Phenotypes associated with this allele
|
Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Terf1tm1.1Blas mutation
(0 available);
any
Terf1 mutation
(35 available)
|
|
|
cellular
|
• mouse embryonic fibroblasts transfected with cre adenovirus exhibit an increase in multitelomeric signals compared to in similarly treated wild-type cells
|
|
• mouse embryonic fibroblasts transfected with cre adenovirus exhibit an increase in telomeres dysfunction-induced foci compared with un-infected cells
|
|
• mouse embryonic fibroblasts transfected with cre adenovirus fail to proliferate due to rapid induction of senescence unlike similarly treated wild-type cells
• however, additional transfection with Trp53 short hairpin RNA restores proliferation
|
|
• mouse embryonic fibroblasts transfected with cre adenovirus fail to proliferate due to rapid induction of senescence unlike similarly treated wild-type cells
• however, additional transfection with Trp53 short hairpin RNA restores normal senescence
|
|
Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Terf1tm1.1Blas mutation
(0 available);
any
Terf1 mutation
(35 available)
Tg(KRT5-cre)1Tak mutation
(0 available)
|
|
|
mortality/aging
|
• although born in Mendelian ratios, only 8% of mice reach P3
|
digestive/alimentary system
|
• in 72% of mice, palate epithelium is dysplastic in areas with nuclear atypia and areas of hyperkeratosis
|
|
• in 78% of mice, tongue epithelium is dysplastic with lack of filiform papillae and severe hyperkeratosis
|
|
• one mouse exhibited a collapsed lumen filled with lamellate keratin
|
|
• hyperkeratosis and dysplasia of the esophagus in 17% of mice
|
|
• in 22% of mice, the non-glandular stomach exhibit dysplasia with nuclear pleomorphism and collapsed lumen with lamellate keratin
|
growth/size/body
|
• in 72% of mice, palate epithelium is dysplastic in areas with nuclear atypia and areas of hyperkeratosis
|
|
• in 78% of mice, tongue epithelium is dysplastic with lack of filiform papillae and severe hyperkeratosis
|
|
• after birth, mice fail to gain weight after birth
|
|
• after birth, mice fail to gain weight after birth
|
homeostasis/metabolism
craniofacial
|
• in 72% of mice, palate epithelium is dysplastic in areas with nuclear atypia and areas of hyperkeratosis
|
|
• in 78% of mice, tongue epithelium is dysplastic with lack of filiform papillae and severe hyperkeratosis
|
endocrine/exocrine glands
cellular
|
• keratinocytes exhibit increased DNA damage foci specifically localized to the telomeres compared to in wild-type cells
|
|
• skin cells exhibit no telomere shortening unlike in wild-type cells
|
immune system
|
• mice exhibit mixed inflammatory infiltration in the dermis
|
pigmentation
|
• severe skin hyperpigmentation
|
integument
|
• mice exhibit skin and follicular papillary atrophy
• skin cells exhibit no telomere shortening unlike in wild-type cells
|
|
• the stratified epithelia of the tongue, palate, esophagus, and nongrandular stomach exhibit severe hyperkeratosis and dysplasia unlike in wild-type mice
|
|
• severe skin hyperpigmentation
|
|
• proliferation of skin cells is decreased compared to in wild-type mice with an arrest in G2/M
• epidermal stem cells fail to form colonies in an clonogenic assay unlike wild-type cells
|
|
• mice exhibit mixed inflammatory infiltration in the dermis
|
|
• keratinocytes fail to form colonies in an clonogenic assay unlike wild-type cells
|
|
Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Terf1tm1.1Blas mutation
(0 available);
any
Terf1 mutation
(35 available)
Tg(KRT5-cre)1Tak mutation
(0 available)
Trp53tm1Tyj mutation
(12 available);
any
Trp53 mutation
(232 available)
|
|
|
mortality/aging
N |
• perinatal and early postnatal lethality is normal
|
neoplasm
|
• in tail and ear skin of older mice
|
craniofacial
digestive/alimentary system
integument
N |
• hair growth and skin pigmentation are normal
|
|
• in tail and ear skin of older mice
|
growth/size/body