All Phenotypes Pard3<tm1Shoh> MGI Mouse

Phenotypes associated with this allele

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Krt14^tm1(cre)Wbm/Krt14⁺ Pard3^tm1Shoh/Pard3^tm1Shoh	either: FVB.129-Pard3^tm1Shoh Krt14^tm1(cre)Wbm or (involves: 129P2/OlaHsd * 129S4/SvJae)	MGI:6258533
cn2	Krt14^tm1(cre)Wbm/Krt14⁺ Pard3^tm1Shoh/Pard3^tm1Shoh Tg(HIST1H2BB/EGFP)1Pa/0	involves: 129 * C57BL/6J	MGI:6272614
cn3	Krt14^tm1(cre)Wbm/Krt14⁺ Pard3^tm1Shoh/Pard3^tm1Shoh	involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6J	MGI:6272603
cn4	Cdk4^tm1.1Bbd/Cdk4^tm1.1Bbd Krt14^tm1(cre)Wbm/Krt14⁺ Pard3^tm1Shoh/Pard3^tm1Shoh Tg(Mt1-Hgf)#Lmb/0	involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6J	MGI:6272611

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

neoplasm

neoplasm ( J:192905 )

N	• untreated mice are viable and reach adulthood with no development of spontaneous skin tumors

decreased incidence of tumors by chemical induction ( J:192905 )

• in a 2-stage DMBA/TPA skin carcinogenesis model, papilloma formation is delayed by ~3 weeks, tumor multiplicity is strongly reduced, and tumors that do form grow slower than in similarly treated wild-type controls

increased incidence of tumors by chemical induction ( J:192905 )

• in a 2-stage DMBA/TPA skin carcinogenesis model, mice show increased incidence of keratoacanthomas (KAs) with typical crater-like morphology, broad tumor base and a keratin-filled center, and tumor sizes that reach >1 cm by 22 weeks post-initiation requiring termination

• at termination, 91% of DMBA/TPA mice are KA-positive versus 27% of wild-type controls

• however, incidence of squamous cell carcinomas (SCCs) is relatively normal

increased metastatic potential ( J:192905 )

• 45% of the relatively small papillomas found in in DMBA/TPA-treated mice show local invasion of tumor cells into the stroma versus 33% of the abundant larger papillomas found in wild-type controls

• 36% of keratoacanthomas (KAs) found in in DMBA/TPA-treated show local invasion into the stroma versus 0% of the KAs found in wild-type controls

decreased tumor growth/size ( J:192905 )

• in response to DMBA/TPA treatment, papillomas that form grow slower than in wild-type controls

• at 14.5 weeks post-DMBA treatment, average papilloma size is significantly smaller than that in wild-type controls

• epidermal cell proliferation is significantly reduced, whereas epidermal apoptosis is significantly increased relative to wild-type controls

increased tumor growth/size ( J:192905 )

• at 22 weeks post-DMBA treatment, keratoacanthomas reach an average size of >1 cm, unlike in wild-type controls

decreased tumor latency ( J:192905 )

• DMBA/TPA-treated mice show accelerated appearance of keratoacanthomas relative to wild-type controls, with KAs first detected at 7 weeks post-DMBA treatment

increased tumor latency ( J:192905 )

• in DMBA/TPA-treated mice, papilloma formation is delayed by ~3 weeks relative to wild-type controls

homeostasis/metabolism

decreased incidence of tumors by chemical induction ( J:192905 )

increased incidence of tumors by chemical induction ( J:192905 )

• at termination, 91% of DMBA/TPA mice are KA-positive versus 27% of wild-type controls

• however, incidence of squamous cell carcinomas (SCCs) is relatively normal

Allelic Composition	Krt14^tm1(cre)Wbm/Krt14⁺ Pard3^tm1Shoh/Pard3^tm1Shoh Tg(HIST1H2BB/EGFP)1Pa/0
Genetic Background	involves: 129 * C57BL/6J

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krt14^tm1(cre)Wbm mutation (0 available); any Krt14 mutation (37 available)
Pard3^tm1Shoh mutation (0 available); any Pard3 mutation (96 available)
Tg(HIST1H2BB/EGFP)1Pa mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

pigmentation

abnormal melanocyte morphology ( J:240961 )

• in P58 tail whole mounts, melanocytes (MCs) show a more stubby dendritic morphology with dendritic shortening and a more spread cell body area relative to MCs in control mice

Allelic Composition	Krt14^tm1(cre)Wbm/Krt14⁺ Pard3^tm1Shoh/Pard3^tm1Shoh
Genetic Background	involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6J

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

neoplasm

increased incidence of tumors by chemical induction ( J:240961 )

• in a 2-stage DMBA/TPA skin carcinogenesis model, mice show increased melanocytic hyperplasia and incidence of melanoma relative to control mice

pigmentation

abnormal hair follicle melanocyte morphology ( J:240961 )

• under non-tumorigenic conditions, mice show a significant increase in melanocyte number per hair follicle in back skin relative to control mice at P0, at 7 weeks, and at 4 and 12 months of age

• both the number of P-cadherin-positive keratinocytes in interfollicular epidermis and melanocyte number contacting dense P-cadherin-positive cell clusters in developing hair follicles are significantly increased relative to controls

abnormal epidermal melanocyte morphology ( J:240961 )

• under non-tumorigenic conditions, newborn (P0) mice show a significant increase in interfollicular melanocytes in back skin relative to control mice

• P-cadherin-positive clusters are enlarged in interfollicular epidermis, with frequent localization of melanocytes to these compartments

increased melanocyte number ( J:240961 )

• in a 2-stage DMBA/TPA skin carcinogenesis model, mice show increased melanocytic hyperplasia in the epidermis relative to control mice

• under non-tumorigenic conditions, mice show a significantly higher melanocyte number in back skin relative to control mice at P0 and all adult ages tested

integument

abnormal hair follicle melanocyte morphology ( J:240961 )

• under non-tumorigenic conditions, mice show a significant increase in melanocyte number per hair follicle in back skin relative to control mice at P0, at 7 weeks, and at 4 and 12 months of age

abnormal epidermal melanocyte morphology ( J:240961 )

• under non-tumorigenic conditions, newborn (P0) mice show a significant increase in interfollicular melanocytes in back skin relative to control mice

• P-cadherin-positive clusters are enlarged in interfollicular epidermis, with frequent localization of melanocytes to these compartments

homeostasis/metabolism

increased incidence of tumors by chemical induction ( J:240961 )

• in a 2-stage DMBA/TPA skin carcinogenesis model, mice show increased melanocytic hyperplasia and incidence of melanoma relative to control mice

Allelic Composition	Cdk4^tm1.1Bbd/Cdk4^tm1.1Bbd Krt14^tm1(cre)Wbm/Krt14⁺ Pard3^tm1Shoh/Pard3^tm1Shoh Tg(Mt1-Hgf)#Lmb/0
Genetic Background	involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6J

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdk4^tm1.1Bbd mutation (0 available); any Cdk4 mutation (58 available)
Krt14^tm1(cre)Wbm mutation (0 available); any Krt14 mutation (37 available)
Pard3^tm1Shoh mutation (0 available); any Pard3 mutation (96 available)
Tg(Mt1-Hgf)#Lmb mutation (0 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

neoplasm

increased incidence of tumors by chemical induction ( J:240961 )

• at 8-15 weeks after DMBA treatment, mice exhibit significantly increased melanoma multiplicity relative to control mice, with primary melanomas invading the dermis and showing tumor-associated angiogenesis

increased metastatic potential ( J:240961 )

• less than 15 weeks after DMBA treatment, mice show increased incidence of distal melanoma metastases in the lungs relative to control mice (57.1% versus 16.7%)

increased tumor growth/size ( J:240961 )

• in DMBA-treated mice, primary melanomas show an increased proliferative index, with a significantly higher number of PCNA^high melanoma cells relative to control mice, consistent with increased melanoma multiplicity

homeostasis/metabolism

increased incidence of tumors by chemical induction ( J:240961 )

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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