All Phenotypes Sdc1<tm1Cma> MGI Mouse

Phenotypes associated with this allele

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Sdc1^tm1Cma/Sdc1^tm1Cma	B6.Cg-Sdc1^tm1Cma	MGI:3525353
hm2	Sdc1^tm1Cma/Sdc1^tm1Cma	either: (involves: 129S4/SvJae * BALB/c) or (involves: 129S4/SvJae * C57BL/6)	MGI:2653535
hm3	Sdc1^tm1Cma/Sdc1^tm1Cma	either: C.Cg-Sdc1^tm1Cma or B6.Cg-Sdc1^tm1Cma	MGI:3525339
hm4	Sdc1^tm1Cma/Sdc1^tm1Cma	involves: 129S4/SvJae	MGI:3717713
hm5	Sdc1^tm1Cma/Sdc1^tm1Cma	involves: 129S4/SvJae * C57BL/6	MGI:3521904
cx6	Sdc1^tm1Cma/Sdc1^tm1Cma Tg(Wnt1)1Hev/0	involves: 129S4/SvJae * C57BL/6 * SJL	MGI:3521901
cx7	Sdc1^tm1Cma/Sdc1⁺ Tg(Wnt1)1Hev/0	involves: 129S4/SvJae * C57BL/6 * SJL	MGI:3521902

Allelic Composition	Sdc1^tm1Cma/Sdc1^tm1Cma
Genetic Background	B6.Cg-Sdc1^tm1Cma

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Sdc1^tm1Cma mutation (0 available); any Sdc1 mutation (23 available)

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

mortality/aging

decreased susceptibility to bacterial infection induced morbidity/mortality ( J:104294 )

• 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

homeostasis/metabolism phenotype ( J:94010 )

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

decreased susceptibility to bacterial infection ( J:104294 )

• 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

decreased susceptibility to bacterial infection induced morbidity/mortality ( J:104294 )

• 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

Allelic Composition	Sdc1^tm1Cma/Sdc1^tm1Cma
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:
Sdc1^tm1Cma mutation (0 available); any Sdc1 mutation (23 available)

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

immune system

decreased susceptibility to bacterial infection ( J:69845 )

• 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

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

homeostasis/metabolism

abnormal cornea wound healing ( J:80682 )

• 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

delayed wound healing ( J:80682 )

• 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

abnormal cell proliferation ( J:80682 )

• 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

increased inflammatory response ( J:80682 )

• 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

abnormal cornea wound healing ( J:80682 )

• 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

Allelic Composition	Sdc1^tm1Cma/Sdc1^tm1Cma
Genetic Background	involves: 129S4/SvJae

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Sdc1^tm1Cma mutation (0 available); any Sdc1 mutation (23 available)

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

immune system

decreased IgG1 level ( J:107378 )

• following infection with Trichinella spiralis, IgG1 production is reduced

decreased interleukin-10 secretion ( J:107378 )

• following infection with Trichinella spiralis, IL-10 production is reduced

decreased interleukin-13 secretion ( J:107378 )

• following infection with Trichinella spiralis, IL-13 production is reduced

increased susceptibility to parasitic infection ( J:107378 )

• following infection with Trichinella spiralis, IL-10, IL-13 and IgG1 production is reduced

hematopoietic system

decreased IgG1 level ( J:107378 )

• following infection with Trichinella spiralis, IgG1 production is reduced

Allelic Composition	Sdc1^tm1Cma/Sdc1^tm1Cma
Genetic Background	involves: 129S4/SvJae * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Sdc1^tm1Cma mutation (0 available); any Sdc1 mutation (23 available)

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

endocrine/exocrine glands

endocrine/exocrine gland phenotype ( J:63122 )

N	• virgin homozygous females exhibit normal mammary gland morphogenesis as well as normal abundance and distribution of mammary myoepithelial cells

reproductive system

reproductive system phenotype ( J:63122 )

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

Allelic Composition	Sdc1^tm1Cma/Sdc1^tm1Cma Tg(Wnt1)1Hev/0
Genetic Background	involves: 129S4/SvJae * C57BL/6 * SJL

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Sdc1^tm1Cma 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

decreased tumor incidence ( J:63122 )

• only 3% of hemizygous females expressing the transgene in a Sdc1^tm1Cma 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

mammary gland hyperplasia ( J:63122 )

• hemizygous females expressing the transgene in a Sdc1^tm1Cma null background exhibit a ~70% inhibition of Wnt1-induced mammary gland hyperplasia relative to hemizygous females of a Sdc1 wild-type background

integument

mammary gland hyperplasia ( J:63122 )

Allelic Composition	Sdc1^tm1Cma/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:
Sdc1^tm1Cma 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

decreased tumor incidence ( J:63122 )

• 30% of hemizygous females expressing the transgene in a Sdc1^tm1Cma 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

Contributing Projects: Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
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