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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tmem258tm1.1(KOMP)Vlcg
targeted mutation 1.1, Velocigene
MGI:5892142
Summary 3 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Tmem258tm1.1(KOMP)Vlcg/Tmem258tm1.1(KOMP)Vlcg involves: C57BL/6NTac MGI:5897843
ht2
Tmem258tm1.1(KOMP)Vlcg/Tmem258+ involves: C57BL/6NTac MGI:5897844
cn3
Gt(ROSA)26Sortm1(CAG-cas9*,-EGFP)Fezh/?
Tmem258tm1.1(KOMP)Vlcg/Tmem258+
involves: C57BL/6NTac MGI:5897845


Genotype
MGI:5897843
hm1
Allelic
Composition
Tmem258tm1.1(KOMP)Vlcg/Tmem258tm1.1(KOMP)Vlcg
Genetic
Background
involves: C57BL/6NTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tmem258tm1.1(KOMP)Vlcg mutation (0 available); any Tmem258 mutation (13 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• no homozygotes are recovered from multiple breeding pairs; no signs of fetal resorption are detected in timed matings, suggesting early embryonic lethality




Genotype
MGI:5897844
ht2
Allelic
Composition
Tmem258tm1.1(KOMP)Vlcg/Tmem258+
Genetic
Background
involves: C57BL/6NTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tmem258tm1.1(KOMP)Vlcg mutation (0 available); any Tmem258 mutation (13 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• DSS-treated heterozygotes exhibit a higher frequency of apoptotic colonic epithelial cells than DSS-treated wild-type controls, as shown by active caspase 3 staining
• DSS-treated heterozygotes exhibit decreased proliferation and disorganized dispersion of colonic epithelial cells relative to DSS-treated wild-type controls, as shown by Ki67 staining
• DSS-treated heterozygotes show more severe colonic crypt destruction than DSS-treated wild-type controls
• DSS-treated heterozygotes show reduced colon length relative to DSS-treated wild-type controls
• at day 8 after oral administration of 2.5% dextran sulfate sodium (DSS), heterozygotes show accelerated weight loss, increased histopathological severity scores (based on severity of inflammation, depth of inflammation and crypt damage), decreased colon length, reduced epithelial proliferation in response to injury, and a marked inflammatory gene expression signature in colonic tissue relative to wild-type controls
• however, untreated heterozygotes exhibit normal intestinal barrier function
• following oral administration of 2.5% DSS for 7 days, heterozygotes show accelerated mortality with a >75% decline in survival at 10 and 15 days post-treatment, unlike in wild-type controls where a ~40% decline in survival does not occur until 15 days post-treatment

growth/size/body
• DSS-treated heterozygotes show accelerated weight loss relative to DSS-treated wild-type controls

immune system
• at day 8 after oral administration of 2.5% dextran sulfate sodium (DSS), heterozygotes show accelerated weight loss, increased histopathological severity scores (based on severity of inflammation, depth of inflammation and crypt damage), decreased colon length, reduced epithelial proliferation in response to injury, and a marked inflammatory gene expression signature in colonic tissue relative to wild-type controls
• however, untreated heterozygotes exhibit normal intestinal barrier function
• following oral administration of 2.5% DSS for 7 days, heterozygotes show accelerated mortality with a >75% decline in survival at 10 and 15 days post-treatment, unlike in wild-type controls where a ~40% decline in survival does not occur until 15 days post-treatment

endocrine/exocrine glands
• DSS-treated heterozygotes show more severe colonic crypt destruction than DSS-treated wild-type controls

cellular
• DSS-treated heterozygotes exhibit a higher frequency of apoptotic colonic epithelial cells than DSS-treated wild-type controls, as shown by active caspase 3 staining
• DSS-treated heterozygotes exhibit decreased proliferation and disorganized dispersion of colonic epithelial cells relative to DSS-treated wild-type controls, as shown by Ki67 staining
• after induction of colitis with DSS, heterozygotes show clear evidence of ER stress in the colonic epithelium, with an increased frequency of HSPA5 (BiP/GRP78)-positive epithelial cells relative to wild-type controls
• however, untreated heterozygotes do not exhibit significant ER stress in colonic epithelium

mortality/aging
• following oral administration of 2.5% DSS for 7 days, heterozygotes show accelerated mortality with a >75% decline in survival at 10 and 15 days post-treatment, unlike in wild-type controls where a ~40% decline in survival does not occur until 15 days post-treatment




Genotype
MGI:5897845
cn3
Allelic
Composition
Gt(ROSA)26Sortm1(CAG-cas9*,-EGFP)Fezh/?
Tmem258tm1.1(KOMP)Vlcg/Tmem258+
Genetic
Background
involves: C57BL/6NTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(CAG-cas9*,-EGFP)Fezh mutation (6 available); any Gt(ROSA)26Sor mutation (992 available)
Tmem258tm1.1(KOMP)Vlcg mutation (0 available); any Tmem258 mutation (13 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• after introduction of single guide RNAs (sgRNAs) targeting exonic Tmem258 sequences (Tmem258 CRISPR) by transduction with lentiviral particles co-encoding Cre recombinase, spheroid cultures derived from colonic crypts exhibit fewer viable Cas9-GFP-positive cells than colonic organoid cultures that have received control sgRNAs targeting noncoding intronic Tmem258 regions
• morphologically, Tmem258 CRISPR organoids contain scattered Cas9-GFP-positive cells within small spheroids that encapsulate numerous dead cells within the lumen, whereas control CRISPR organoids appear healthier and larger with contiguous Cas9-GFP-positive cells suggestive of active proliferation
• after simultaneous delivery of Cre recombinase and sgRNA targeting of Tmem258 sequences by lentiviral transduction, Tmem258 CRISPR organoid cultures contain more in-frame mutations in Cas9-GFP-positive cells than control CRISPR organoids, suggesting that out-of-frame alleles are negatively selected, consistent with increased ER stress





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last database update
10/29/2024
MGI 6.24
The Jackson Laboratory