All Phenotypes Ica1<tm1Mdos> MGI Mouse

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Phenotypes associated with this allele

Allele Symbol
Allele Name
Allele ID

Ica1^tm1Mdos
targeted mutation 1, H Michael Dosch
MGI:2662437

Summary

3 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Ica1^tm1Mdos/Ica1^tm1Mdos	involves: 129S1/Sv * 129X1/SvJ	MGI:3831658
hm2	Ica1^tm1Mdos/Ica1^tm1Mdos	NOD.129-Ica1^tm1Mdos	MGI:2662441
cx3	Ica1^tm1Mdos/Ica1^tm1Mdos Ica1l^em1Jxia/Ica1l^em1Jxia	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA	MGI:5806228

Allelic Composition	Ica1^tm1Mdos/Ica1^tm1Mdos
Genetic Background	involves: 129S1/Sv * 129X1/SvJ

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ica1^tm1Mdos mutation (1 available); any Ica1 mutation (41 available)

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

normal phenotype

no abnormal phenotype detected ( J:83526 )

• mutants have no obvious phenotype and age normally

reproductive system

reproductive system phenotype ( J:233657 )

N	• mice exhibit normal fertility with no significant difference in total, mobile and linear mobile sperm

Allelic Composition	Ica1^tm1Mdos/Ica1^tm1Mdos
Genetic Background	NOD.129-Ica1^tm1Mdos

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ica1^tm1Mdos mutation (1 available); any Ica1 mutation (41 available)

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

mortality/aging

premature death ( J:83526 )

• a subset of females die spontaneously without prodromal symptoms around 4-5 months of age

homeostasis/metabolism

abnormal glucose homeostasis ( J:83526 )

• diabetes develops around 20 weeks of age, 4 weeks later than wild-type NOD mice

immune system

abnormal T cell physiology ( J:83526 )

• mutants fail to generate, even after immunization, cross-reactive T cells that recognize the dominant Tep69 epitope in Ica1, and the ABBOS epitope in BSA

decreased susceptibility to autoimmune diabetes ( J:83526 )

• mutants are resistant to cyclophosphamide-accelerated diabetes

• although mutants develop diabetes at around 20 weeks of age, this is 4 weeks later than wild-type NOD mice

hematopoietic system

abnormal T cell physiology ( J:83526 )

• mutants fail to generate, even after immunization, cross-reactive T cells that recognize the dominant Tep69 epitope in Ica1, and the ABBOS epitope in BSA

Allelic Composition	Ica1^tm1Mdos/Ica1^tm1Mdos Ica1l^em1Jxia/Ica1l^em1Jxia
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ica1l^em1Jxia mutation (0 available); any Ica1l mutation (25 available)
Ica1^tm1Mdos mutation (1 available); any Ica1 mutation (41 available)

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

reproductive system

abnormal sperm mitochondrial sheath morphology ( J:233657 )

oligozoospermia ( J:233657 )

• severe reduction in total and mobile sperm number with complete loss of linear mobile sperm

• in cauda epididymis

abnormal acrosome morphology ( J:233657 )

• fragmented or completely lost

globozoospermia ( J:233657 )

absent acrosome ( J:233657 )

• in some sperm

abnormal sperm nucleus morphology ( J:233657 )

• smaller and irregular compared with wild-type sperm

abnormal spermiogenesis ( J:233657 )

• with round nuclei sperm

male infertility ( J:233657 )

cellular

abnormal sperm mitochondrial sheath morphology ( J:233657 )

oligozoospermia ( J:233657 )

• severe reduction in total and mobile sperm number with complete loss of linear mobile sperm

• in cauda epididymis

abnormal acrosome morphology ( J:233657 )

• fragmented or completely lost

globozoospermia ( J:233657 )

absent acrosome ( J:233657 )

• in some sperm

abnormal sperm nucleus morphology ( J:233657 )

• smaller and irregular compared with wild-type sperm

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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