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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Sdc1tm1Cma
targeted mutation 1, Caroline M Alexander
MGI:1934652
Summary 7 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Sdc1tm1Cma/Sdc1tm1Cma B6.Cg-Sdc1tm1Cma MGI:3525353
hm2
Sdc1tm1Cma/Sdc1tm1Cma either: (involves: 129S4/SvJae * BALB/c) or (involves: 129S4/SvJae * C57BL/6) MGI:2653535
hm3
Sdc1tm1Cma/Sdc1tm1Cma either: C.Cg-Sdc1tm1Cma or B6.Cg-Sdc1tm1Cma MGI:3525339
hm4
Sdc1tm1Cma/Sdc1tm1Cma involves: 129S4/SvJae MGI:3717713
hm5
Sdc1tm1Cma/Sdc1tm1Cma involves: 129S4/SvJae * C57BL/6 MGI:3521904
cx6
Sdc1tm1Cma/Sdc1tm1Cma
Tg(Wnt1)1Hev/0
involves: 129S4/SvJae * C57BL/6 * SJL MGI:3521901
cx7
Sdc1tm1Cma/Sdc1+
Tg(Wnt1)1Hev/0
involves: 129S4/SvJae * C57BL/6 * SJL MGI:3521902


Genotype
MGI:3525353
hm1
Allelic
Composition
Sdc1tm1Cma/Sdc1tm1Cma
Genetic
Background
B6.Cg-Sdc1tm1Cma
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Sdc1tm1Cma mutation (0 available); any Sdc1 mutation (23 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• following skin burning, mice are less susceptible to Pseudomonas aeruginosa infection with 13% of mice dying following treatment while 80% of wild-type mice die 48 hours following treatment
• administration of heparin sulfate increases mortality following burning and infection

homeostasis/metabolism
N
• homozygotes display normal heparan sulfate (HS) biosynthesis relative to wild-type
• no changes in HS tissue-specific structures are noted in kidney, lung, skin or spleen with respect to disaccharide species or sulfation degree

immune system
• 24 hours following burning and infection, no bacteria are recovered from the liver whereas wild-type livers contain 3.4x105+/-9x104 colony forming units
• 24 hours following burning and infection, no perivascular cuffing or thrombosis is detected whereas the addition of heparin sulfate results in extensive perivascular cuffing
• following skin burning, mice are less susceptible to Pseudomonas aeruginosa infection with 13% of mice dying following treatment while 80% of wild-type mice die 48 hours following treatment
• administration of heparin sulfate increases mortality following burning and infection




Genotype
MGI:2653535
hm2
Allelic
Composition
Sdc1tm1Cma/Sdc1tm1Cma
Genetic
Background
either: (involves: 129S4/SvJae * BALB/c) or (involves: 129S4/SvJae * C57BL/6)
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Sdc1tm1Cma mutation (0 available); any Sdc1 mutation (23 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• at 7 days, mutant newborns are resistant to P. aeruginosa (strain PAO1) lung infection induced through intranasal administration
• mutant newborns exhibit reduced lung and spleen colonization by P. aeruginosa and survive the infection with little or no formation of inflammatory lung foci
• resistance to P. aeruginosa infection can be reversed by administering purified shed syndecan-1 ectodomains or heparin but not heparan sulphate-free syndecan-1 core protein or chondroitin sulphate
• notably, mutant newborns are as susceptible as wild-type mice to P. aeruginosa infection induced through intraperitoneal inoculation




Genotype
MGI:3525339
hm3
Allelic
Composition
Sdc1tm1Cma/Sdc1tm1Cma
Genetic
Background
either: C.Cg-Sdc1tm1Cma or B6.Cg-Sdc1tm1Cma
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Sdc1tm1Cma mutation (0 available); any Sdc1 mutation (23 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• in response to corneal epithelial wounding, homozygotes re-epithelialize debridement wounds at a slower rate (8-hour delay in the 50% wound closure time relative to wild-type)
• in contrast to wild-type, mutant corneal epithelial cells fail to re-stratify properly by 2 weeks and exhibit prolonged hypoplasia
• in response to corneal epithelial wounding, homozygotes re-epithelialize debridement wounds at a slower rate (8-hour delay in the 50% wound closure time relative to wild-type)
• in contrast to wild-type, mutant corneal epithelial cells fail to re-stratify properly by 2 weeks and exhibit prolonged hypoplasia
• homozygotes show normal cell migration but delayed re-epithelialization of full-thickness cutaneous wounds; hypoplasia of epithelial tissues within the wound bed is observed
• in response to dermabrasion, homozygotes show delayed skin healing at both 2 and 5 days after wounding

cellular
• relative to wild-type cells, mutant corneal epithelial cells display a higher cell proliferation rate prior to wounding
• similarly, mutant epidermal keratinocytes proliferate at a significantly higher rate prior to dermabrasion
• wild-type corneal epithelial cells increase proliferation at 24 hours after wounding; in contrast, mutant corneal epithelial cells show reduced localization of alpha9 integrin during closure of wounds and fail to increase their proliferation rate 24 hours after wounding
• at 2 days after dermabrasion, mutant epidermal keratinocytes show only a slight increase in cell proliferation; in wild-type skin, cell proliferation increases >3-fold
• in mutants, extracts from full-thickness skin show increased levels of alpha3 and alpha9 integrins both prior to injury and after hair removal but no increase 2 days after dermabrasion

immune system
• after corneal epithelial wounding, homozygotes show a transient increase in inflammatory cells in the corneal stroma
• 18 hours after wounding, more inflammatory cells are found beneath the migrating mutant epithelial sheet than in the wild-type
• in response to dermabrasion, mutant skin wounds appear deeper and tissues more inflamed relative to wild-type

vision/eye
• in response to corneal epithelial wounding, homozygotes re-epithelialize debridement wounds at a slower rate (8-hour delay in the 50% wound closure time relative to wild-type)
• in contrast to wild-type, mutant corneal epithelial cells fail to re-stratify properly by 2 weeks and exhibit prolonged hypoplasia




Genotype
MGI:3717713
hm4
Allelic
Composition
Sdc1tm1Cma/Sdc1tm1Cma
Genetic
Background
involves: 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Sdc1tm1Cma mutation (0 available); any Sdc1 mutation (23 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• following infection with Trichinella spiralis, IgG1 production is reduced
• following infection with Trichinella spiralis, IL-10 production is reduced
• following infection with Trichinella spiralis, IL-13 production is reduced
• following infection with Trichinella spiralis, IL-10, IL-13 and IgG1 production is reduced

hematopoietic system
• following infection with Trichinella spiralis, IgG1 production is reduced




Genotype
MGI:3521904
hm5
Allelic
Composition
Sdc1tm1Cma/Sdc1tm1Cma
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Sdc1tm1Cma mutation (0 available); any Sdc1 mutation (23 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
N
• virgin homozygous females exhibit normal mammary gland morphogenesis as well as normal abundance and distribution of mammary myoepithelial cells

reproductive system
N
• homozygotes are fertile and appear phenotypically normal under normal laboratory conditions




Genotype
MGI:3521901
cx6
Allelic
Composition
Sdc1tm1Cma/Sdc1tm1Cma
Tg(Wnt1)1Hev/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Sdc1tm1Cma mutation (0 available); any Sdc1 mutation (23 available)
Tg(Wnt1)1Hev mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• only 3% of hemizygous females expressing the transgene in a Sdc1tm1Cma null background develop mammary tumors (median time: ~36 weeks) versus 34% of hemizygous females in a Sdc1 wild-type background (median time: ~21 weeks)
• these Wnt1-induced tumors are predominantly alveolar adenocarcinomas

endocrine/exocrine glands
• hemizygous females expressing the transgene in a Sdc1tm1Cma null background exhibit a ~70% inhibition of Wnt1-induced mammary gland hyperplasia relative to hemizygous females of a Sdc1 wild-type background

integument
• hemizygous females expressing the transgene in a Sdc1tm1Cma null background exhibit a ~70% inhibition of Wnt1-induced mammary gland hyperplasia relative to hemizygous females of a Sdc1 wild-type background




Genotype
MGI:3521902
cx7
Allelic
Composition
Sdc1tm1Cma/Sdc1+
Tg(Wnt1)1Hev/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Sdc1tm1Cma mutation (0 available); any Sdc1 mutation (23 available)
Tg(Wnt1)1Hev mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 30% of hemizygous females expressing the transgene in a Sdc1tm1Cma heterozygous null background develop mammary tumors (median time: ~25 weeks) versus 34% of hemizygous females in a Sdc1 wild-type background (median time: ~21 weeks)
• these Wnt1-induced tumors are predominantly alveolar adenocarcinomas





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last database update
09/17/2024
MGI 6.24
The Jackson Laboratory