Phenotypes associated with this allele

• Allele Symbol: Sod2^tm1Smel
• Allele Name: targeted mutation 1, Simon Melov
• Allele ID: MGI:5788667
• Summary: 1 genotype

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Sod2^tm1Smel/Sod2^tm1Smel Tg(KRT14-cre/ERT)20Efu/0	involves: C57BL/6J * CD-1	MGI:5804631

Genotype
MGI:5804631

cn1

• Allelic Composition: Sod2^tm1Smel/Sod2^tm1Smel; Tg(KRT14-cre/ERT)20Efu/0
• Genetic Background: involves: C57BL/6J * CD-1

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

homeostasis/metabolism

delayed wound healing ( J:226565 )

• after a skin biopsy, 14-mo-old mice treated with TAM at 4 months show delayed wound closure relative to vehicle-treated mice

• faster wound closure noted in 8-mo-old mice is lost at 11 months of age (i.e. at 7 months after TAM treatment)

enhanced wound healing ( J:226565 )

• 8-mo-old mice treated with TAM at 4 months show accelerated wound closure after a skin biopsy relative to vehicle-treated mice

• young TAM-treated mice show an unusually thick layer of epidermal cells near the wound edges but no difference in collagen formation, suggesting rapid re-epithelialization

• faster wound closure in young TAM-treated mice is likely due to a transient increase in epidermal differentiation, rather than increased cell proliferation

cellular

abnormal keratinocyte differentiation ( J:226565 )

• at 6 days after skin injury, wounds in young TAM-treated mice show a few cells in the stratum basale (SB) layer and a prominent stratum granulosum (SG) layer, suggesting accelerated epidermal differentiation during wound healing

• however, acceleration is only transient, as no difference in epidermal stratification is noted between young TAM- and vehicle-treated mice at 10 days after injury

decreased keratinocyte proliferation ( J:226565 )

• whereas TPA treatment enhances epidermal proliferation in vehicle-treated mice, TPA induces less proliferation in the epidermis of 8-mo-old mice pretreated with TAM at 4 months, as determined by Ki67 staining

early cellular replicative senescence ( J:226565 )

• 8-mo-old mice treated with TAM at 4 months show a 2.5-fold higher senescence-associated beta-galactosidase activity in the epidermis relative to vehicle treated mice; staining is more evident in the stratum corneum or more differentiated layers

• epidermal p16^INK4a mRNA is detectable in most (>70%) skin samples at 4 months and even at 10 months after TAM treatment

abnormal mitochondrial ATP synthesis coupled electron transport ( J:226565 )

• 8-mo-old mice treated with TAM at 4 months show significantly less succinate dehydrogenase (complex II) activity in epidermis/hair follicles, but not in skeletal muscle beneath the stratum corneum layer, relative to vehicle-treated mice

• however, mitochondrial complex IV (COX) activity is similar in TAM- and vehicle-treated mice

integument

abnormal keratinocyte differentiation ( J:226565 )

• at 6 days after skin injury, wounds in young TAM-treated mice show a few cells in the stratum basale (SB) layer and a prominent stratum granulosum (SG) layer, suggesting accelerated epidermal differentiation during wound healing

• however, acceleration is only transient, as no difference in epidermal stratification is noted between young TAM- and vehicle-treated mice at 10 days after injury

decreased keratinocyte proliferation ( J:226565 )

• whereas TPA treatment enhances epidermal proliferation in vehicle-treated mice, TPA induces less proliferation in the epidermis of 8-mo-old mice pretreated with TAM at 4 months, as determined by Ki67 staining

abnormal epidermis stratum corneum morphology ( J:226565 )

• TPA treatment causes stratum corneum (SC) separation in 8-mo-old mice pretreated with TAM at 4 months of age

thick epidermis ( J:226565 )

• after a skin biopsy, 8-mo-old mice treated with TAM at 4 months show an unusually thick layer of epidermal cells near the wound edges relative to vehicle-treated mice

thin epidermis ( J:226565 )

• TAM-treated mice exhibit faster age-related epidermal thinning with a significant decline in epidermal thickness at 7 months after TAM treatment, whereas vehicle-treated mice show epidermal thinning after 10 months of vehicle treatment

• TPA (12-O-tetradecanoylphorbol-13-acetate) treatment fails to promote epidermal thickening in TAM-treated mice, unlike in vehicle-treated mice

skin lesions ( J:226565 )

• TPA treatment causes epidermal lesions in 8-mo-old mice pretreated with TAM at 4 months of age

decreased epidermal stem cell number ( J:226565 )

• 14-mo-old mice treated with TAM at 4 months show a marked reduction in epidermal bulge stem cells (CD49f^hi/CD34⁺), suprabasal bulge stem cells (CD49f^lo/CD34⁺), and junctional zone stem cells (CD49f^hi/CD34^-/Sca1^-) relative to vehicle-treated mice, indicating epidermal stem cell exhaustion