J.Cg-Nrastm1.1Nesh Cdkn2atm2.1Nesh Tg(Tyr-cre/ERT2)13Bos
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm2.1Nesh mutation (4 available); any Cdkn2a mutation (50 available)
Nrastm1.1Nesh mutation (2 available); any Nras mutation (22 available)
Tg(Tyr-cre/ERT2)13Bos mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• melanocytes treated with 4-hydroxytamoxifen (4-OHT) to induce cre activity exhibit decreased proliferation in culture and cease to proliferate after 2-3 passages

integument
• mice treated with 4-OHT neonatally readily develop melanoma with 70% penetrance and a median latency of 26.3 weeks
• melanomas contain both spindle-cell and desmoplastic cell types with no overt signs of macrometastatic spread

pigmentation
• melanocytes treated with 4-hydroxytamoxifen (4-OHT) to induce cre activity exhibit decreased proliferation in culture and cease to proliferate after 2-3 passages
• mice treated with 4-OHT neonatally exhibit the presence of nevi and hyperpigmented regions on the paws and tails

neoplasm
• mice treated with 4-OHT neonatally readily develop melanoma with 70% penetrance and a median latency of 26.3 weeks
• melanomas contain both spindle-cell and desmoplastic cell types with no overt signs of macrometastatic spread




Genotype
MGI:5752233
cn5
Allelic
Composition
Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh
Nrastm1Tyj/Nrastm1Tyj
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
B6J.Cg-Nrastm1Tyj Cdkn2atm2.1Nesh Tg(Tyr-cre/ERT2)13Bos
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm2.1Nesh mutation (4 available); any Cdkn2a mutation (50 available)
Nrastm1Tyj mutation (1 available); any Nras mutation (22 available)
Tg(Tyr-cre/ERT2)13Bos mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• melanocytes treated with 4-hydroxytamoxifen (4-OHT) to induce cre activity exhibit decreased proliferation in culture and cease to proliferate after 2-3 passages

integument
• melanoma is very rare in mice treated with 4-OHT neonatally, with 1 in 29 mice developing tumors when observed for 80 weeks

pigmentation
• melanocytes treated with 4-hydroxytamoxifen (4-OHT) to induce cre activity exhibit decreased proliferation in culture and cease to proliferate after 2-3 passages
• mice treated with 4-OHT neonatally exhibit the presence of nevi and hyperpigmented regions on the paws and tails

neoplasm
• melanoma is very rare in mice treated with 4-OHT neonatally, with 1 in 29 mice developing tumors when observed for 80 weeks




Genotype
MGI:5702889
cn6
Allelic
Composition
Gt(ROSA)26Sortm1(GNAQ*)Cvr/Gt(ROSA)26Sor+
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
C3FeJ.Cg-Gt(ROSA)26Sortm1(GNAQ*)Cvr Tg(Tyr-cre/ERT2)13Bos
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(GNAQ*)Cvr mutation (0 available); any Gt(ROSA)26Sor mutation (497 available)
Tg(Tyr-cre/ERT2)13Bos mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
pigmentation
• melanocytic hyperplasia in tamoxifen treated mice after 2 and 6.5 months
• 2 months after tamoxifen treatment

vision/eye
• 2 months after tamoxifen treatment

behavior/neurological
N
• tamoxifen-treated mice do not exhibit any behavioral abnormalities

neoplasm
N
• tamoxifen-treated mice fail to develop uveal melanoma




Genotype
MGI:5645995
cn7
Allelic
Composition
Trp53tm1Brn/Trp53tm1Brn
Tg(Tyr-cre/ERT2)13Bos/0
Tg(Tyr-NRAS*Q61K)1Bee/0
Genetic
Background
FVB.Cg-Trp53tm1Brn Tg(Tyr-cre/ERT2)13Bos Tg(Tyr-NRAS*Q61K)1Bee
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Tyr-cre/ERT2)13Bos mutation (4 available)
Tg(Tyr-NRAS*Q61K)1Bee mutation (1 available)
Trp53tm1Brn mutation (13 available); any Trp53 mutation (150 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• spontaneous development of malignant melanoma by 200 days of age in all mice treated with tamoxifen
• tumors of tamoxifen-treated mice are relatively small, with regular ovoid shape and high levels of Ki-67 staining
• naevi are not seen above dermal malignant melanomas in tamoxifen treated mice, although small nests of melanocytes in a subepidermal location are occasionally seen
• early lesions of tamoxifen treated mice do not show evidence of tumor derivation from the upper dermis and appear to be derived from follicular or other deep dermal precursors
• majority of tumors of tamoxifen treated mice are located on the back
• all mice treated with tamoxifen develop malignant melanoma before 150 days of age after a single neonatal UVB dose
• tamoxifen-treated mice show a diminished response of melanocyte emigration from the upper regions of hair follicles to the epidermal basal layer 3-5 days after neonatal UV radiation compared to controls

integument
• spontaneous development of malignant melanoma by 200 days of age in all mice treated with tamoxifen
• tumors of tamoxifen-treated mice are relatively small, with regular ovoid shape and high levels of Ki-67 staining
• naevi are not seen above dermal malignant melanomas in tamoxifen treated mice, although small nests of melanocytes in a subepidermal location are occasionally seen
• early lesions of tamoxifen treated mice do not show evidence of tumor derivation from the upper dermis and appear to be derived from follicular or other deep dermal precursors
• majority of tumors of tamoxifen treated mice are located on the back




Genotype
MGI:5902129
cn8
Allelic
Composition
Braftm1Mmcm/Braf+
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Braftm1Mmcm mutation (2 available); any Braf mutation (13 available)
Ptentm2.1Ppp mutation (0 available); any Pten mutation (39 available)
Tg(Tyr-cre/ERT2)13Bos mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
integument
• 7-10 days following 4-hydroxytamoxifen (4-HT) treatment, all mice show expansion of highly pigmented cells that develop into pigmented malignant lesions in locations of 4-HT administration such as the face, flank, or tail skin
• pigmented melanoma cells are seen throughout the dermis and subcutis of 4-HT treated mice and show pagetoid spread into the epidermis
• lesions in 4-HT treated mice progress rapidly to advanced malignancy such that all mice require euthanasia 25-50 days following 4-HT administration
• treatment of 4-HT treated mice with the MEK1/2 inhibitor PD325901 or the mTorc1 inhibitor rapamycin inhibits melanoma formation
• mice in which drug treatment is ceased subsequently develop malignant melanoma
• mice treated once with PD325901 to prevent melanoma remain sensitive to the anti-melanoma action of a second round of PD325901 administration

neoplasm
• 7-10 days following 4-hydroxytamoxifen (4-HT) treatment, all mice show expansion of highly pigmented cells that develop into pigmented malignant lesions in locations of 4-HT administration such as the face, flank, or tail skin
• pigmented melanoma cells are seen throughout the dermis and subcutis of 4-HT treated mice and show pagetoid spread into the epidermis
• lesions in 4-HT treated mice progress rapidly to advanced malignancy such that all mice require euthanasia 25-50 days following 4-HT administration
• treatment of 4-HT treated mice with the MEK1/2 inhibitor PD325901 or the mTorc1 inhibitor rapamycin inhibits melanoma formation
• mice in which drug treatment is ceased subsequently develop malignant melanoma
• mice treated once with PD325901 to prevent melanoma remain sensitive to the anti-melanoma action of a second round of PD325901 administration
• spread of melanoma in 4-HT treated mice is seen into the regional draining lymph nodes in 100% of mice and to the lungs in some cases




Genotype
MGI:5902136
cn9
Allelic
Composition
Braftm1Mmcm/Braf+
Ptentm2.1Ppp/Pten+
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Braftm1Mmcm mutation (2 available); any Braf mutation (13 available)
Ptentm2.1Ppp mutation (0 available); any Pten mutation (39 available)
Tg(Tyr-cre/ERT2)13Bos mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
integument
• 4-HT treated mice eventually develop focal malignant melanomas

neoplasm
• 4-HT treated mice eventually develop focal malignant melanomas

pigmentation
• 4-hydroxytamoxifen (4-HT) treated mice initially develop benign melanocytic lesions but they eventually develop focal malignant melanomas




Genotype
MGI:4835041
cn10
Allelic
Composition
Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm2.1Nesh mutation (4 available); any Cdkn2a mutation (50 available)
Krastm4Tyj mutation (6 available); any Kras mutation (35 available)
Tg(Tyr-cre/ERT2)13Bos mutation (4 available)
Trp53tm1Brn mutation (13 available); any Trp53 mutation (150 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• all mice treated with tamoxifen neonatally die within 14 weeks of treatment due to aggressive melanomas with spindle-like morphology unlike control mice in which only one mouse develops melanoma over a period of 60 weeks

neoplasm
• tumor growth is more aggressive than in Cdkn2atm1Rdp/Cdkn2atm1Rdp Tg(Tyr-HRAS)60Lc mice
• tamoxifen-treated mice develop melanomas with spindle-like morphology
• all mice treated with tamoxifen neonatally die within 14 weeks of treatment due to aggressive melanomas with spindle-like morphology unlike control mice in which only one mouse develops melanoma over a period of 60 weeks
• tumors in tamoxifen-treated mice occur on the flank, ear, and tail
• the number of tumors in tamoxifen-treated mice is greater than in similarly treated Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh Krastm4Tyj/Kras+ Tg(Tyr-cre/ERT2)13Bos mice or Krastm4Tyj/Kras+ Trp53tm1Brn/Trp53tm1Brn Tg(Tyr-cre/ERT2)13Bos mice
• by 15 weeks, 17 of 27 adult mice treated with tamoxifen develop melanomas at the site of application and depilation
• however, no uveal tumors are observed

pigmentation
• tamoxifen-treated mice exhibit melanocytic proliferation unlike wild-type mice
• tamoxifen-treated mice develop pigmented macules in the paws and tail unlike wild-type mice




Genotype
MGI:4835042
cn11
Allelic
Composition
Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh
Trp53tm1Brn/Trp53tm1Brn
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm2.1Nesh mutation (4 available); any Cdkn2a mutation (50 available)
Tg(Tyr-cre/ERT2)13Bos mutation (4 available)
Trp53tm1Brn mutation (13 available); any Trp53 mutation (150 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 1 in 19 (5%) mice treated with tamoxifen neonatally develop melanomas with spindle-like morphology at a median latency of greater than 52 weeks

pigmentation
• tamoxifen-treated mice exhibit melanocytic proliferation unlike wild-type mice
• tamoxifen-treated mice develop pigmented macules in the paws and tail unlike wild-type mice




Genotype
MGI:4835045
cn12
Allelic
Composition
Cdkn2atm2.1Nesh/Cdkn2a+
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm2.1Nesh mutation (4 available); any Cdkn2a mutation (50 available)
Krastm4Tyj mutation (6 available); any Kras mutation (35 available)
Tg(Tyr-cre/ERT2)13Bos mutation (4 available)
Trp53tm1Brn mutation (13 available); any Trp53 mutation (150 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• tamoxifen-treated mice develop melanomas with spindle-like morphology
• 3 of 7 (43%) mice treated with tamoxifen neonatally develop melanomas with spindle-like morphology at a median latency greater than 52 weeks compared with Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh Krastm4Tyj/Kras+ Trp53tm1Brn/Trp53tm1Brn Tg(Tyr-cre/ERT2)13Bos mice whose median latency is 14 weeks

pigmentation
• tamoxifen-treated mice exhibit melanocytic proliferation unlike wild-type mice
• tamoxifen-treated mice develop pigmented macules in the paws and tail unlike wild-type mice




Genotype
MGI:4835046
cn13
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (6 available); any Kras mutation (35 available)
Tg(Tyr-cre/ERT2)13Bos mutation (4 available)
Trp53tm1Brn mutation (13 available); any Trp53 mutation (150 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• tamoxifen-treated mice develop melanomas with spindle-like morphology
• 5 of 11 mice treated with tamoxifen neonatally develop melanomas with spindle-like morphology at a longer latency (median latency 31 weeks) than in Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh Krastm4Tyj/Kras+ Trp53tm1Brn/Trp53tm1BrnTg(Tyr-cre/ERT2)13Bos mice (median latency 14 weeks)

pigmentation
• tamoxifen-treated mice exhibit melanocytic proliferation unlike wild-type mice
• tamoxifen-treated mice develop pigmented macules in the paws and tail unlike wild-type mice




Genotype
MGI:5902132
cn14
Allelic
Composition
Braftm1Mmcm/Braf+
Ptentm1Rdp/Ptentm1Rdp
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Braftm1Mmcm mutation (2 available); any Braf mutation (13 available)
Ptentm1Rdp mutation (0 available); any Pten mutation (39 available)
Tg(Tyr-cre/ERT2)13Bos mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
integument
• 7-10 days following 4-hydroxytamoxifen (4-HT) treatment, all mice show expansion of highly pigmented cells that develop into pigmented malignant lesions in locations of 4-HT administration such as the face, flank, or tail skin
• pigmented melanoma cells are seen throughout the dermis and subcutis of 4-HT treated mice and show pagetoid spread into the epidermis
• lesions in 4-HT treated mice progress rapidly to advanced malignancy such that all mice require euthanasia 25-50 days following 4-HT administration
• treatment of 4-HT treated mice with the MEK1/2 inhibitor PD325901 or the mTorc1 inhibitor rapamycin inhibits melanoma formation
• mice in which drug treatment is ceased subsequently develop malignant melanoma
• mice treated once with PD325901 to prevent melanoma remain sensitive to the anti-melanoma action of a second round of PD325901 administration
• treatment of melanoma bearing mice with either PD325901 or rapamycin inhibits further tumor growth but has little or no effect on tumor regression
• treatment of melanoma bearing with both PD325901 or rapamycin results in a 20% reduction in tumor size

neoplasm
• 7-10 days following 4-hydroxytamoxifen (4-HT) treatment, all mice show expansion of highly pigmented cells that develop into pigmented malignant lesions in locations of 4-HT administration such as the face, flank, or tail skin
• pigmented melanoma cells are seen throughout the dermis and subcutis of 4-HT treated mice and show pagetoid spread into the epidermis
• lesions in 4-HT treated mice progress rapidly to advanced malignancy such that all mice require euthanasia 25-50 days following 4-HT administration
• treatment of 4-HT treated mice with the MEK1/2 inhibitor PD325901 or the mTorc1 inhibitor rapamycin inhibits melanoma formation
• mice in which drug treatment is ceased subsequently develop malignant melanoma
• mice treated once with PD325901 to prevent melanoma remain sensitive to the anti-melanoma action of a second round of PD325901 administration
• treatment of melanoma bearing mice with either PD325901 or rapamycin inhibits further tumor growth but has little or no effect on tumor regression
• treatment of melanoma bearing with both PD325901 or rapamycin results in a 20% reduction in tumor size
• spread of melanoma is seen into the regional draining lymph nodes in 100% of mice and to the lungs in some cases




Genotype
MGI:5515811
cn15
Allelic
Composition
Sox10tm7.1(Sox10)Weg/Sox10+
Tg(Tyr-cre/ERT2)13Bos/0
Tg(Tyr-NRAS*Q61K)1Bee/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J * DBA/2 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Sox10tm7.1(Sox10)Weg mutation (0 available); any Sox10 mutation (7 available)
Tg(Tyr-cre/ERT2)13Bos mutation (4 available)
Tg(Tyr-NRAS*Q61K)1Bee mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
pigmentation
N
• mice injected with tamoxifen at 2 months of age do not exhibit hyperpigmentation in the back skin, snout and paws at 12 months of age, indicating reversion of lesions that are seen in single Tg(Tyr-NRAS*Q61K)1Bee mutants




Genotype
MGI:5902125
cn16
Allelic
Composition
Braftm1Mmcm/Braf+
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
involves: 129P2/OlaHsd * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Braftm1Mmcm mutation (2 available); any Braf mutation (13 available)
Tg(Tyr-cre/ERT2)13Bos mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
pigmentation
• pigmented lesions in 4-HT treated mice are frequently located at the dermal-epidermal junction with extension into the dermis, indicating melanocytic nevi
• other melanocytic proliferations form in the dermis with no junctional component in 4-HT treated mice

integument
• mice treated with 4-hydroxytamoxifen (4-HT) either topically or systemically develop highly pigmented lesions that are detected by 21-28 days after 4-HT administration; these are small papular pigmented lesions that are not malignant
• topical administration of high concentrations of 4-HT occasionally results in periocular lesions on the face and on the glabrous skin of the paws




Genotype
MGI:5902126
cn17
Allelic
Composition
Braftm1Mmcm/Braftm1Mmcm
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
involves: 129P2/OlaHsd * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Braftm1Mmcm mutation (2 available); any Braf mutation (13 available)
Tg(Tyr-cre/ERT2)13Bos mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
pigmentation
• topical administration of 4-hydroxytamoxifen (4-HT) to the ear, tail or flank results in the development of benign melanocytic hyperplasias that are larger and more highly pigmented than in conditional heterozygotes




Genotype
MGI:6269398
cn18
Allelic
Composition
Ednrbtm1Nrd/Ednrbtm1Nrd
Gt(ROSA)26Sortm14(CAG-tdTomato)Hze/Gt(ROSA)26Sor+
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
involves: 129S1/Sv * 129S6/SvEvTac * 129X1/SvJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ednrbtm1Nrd mutation (1 available); any Ednrb mutation (45 available)
Gt(ROSA)26Sortm14(CAG-tdTomato)Hze mutation (3 available); any Gt(ROSA)26Sor mutation (497 available)
Tg(Tyr-cre/ERT2)13Bos mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
integument
• following induction of Cre-mediated recombination by TAM treatment at 3 weeks of age (1st telogen), mice show a noticeable hair-graying phenotype by the 2nd telogen; hair graying persists through the next hair cycle (3rd telogen), unlike in control mice
• following TAM treatment at 3 weeks of age (1st telogen), mice exhibit unpigmented hair follicles that contain fewer differentiated melanocytes in the bulb by anagen IV
• following TAM treatment at 3 weeks of age (1st telogen), mice exhibit unpigmented hair follicles unlike control mice
• following TAM treatment at 3 weeks of age (1st telogen), >65% of hair shafts lack melanin, leading to a hair-graying phenotype at the 2nd and 3rd telogen

pigmentation
• following TAM treatment at 3 weeks of age (1st telogen), melanocyte stem cells (McSCs) in unpigmented hair follicles show less BrdU incorporation than those in pigmented hair follicles of control mice at anagen III
• following induction of Cre-mediated recombination by TAM treatment at 3 weeks of age (1st telogen), mice show a noticeable hair-graying phenotype by the 2nd telogen; hair graying persists through the next hair cycle (3rd telogen), unlike in control mice
• following TAM treatment at 3 weeks of age (1st telogen), mice exhibit unpigmented hair follicles that contain fewer differentiated melanocytes in the bulb by anagen IV
• following TAM treatment at 3 weeks of age (1st telogen), mice exhibit unpigmented hair follicles unlike control mice
• following TAM treatment at 3 weeks of age (1st telogen), >65% of hair shafts lack melanin, leading to a hair-graying phenotype at the 2nd and 3rd telogen
• following TAM treatment at 3 weeks of age (1st telogen), unpigmented hair follicles contain fewer differentiated melanocytes in the bulb by anagen IV, as shown by a decreased number of tomato+ melanocytes expressing differentiation markers Dct, MITF, and S100
• % of apoptotic (Casp3+) bulb melanocytes is significantly increased relative to that in control mice at anagen VI

cellular
• following TAM treatment at 3 weeks of age (1st telogen), melanocyte stem cells (McSCs) in unpigmented hair follicles show less BrdU incorporation than those in pigmented hair follicles of control mice at anagen III




Genotype
MGI:6269406
cn19
Allelic
Composition
Ednrbtm1Nrd/Ednrbtm1Nrd
Tg(Dct-lacZ)#Ove/0
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ednrbtm1Nrd mutation (1 available); any Ednrb mutation (45 available)
Tg(Dct-lacZ)#Ove mutation (0 available)
Tg(Tyr-cre/ERT2)13Bos mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
pigmentation
• following TAM treatment immediately after wounding at 8 weeks of age, mice show a significantly reduced number of epidermal melanocytes in the wound area both at day 0 and day 8 after re- epithelialization relative to control mice
• however, no signs of apoptosis are observed, suggesting normal survival of epidermal melanocytes after wounding
• following initial TAM treatment during 2nd anagen, the number of Dct-LacZ+ melanocyte stem cells (McSCs) in unpigmented hair follicles is significantly lower than that in control mice by the 2nd telogen; most unpigmented hair follicles completely lack McSCs by the 3rd and 4th telogen

integument
• following TAM treatment immediately after wounding at 8 weeks of age, mice show a significantly reduced number of epidermal melanocytes in the wound area both at day 0 and day 8 after re- epithelialization relative to control mice
• however, no signs of apoptosis are observed, suggesting normal survival of epidermal melanocytes after wounding




Genotype
MGI:5902133
cn20
Allelic
Composition
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
involves: 129S1/Sv * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm2.1Ppp mutation (0 available); any Pten mutation (39 available)
Tg(Tyr-cre/ERT2)13Bos mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
pigmentation
N
• mice treated with 4-hydroxytamoxifen do not show any melanocytic phenotype over 18 months




Genotype
MGI:4835044
cn21
Allelic
Composition
Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh
Krastm4Tyj/Kras+
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm2.1Nesh mutation (4 available); any Cdkn2a mutation (50 available)
Krastm4Tyj mutation (6 available); any Kras mutation (35 available)
Tg(Tyr-cre/ERT2)13Bos mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• tamoxifen-treated mice develop melanomas with spindle-like morphology
• 8 of 11 (73%) mice treated with tamoxifen neonatally develop melanomas with spindle-like morphology formation at a longer latency (median latency 24 weeks) than in Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh Krastm4Tyj/Kras+ Trp53tm1Brn/Trp53tm1Brn Tg(Tyr-cre/ERT2)13Bos mice (median latency 14 weeks)

pigmentation
• tamoxifen-treated mice exhibit melanocyte proliferation unlike wild-type mice
• tamoxifen-treated mice develop pigmented macules in the paws and tail unlike wild-type mice




Genotype
MGI:4835047
cn22
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
involves: 129S4/SvJae * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (6 available); any Kras mutation (35 available)
Tg(Tyr-cre/ERT2)13Bos mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 1 in 14 tamoxifen treated mice develops melanoma with a median tumor latency greater than 52 weeks

pigmentation
• tamoxifen-treated mice exhibit melanocytic proliferation unlike wild-type mice
• tamoxifen-treated mice develop pigmented macules in the paws and tail unlike wild-type mice




Genotype
MGI:5902135
cn23
Allelic
Composition
Ptentm1Rdp/Ptentm1Rdp
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm1Rdp mutation (0 available); any Pten mutation (39 available)
Tg(Tyr-cre/ERT2)13Bos mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
pigmentation
N
• mice treated with 4-hydroxytamoxifen do not show any melanocytic phenotype over 18 months




Genotype
MGI:6269418
cn24
Allelic
Composition
Mc1rtm1.1Mymi/Mc1rtm1.1Mymi
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6J * C57BL/6NTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mc1rtm1.1Mymi mutation (1 available); any Mc1r mutation (28 available)
Tg(Tyr-cre/ERT2)13Bos mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
pigmentation
• following TAM treatment, mice exhibit a yellow coat color at 2nd telogen, similar to mice homozygous for the Mc1re allele

integument
• following TAM treatment, mice exhibit a yellow coat color at 2nd telogen, similar to mice homozygous for the Mc1re allele




Genotype
MGI:6269451
cn25
Allelic
Composition
Mc1rtm1.1Mymi/Mc1rtm1.1Mymi
Tg(KRT14-rtTA)F42Efu/0
Tg(tetO-EDN1,-lacZ)9Mhus/0
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6J * C57BL/6NTac * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mc1rtm1.1Mymi mutation (1 available); any Mc1r mutation (28 available)
Tg(KRT14-rtTA)F42Efu mutation (1 available)
Tg(tetO-EDN1,-lacZ)9Mhus mutation (1 available)
Tg(Tyr-cre/ERT2)13Bos mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
pigmentation
• following wounding, mice show a significant increase of epidermal melanocytes containing dark pigment in the wound site, indicating that Edn1 overexpression in epithelial cells can rescue the defect of epidermal melanocyte regeneration caused by MC1R loss in the melanocyte lineage

integument
• following wounding, mice show a significant increase of epidermal melanocytes containing dark pigment in the wound site, indicating that Edn1 overexpression in epithelial cells can rescue the defect of epidermal melanocyte regeneration caused by MC1R loss in the melanocyte lineage




Genotype
MGI:6269447
cn26
Allelic
Composition
Mc1rtm1.1Mymi/Mc1rtm1.1Mymi
Tg(Dct-lacZ)#Ove/0
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6J * C57BL/6NTac * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mc1rtm1.1Mymi mutation (1 available); any Mc1r mutation (28 available)
Tg(Dct-lacZ)#Ove mutation (0 available)
Tg(Tyr-cre/ERT2)13Bos mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
pigmentation
• following wounding, mice show a significant reduction of epidermal melanocytes in the wound site relative to control mice

integument
• following wounding, mice show a significant reduction of epidermal melanocytes in the wound site relative to control mice




Genotype
MGI:5318067
cn27
Allelic
Composition
Braftm1Tuv/Braftm1Tuv
Gt(ROSA)26Sortm1(sb13)Tuv/Gt(ROSA)26Sor+
Tg(Tyr-cre/ERT2)13Bos/0
TgTn(sb-T2/Onc)#Dla/0
Genetic
Background
involves: 129S6/SvEvTac * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Braftm1Tuv mutation (0 available); any Braf mutation (13 available)
Gt(ROSA)26Sortm1(sb13)Tuv mutation (0 available); any Gt(ROSA)26Sor mutation (497 available)
TgTn(sb-T2/Onc)#Dla mutation (0 available)
Tg(Tyr-cre/ERT2)13Bos mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• in tamoxifen-treated mice




Genotype
MGI:4418448
cn28
Allelic
Composition
Cdkn2atm1Rdp/Cdkn2atm1Rdp
Ptentm1Rps/Ptentm1Rps
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
involves: 129/Sv * 129S1/Sv * C57BL/6J * FVB/N * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm1Rdp mutation (6 available); any Cdkn2a mutation (50 available)
Ptentm1Rps mutation (1 available); any Pten mutation (39 available)
Tg(Tyr-cre/ERT2)13Bos mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• following 4-hydroxytamoxifen (4-OHT) application, all mice develop melanoma over a 9 month period unlike wild-type mice

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
melanoma DOID:1909 OMIM:155600
J:155731




Genotype
MGI:4418449
cn29
Allelic
Composition
Cdkn2atm1Rdp/Cdkn2atm1Rdp
Ctnnb1tm1Mmt/Ctnnb1tm1Mmt
Ptentm1Rps/Ptentm1Rps
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
involves: 129/Sv * C57BL/6J * FVB * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm1Rdp mutation (6 available); any Cdkn2a mutation (50 available)
Ctnnb1tm1Mmt mutation (0 available); any Ctnnb1 mutation (21 available)
Ptentm1Rps mutation (1 available); any Pten mutation (39 available)
Tg(Tyr-cre/ERT2)13Bos mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• following 4-hydroxytamoxifen (4-OHT) application, all mice develop melanoma over a 9 month period unlike wild-type mice

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
melanoma DOID:1909 OMIM:155600
J:155731




Genotype
MGI:5700641
cn30
Allelic
Composition
Cdkn2atm1Rdp/Cdkn2atm1Rdp
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Ptentm1Rdp/Ptentm1Rdp
Tg(tetO-BRAF*V600E)29Lc/0
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
involves: 129/Sv * C57BL/6J * FVB * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm1Rdp mutation (6 available); any Cdkn2a mutation (50 available)
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy mutation (2 available); any Gt(ROSA)26Sor mutation (497 available)
Ptentm1Rdp mutation (0 available); any Pten mutation (39 available)
Tg(tetO-BRAF*V600E)29Lc mutation (0 available)
Tg(Tyr-cre/ERT2)13Bos mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• tamoxifen treated mice administered doxycycline in the diet develop melanoma with a median latency of 60 days and with 85% penetrance
• withdrawal of doxycycline leads to rapid tumor regression
• treatment with PLX4720 BRAF inhibitor results in tumor growth inhibition in mutants, however, after continual administration of this inhibitor, mice develop drug resistance




Genotype
MGI:6256964
cn31
Allelic
Composition
Pikfyvetm2.1Tssk/Pikfyvetm2.1Tssk
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
involves: C57BL/6 * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pikfyvetm2.1Tssk mutation (0 available); any Pikfyve mutation (5 available)
Tg(Tyr-cre/ERT2)13Bos mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Hair greying in tamoxifen-treated Pikfyvetm2.1Tssk/Pikfyvetm2.1Tssk Tg(Tyr-cre/ERT2)13Bos/0 mice

pigmentation
• after tamoxifen (4-OHT) treatment for 21 days (P28-P50) followed by shave depilation at P50 to induce the 3rd hair cycle, both pigmented and unpigmented hairs are noted at P60, whereas control mice fed a normal diet show fully pigmented hair growth
• after 4-OHT treatment (P28-P50) followed by shave depilation at P50, some, but not all, anagen hair follicles (HFs) show a vacuolated phenotype, indicating that Cre-mediated deletion is not 100% efficient; some HFs show normal melanocyte morphology ("normal"), some HFs exhibit accumulation of cells with intracellular vesicles with some residual pigment ("intermediate"), while others show accumulation of cells with intracellular vesicles with little to no pigment ("abnormal")
• EM of skin biopsies taken at P60 show anagen hair bulbs containing melanocytes in various conditions: ~40% appear normal, another ~40% show severe vacuolization exhibiting vesicles within vacuoles resembling multivesicular bodies with very few if any melanosomes, and ~20% show an intermediate phenotype with fewer melanosomes generally of earlier stages
• dorsal hairs from 4-OHT-treated mice accumulate ~50% less melanin relative to hairs from control mice at P85, P105, and P365
• after 4-OHT treatment for 29 days (P21-P50) followed by shave depilation of a dorsal region at P50, mice exhibit hair greying with white hairs first seen in the depilated area at P85
• when mice are switched off tamoxifen and fed a normal chow starting at P50, more white hairs are visually apparent at P105
• numerous white hairs accumulate on the head and upper back (areas that have never been shave depilated) by P365, indicating that greying is accelerated but not induced by depilation
• greying is not progressive as mice continue to maintain the same relative level of depigmentation over the course of a year
• after DOPA incubation, some of the multivesicular endosome-like structures observed in epidermal melanocytes of 4-OHT-treated mice contain DOPA reaction product, suggesting that TYR may be trapped within this compartment
• after 4-OHT treatment, primary melanocytes isolated from newborn mice show a significantly reduced number of pigmented melanosomes per cell relative to vehicle-treated melanocytes
• 4-OHT-treated primary melanocytes exhibit accumulation of full length premelanosome protein (PMEL) relative to vehicle-treated melanocytes
• in culture, some 4-OHT-treated melanocytes accumulate single membrane structures resembling multivesicular endosomes with few stage IV melanosomes, while others accumulate early and late stage melanosomes with a few single membrane structures

integument
• after tamoxifen (4-OHT) treatment for 21 days (P28-P50) followed by shave depilation at P50 to induce the 3rd hair cycle, both pigmented and unpigmented hairs are noted at P60, whereas control mice fed a normal diet show fully pigmented hair growth
• after 4-OHT treatment (P28-P50) followed by shave depilation at P50, some, but not all, anagen hair follicles (HFs) show a vacuolated phenotype, indicating that Cre-mediated deletion is not 100% efficient; some HFs show normal melanocyte morphology ("normal"), some HFs exhibit accumulation of cells with intracellular vesicles with some residual pigment ("intermediate"), while others show accumulation of cells with intracellular vesicles with little to no pigment ("abnormal")
• EM of skin biopsies taken at P60 show anagen hair bulbs containing melanocytes in various conditions: ~40% appear normal, another ~40% show severe vacuolization exhibiting vesicles within vacuoles resembling multivesicular bodies with very few if any melanosomes, and ~20% show an intermediate phenotype with fewer melanosomes generally of earlier stages
• dorsal hairs from 4-OHT-treated mice accumulate ~50% less melanin relative to hairs from control mice at P85, P105, and P365
• after 4-OHT treatment for 29 days (P21-P50) followed by shave depilation of a dorsal region at P50, mice exhibit hair greying with white hairs first seen in the depilated area at P85
• when mice are switched off tamoxifen and fed a normal chow starting at P50, more white hairs are visually apparent at P105
• numerous white hairs accumulate on the head and upper back (areas that have never been shave depilated) by P365, indicating that greying is accelerated but not induced by depilation
• greying is not progressive as mice continue to maintain the same relative level of depigmentation over the course of a year




Genotype
MGI:6256968
cn32
Allelic
Composition
Gt(ROSA)26Sortm4(ACTB-tdTomato,-EGFP)Luo/Gt(ROSA)26Sor+
Pikfyvetm2.1Tssk/Pikfyvetm2.1Tssk
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
involves: C57BL/6 * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm4(ACTB-tdTomato,-EGFP)Luo mutation (6 available); any Gt(ROSA)26Sor mutation (497 available)
Pikfyvetm2.1Tssk mutation (0 available); any Pikfyve mutation (5 available)
Tg(Tyr-cre/ERT2)13Bos mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Early greying in Pikfyvetm2.1Tssk/Pikfyvetm2.1Tssk Tg(Tyr-cre/ERT2)13Bos/0 Gt(ROSA)26Sortm4(ACTB-tdTomato,-EGFP)Luo/Gt(ROSA)26Sor+ mice

pigmentation
• after 4-OHT treatment (P21-P50) mice exhibit an early greying phenotype at P50
• however, GFP+ cells associated with hair follicles are present at P100, indicating that melanocyte survival is not significantly affected

integument
• after 4-OHT treatment (P21-P50) mice exhibit an early greying phenotype at P50
• however, GFP+ cells associated with hair follicles are present at P100, indicating that melanocyte survival is not significantly affected




Genotype
MGI:6269417
cn33
Allelic
Composition
Ctnnb1tm2Kem/Ctnnb1tm2Kem
Tg(KRT14-rtTA)F42Efu/0
Tg(tetO-EDN1,-lacZ)9Mhus/0
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
involves: C57BL/6J * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ctnnb1tm2Kem mutation (1 available); any Ctnnb1 mutation (21 available)
Tg(KRT14-rtTA)F42Efu mutation (1 available)
Tg(tetO-EDN1,-lacZ)9Mhus mutation (1 available)
Tg(Tyr-cre/ERT2)13Bos mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
pigmentation
• following depletion of beta-catenin in McSCs during anagen, McSCs fail to differentiate as shown by the absence of pigment and Tyr expression in McSCs at anagen onset
• following depletion of beta-catenin in McSCs during anagen, McSCs fail to proliferate as shown by the absence of Ki67 expression in McSCs at anagen onset; this is in contrast to control littermates that overexpress Edn1 with intact Wnt signaling
• following depletion of beta-catenin in McSCs during anagen, mice develop a hair-graying phenotype by the 2nd telogen; this is in contrast to control littermates that overexpress Edn1 with intact Wnt signaling
• following depletion of beta-catenin in McSCs during anagen, wounded mice show a significant reduction in the number of epidermal melanocytes relative to control littermates that overexpress Edn1 with intact Wnt signaling

integument
• following depletion of beta-catenin in McSCs during anagen, mice develop a hair-graying phenotype by the 2nd telogen; this is in contrast to control littermates that overexpress Edn1 with intact Wnt signaling
• following depletion of beta-catenin in McSCs during anagen, wounded mice show a significant reduction in the number of epidermal melanocytes relative to control littermates that overexpress Edn1 with intact Wnt signaling

cellular
• following depletion of beta-catenin in McSCs during anagen, McSCs fail to differentiate as shown by the absence of pigment and Tyr expression in McSCs at anagen onset
• following depletion of beta-catenin in McSCs during anagen, McSCs fail to proliferate as shown by the absence of Ki67 expression in McSCs at anagen onset; this is in contrast to control littermates that overexpress Edn1 with intact Wnt signaling





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
09/10/2019
MGI 6.14
The Jackson Laboratory