Phenotypes associated with this allele

• Allele Symbol: Krt14^tm1(cre)Wbm
• Allele Name: targeted mutation 1, Walter Birchmeier
• Allele ID: MGI:2148596
• Summary: 13 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Arpc4^tm1c(EUCOMM)Wtsi/Arpc4^tm1c(EUCOMM)Wtsi Krt14^tm1(cre)Wbm/Krt14^+	B6.Cg-Arpc4^tm1c(EUCOMM)Wtsi Krt14^tm1(cre)Wbm	MGI:6115481
cn2	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
cn3	Cd151^tm2Nki/Cd151^tm2Nki Itga3^tm1Son/Itga3^+ Krt14^tm1(cre)Wbm/?	FVB.129P2-Cd151^tm2Nki Itga3^tm1Son Krt14^tm1(cre)Wbm	MGI:5550138
cn4	Cd151^tm2Nki/Cd151^tm2Nki Krt14^tm1(cre)Wbm/?	FVB.129P2-Cd151^tm2Nki Krt14^tm1(cre)Wbm	MGI:5550137
cn5	Krt14^tm1(cre)Wbm/Krt14^+ Pard3^tm1Shoh/Pard3^tm1Shoh Tg(HIST1H2BB/EGFP)1Pa/0	involves: 129 * C57BL/6J	MGI:6272614
cn6	Ctnnb1^tm4Wbm/Ctnnb1^tm4Wbm Krt14^tm1(cre)Wbm/Krt14^+	involves: 129P2/OlaHsd	MGI:5547809
cn7	Zbtb17^tm1Cksn/Zbtb17^tm1.1Cksn Krt14^tm1(cre)Wbm/Krt14^+	involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ	MGI:3721960
cn8	Zbtb17^tm1Cksn/Zbtb17^tm1Cksn Krt14^tm1(cre)Wbm/Krt14^+	involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ	MGI:3721959
cn9	Krt14^tm1(cre)Wbm/Krt14^+ Pard3^tm1Shoh/Pard3^tm1Shoh	involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6J	MGI:6272603
cn10	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
cn11	Ctnnb1^tm4Wbm/Ctnnb1^tm4Wbm Krt14^tm1(cre)Wbm/Krt14^+	involves: 129P2/OlaHsd * C57BL/6	MGI:2673246
cn12	Wls^tm1.1Arte/Wls^tm1.1Arte Krt14^tm1(cre)Wbm/Krt14^+	involves: 129P2/OlaHsd * C57BL/6	MGI:5547811
cn13	Itga3^tm1Son/Itga3^tm1Son Krt14^tm1(cre)Wbm/Krt14^+	involves: 129P2/OlaHsd * FVB/N	MGI:3836769

Genotype
MGI:6115481

cn1

• Allelic Composition: Arpc4^{tm1c(EUCOMM)Wtsi}/Arpc4^{tm1c(EUCOMM)Wtsi}; Krt14^tm1(cre)Wbm/Krt14⁺
• Genetic Background: B6.Cg-Arpc4^{tm1c(EUCOMM)Wtsi} Krt14^tm1(cre)Wbm
• Cell Lines: EPD0058_1_A11

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

integument

abnormal keratinocyte differentiation ( J:253986 )

• molecular analysis revealed disrupted keratinocyte differentiation

absent sebaceous gland ( J:253986 )

• at P7, hair follicles in psoriasis-like lesions often lack the sebaceous gland

abnormal head skin morphology ( J:253986 )

• at P1, local thickening of the epidermis, mainly the cornified layer, and scattered ghost (anucleated) cells are mostly evident in the head region

alopecia ( J:253986 )

• at P5, pups exhibit uneven skin thickening with alopecic areas

• at P7, hair follicles in psoriasis-like lesions often lack the shaft

sparse hair ( J:253986 )

• at P5, body and extremities show poorly furred skin

decreased hair follicle number ( J:253986 )

• at P7, hair follicles in psoriasis-like lesions are rare

hyperkeratosis ( J:253986 )

• at P7, the cornified layer is abnormally thickened

parakeratosis ( J:253986 )

• at P7, the thickened cornified layer is characterized by the presence of nuclei and microabscesses

acanthosis ( J:253986 )

• at P7, the epidermal squamous cells exhibit hyperplasia (acanthosis)

thick epidermis ( J:253986 )

• at P1, local thickening of the epidermis, mainly the cornified layer, are mostly evident in the head region

• at P5, body and extremities show unevenly thickened skin

abnormal skin appearance ( J:253986 )

• at P5, pups exhibit abnormal skin appearance with uneven thickening accompanied by alopecic areas

dry skin ( J:253986 )

• at P5, body and extremities show dry skin

scaly skin ( J:253986 )

• over time, psoriasis-like lesions acquire an ichthyosis-like appearance

skin lesions ( J:253986 )

• initial skin lesions are detected microscopically at P1; mice have to be euthanized by P21 due to the severity of skin lesions

psoriasis ( J:253986 )

• at P1, local thickening of the epidermis, mainly the cornified layer, and scattered ghost (anucleated) cells are mostly evident in the head region

• initial skin lesions develop progressively into macroscopic psoriasis-like plaques

• psoriasis-like lesions are variable in size and usually more severe in the dorsal than in the ventral trunk, extremities and head

• over time, psoriasis-like lesions acquire an ichthyosis-like appearance

• psoriatic epidermis exhibits hyperactivation of transcription factor Nrf2 and decreased F-actin levels

• however, mice do not exhibit any outside-in epidermal permeability barrier defects

abnormal skin physiology ( J:253986 )

• skin lesions show increased Ki67 positivity in both the basal and the suprabasal epidermal layers

• at P4, the mutant epidermis shows increased nuclear Nrf2 levels; whereas the number of Nrf2-positive interfollicular keratinocytes declines with age in wild-type epidermis, Nrf2 expression remains ubiquitous in psoriasis-like lesions at P14, indicating Nrf2 hyperactivation

dermatitis ( J:253986 )

• at P7, P14 and P21, inflammatory infiltrations mainly consisting of lymphocytic cells are detected in the dermis

cellular

abnormal keratinocyte differentiation ( J:253986 )

• molecular analysis revealed disrupted keratinocyte differentiation

endocrine/exocrine glands

absent sebaceous gland ( J:253986 )

• at P7, hair follicles in psoriasis-like lesions often lack the sebaceous gland

growth/size/body

abnormal head skin morphology ( J:253986 )

• at P1, local thickening of the epidermis, mainly the cornified layer, and scattered ghost (anucleated) cells are mostly evident in the head region

immune system

dermatitis ( J:253986 )

• at P7, P14 and P21, inflammatory infiltrations mainly consisting of lymphocytic cells are detected in the dermis

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
psoriasis		DOID:8893	OMIM:PS177900	J:253986

Genotype
MGI:6258533

cn2

• Allelic Composition: Krt14^tm1(cre)Wbm/Krt14⁺; Pard3^tm1Shoh/Pard3^tm1Shoh
• Genetic Background: either: FVB.129-Pard3^tm1Shoh Krt14^tm1(cre)Wbm or (involves: 129P2/OlaHsd * 129S4/SvJae)

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 )

• 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

Genotype
MGI:5550138

cn3

• Allelic Composition: Cd151^tm2Nki/Cd151^tm2Nki; Itga3^tm1Son/Itga3⁺; Krt14^tm1(cre)Wbm/?
• Genetic Background: FVB.129P2-Cd151^tm2Nki Itga3^tm1Son Krt14^tm1(cre)Wbm

neoplasm

decreased incidence of tumors by chemical induction ( J:205736 )

• reduced tumor volume and incidents in DMBA- and TPA-treated mice more so than in Cd151^tm2Nki/Cd151^tm2Nki Krt14^tm1(cre)Wbm mice

• however, overall benign and malignant histology is normal

decreased tumor growth/size ( J:205736 )

• reduced tumor volume and incidents in DMBA- and TPA-treated mice more so than in Cd151^tm2Nki/Cd151^tm2Nki Krt14^tm1(cre)Wbm mice

integument

decreased keratinocyte proliferation ( J:205736 )

• in papillomas of DMBA- and TPA-treated mice

homeostasis/metabolism

decreased incidence of tumors by chemical induction ( J:205736 )

• reduced tumor volume and incidents in DMBA- and TPA-treated mice more so than in Cd151^tm2Nki/Cd151^tm2Nki Krt14^tm1(cre)Wbm mice

• however, overall benign and malignant histology is normal

cellular

decreased keratinocyte proliferation ( J:205736 )

• in papillomas of DMBA- and TPA-treated mice

Genotype
MGI:5550137

cn4

• Allelic Composition: Cd151^tm2Nki/Cd151^tm2Nki; Krt14^tm1(cre)Wbm/?
• Genetic Background: FVB.129P2-Cd151^tm2Nki Krt14^tm1(cre)Wbm

integument

increased keratinocyte migration ( J:205736 )

• keratinocytes expressing a hair bulge marker are found in the infundibulum and the interfollicular epidermis

• short-term TPA treatment increases the number of keratinocytes expressing a hair bulge marker found in the suprabasal layer

decreased keratinocyte proliferation ( J:205736 )

• in papillomas of DMBA- and TPA-treated mice

abnormal hair follicle morphology ( J:205736 )

• contains fewer long-lived, slow-cycling label-retaining cells (keratinocytes expressing the hair bulge marker)

thin epidermis ( J:205736 )

neoplasm

decreased incidence of tumors by chemical induction ( J:205736 )

• reduced tumor volume and incidents in DMBA- and TPA-treated mice compared with control mice

• however, overall benign and malignant histology is normal

decreased tumor growth/size ( J:205736 )

• reduced tumor volume and incidents in DMBA- and TPA-treated mice compared with control mice

• mildly decreases tumor progression of squamous cell carcinoma induced by DMBA and TPA

homeostasis/metabolism

decreased incidence of tumors by chemical induction ( J:205736 )

• reduced tumor volume and incidents in DMBA- and TPA-treated mice compared with control mice

• however, overall benign and malignant histology is normal

cellular

increased keratinocyte migration ( J:205736 )

• keratinocytes expressing a hair bulge marker are found in the infundibulum and the interfollicular epidermis

• short-term TPA treatment increases the number of keratinocytes expressing a hair bulge marker found in the suprabasal layer

decreased keratinocyte proliferation ( J:205736 )

• in papillomas of DMBA- and TPA-treated mice

Genotype
MGI:6272614

cn5

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

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

Genotype
MGI:5547809

cn6

• Allelic Composition: Ctnnb1^tm4Wbm/Ctnnb1^tm4Wbm; Krt14^tm1(cre)Wbm/Krt14⁺
• Genetic Background: involves: 129P2/OlaHsd

immune system

increased neutrophil cell number ( J:202499 )

• enhanced infiltration in the skin

decreased gamma-delta T cell number ( J:202499 )

• decrease in gamma-delta TCR+ T cells (dendritic epidermal T cells) in the skin

hematopoietic system

increased neutrophil cell number ( J:202499 )

• enhanced infiltration in the skin

decreased gamma-delta T cell number ( J:202499 )

• decrease in gamma-delta TCR+ T cells (dendritic epidermal T cells) in the skin

Genotype
MGI:3721960

cn7

• Allelic Composition: Zbtb17^tm1Cksn/Zbtb17^tm1.1Cksn; Krt14^tm1(cre)Wbm/Krt14⁺
• Genetic Background: involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ

integument

rough coat ( J:123966 )

• 100% of mice have rough fur

• initially rough areas appear in stripes

Genotype
MGI:3721959

cn8

• Allelic Composition: Zbtb17^tm1Cksn/Zbtb17^tm1Cksn; Krt14^tm1(cre)Wbm/Krt14⁺
• Genetic Background: involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ

pigmentation

darkened coat color ( J:123966 )

• at one year of age mice have darker coat and skin than wild-type mice

• in areas of substantial hair loss a black dot-like area is visible

• light-tipped zigzag hairs are decreased in number

abnormal hair follicle melanocyte morphology ( J:123966 )

• back skin displays abnormal content distribution of melanin

• in areas of substantial hair loss a black dot-like area is visible

• mice exhibit focal areas in the dermis and subcutis around hair follicles with high melanin content

integument

increased keratinocyte proliferation ( J:123966 )

• keratinocyte located at the orifice of the hair funnel exhibit increased proliferation

• proliferation of keratinocyte in the anagen but not the catagen of the hair cycle is increased

abnormal coat/ hair morphology ( J:123966 )

darkened coat color ( J:123966 )

• at one year of age mice have darker coat and skin than wild-type mice

• in areas of substantial hair loss a black dot-like area is visible

• light-tipped zigzag hairs are decreased in number

abnormal hair follicle melanocyte morphology ( J:123966 )

• back skin displays abnormal content distribution of melanin

• in areas of substantial hair loss a black dot-like area is visible

• mice exhibit focal areas in the dermis and subcutis around hair follicles with high melanin content

focal dorsal hair loss ( J:123966 )

• mice experience hair loss on the back skin without a reduction in the number of hair follicles

sparse hair ( J:123966 )

• hair density is decreased

rough coat ( J:123966 )

• 100% of mice have rough fur

• initially rough areas appear in stripes

decreased curvature of zigzag hairs ( J:123966 )

decreased zigzag hair amount ( J:123966 )

• only 24% to 54% of hairs are of the zigzag type compared to 70% in wild-type mice

abnormal hair follicle morphology ( J:123966 )

• hair follicle length is highly variable relative to in wild-type mice

• cyst-like hair follicles containing hair remnants are observed in some areas

• cystic alterations occur in the upper part of the follicle and epithelium of the cyst-like structure is continuous with the epidermis

• the number of hair follicles extending into the subcutis is increased relative to in wild-type mice

• catagen during the hair cycle is delayed

• at one year of age, numerous back skin hair follicles are thickened

abnormal hair follicle orientation ( J:123966 )

• the orientation of hair follicles is altered relative to in wild-type mice

abnormal epidermal layer morphology ( J:123966 )

• the number of interfollicular epidermal layers is increased

hyperkeratosis ( J:123966 )

cellular

increased keratinocyte proliferation ( J:123966 )

• keratinocyte located at the orifice of the hair funnel exhibit increased proliferation

• proliferation of keratinocyte in the anagen but not the catagen of the hair cycle is increased

Genotype
MGI:6272603

cn9

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

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

• 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

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

Genotype
MGI:6272611

cn10

• 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

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 )

• 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

Genotype
MGI:2673246

cn11

• Allelic Composition: Ctnnb1^tm4Wbm/Ctnnb1^tm4Wbm; Krt14^tm1(cre)Wbm/Krt14⁺
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6

integument

abnormal hair growth ( J:69463 )

alopecia ( J:69463 )

• hairless patches at 8 days of age

• hair placodes absent where Catnb is not expressed

• initial phase hair growth occurs until 16 days

• reduced number of zigzag hairs

• hair lost around 4 weeks of age and no regrowth

Genotype
MGI:5547811

cn12

• Allelic Composition: Wls^tm1.1Arte/Wls^tm1.1Arte; Krt14^tm1(cre)Wbm/Krt14⁺
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6

mortality/aging

premature death ( J:202499 )

• mice die within 10 weeks

integument

epidermal spongiosis ( J:202499 )

abnormal hair growth ( J:202499 )

• hair loss begins during the first hair cycle

sparse hair ( J:202499 )

• less dense at P6

thin hypodermis ( J:202499 )

decreased hair follicle number ( J:202499 )

• fewer follicles develop and degenerate to cyst-like structures

hair follicle degeneration ( J:202499 )

• degenerate to cyst-like structures

thin dermal layer ( J:202499 )

abnormal skin appearance ( J:202499 )

• irritated, flaky and thin skin with exposed blood vessels

• Munro's microabscesses all over the skin

flaky skin ( J:202499 )

reddish skin ( J:202499 )

• red-nose phenotype at P6

scaly skin ( J:202499 )

thin skin ( J:202499 )

abnormal skin physiology ( J:202499 )

• hyperproliferative epidermis with increased proportion of proliferating basal cells but fewer number of proliferating cells in the bulb

increased keratinocyte proliferation ( J:202499 )

impaired skin barrier function ( J:202499 )

• at P6, but not in neonates

skin inflammation ( J:202499 )

• with fluid retention

• neutrophil infiltration in the dermis at P16 that is not reduced by antibiotic treatment

immune system

small thymus medulla ( J:202499 )

• reduced at P90, but not P4 or P28

decreased thymus weight ( J:202499 )

• relative weight at P21 and P65, but not P4

thymus atrophy ( J:202499 )

thymus hypoplasia ( J:202499 )

• at P40, but not P4

abnormal T cell differentiation ( J:202499 )

• T cell maturation is shifted away from alpha/beta T cells in the thymus at P40

increased double-negative T cell number ( J:202499 )

• at P40 in the thymus

decreased double-positive T cell number ( J:202499 )

• at P40 in the thymus

cutaneous mastocytosis ( J:202499 )

• increased mast cell number in the skin

increased neutrophil cell number ( J:202499 )

• neutrophil infiltration in the dermis at P16 that is not reduced by antibiotic treatment

abnormal T cell subpopulation ratio ( J:202499 )

• the ratio of CD4 to CD8 T cells is decreased at P40 in the thymus, lymph node and blood

decreased T cell number ( J:202499 )

• reduced CD3+ T cells in the thymus

decreased gamma-delta T cell number ( J:202499 )

• age-dependent decrease in gamma-delta TCR+ T cells (dendritic epidermal T cells) in the skin

increased macrophage cell number ( J:202499 )

• in the skin

abnormal T cell physiology ( J:202499 )

• dendritic epidermal T cell survival is impaired

increased T cell proliferation ( J:202499 )

• of dendritic epidermal T cell

skin inflammation ( J:202499 )

• with fluid retention

• neutrophil infiltration in the dermis at P16 that is not reduced by antibiotic treatment

vision/eye

abnormal eye morphology ( J:202499 )

• swollen eye

hearing/vestibular/ear

abnormal ear morphology ( J:202499 )

craniofacial

abnormal nose morphology ( J:202499 )

• red-nose phenotype at P6

respiratory system

abnormal nose morphology ( J:202499 )

• red-nose phenotype at P6

adipose tissue

abnormal adipose tissue physiology ( J:202499 )

• mice exhibit lack of fat tissue sustainment

growth/size/body

abnormal nose morphology ( J:202499 )

• red-nose phenotype at P6

decreased body size ( J:202499 )

postnatal growth retardation ( J:202499 )

homeostasis/metabolism

decreased body surface temperature ( J:202499 )

• in adult mice

epidermal spongiosis ( J:202499 )

impaired skin barrier function ( J:202499 )

• at P6, but not in neonates

hematopoietic system

small thymus medulla ( J:202499 )

• reduced at P90, but not P4 or P28

decreased thymus weight ( J:202499 )

• relative weight at P21 and P65, but not P4

thymus atrophy ( J:202499 )

thymus hypoplasia ( J:202499 )

• at P40, but not P4

abnormal T cell differentiation ( J:202499 )

• T cell maturation is shifted away from alpha/beta T cells in the thymus at P40

increased double-negative T cell number ( J:202499 )

• at P40 in the thymus

cutaneous mastocytosis ( J:202499 )

• increased mast cell number in the skin

increased neutrophil cell number ( J:202499 )

• neutrophil infiltration in the dermis at P16 that is not reduced by antibiotic treatment

abnormal T cell subpopulation ratio ( J:202499 )

• the ratio of CD4 to CD8 T cells is decreased at P40 in the thymus, lymph node and blood

decreased T cell number ( J:202499 )

• reduced CD3+ T cells in the thymus

decreased double-positive T cell number ( J:202499 )

• at P40 in the thymus

decreased gamma-delta T cell number ( J:202499 )

• age-dependent decrease in gamma-delta TCR+ T cells (dendritic epidermal T cells) in the skin

increased macrophage cell number ( J:202499 )

• in the skin

abnormal T cell physiology ( J:202499 )

• dendritic epidermal T cell survival is impaired

increased T cell proliferation ( J:202499 )

• of dendritic epidermal T cell

cellular

increased T cell proliferation ( J:202499 )

• of dendritic epidermal T cell

increased keratinocyte proliferation ( J:202499 )

endocrine/exocrine glands

small thymus medulla ( J:202499 )

• reduced at P90, but not P4 or P28

decreased thymus weight ( J:202499 )

• relative weight at P21 and P65, but not P4

thymus atrophy ( J:202499 )

thymus hypoplasia ( J:202499 )

• at P40, but not P4

Genotype
MGI:3836769

cn13

• Allelic Composition: Itga3^tm1Son/Itga3^tm1Son; Krt14^tm1(cre)Wbm/Krt14⁺
• Genetic Background: involves: 129P2/OlaHsd * FVB/N

homeostasis/metabolism

enhanced wound healing ( J:145988 )

• wound healing of the epidermis is accelerated

• about 90% of experimental wounds are closed after one week compared to about 60% in controls

• this enhanced wound healing is due to accelerated keratinocyte migration from sides of wound and not from increased proliferation

immune system

skin inflammation ( J:145988 )

• inflammation occurs frequently around 3 to 4 months of age at the ears and around the eyes

integument

skin inflammation ( J:145988 )

• inflammation occurs frequently around 3 to 4 months of age at the ears and around the eyes

alopecia ( J:145988 )

• alopecia starts at 3- to 4- months after birth and progresses with age

blistering ( J:145988 )

• microblisters occur at the dermis-epidermis junction

thick skin ( J:145988 )

• epidermis is thickened around the ears, the eyes, and at sites of microblistering