Summary | ||||||||
Mutation origin |
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Mutation description |
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Phenotypes |
View phenotypes and curated references for all genotypes (concatenated display).
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Expression |
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Find Mice (IMSR) |
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Notes |
Wakasugi (J:5498) postulated the existence of a mutant gene in the DDK strain to explain the much reduced litter size of DDK females mated to males of other strains. Reciprocal crosses and matings within the DDK strain were fully fertile. Reduced litter size was due to a defect in the eggs of the DDK females, not in the uterine environment. To explain the results of breeding tests, Wakasugi assumed the DDK strain to be homozygous for Om, a gene that produces a substance in ova differing from that produced by other strains. The gene locus also produces a substance in sperm. The abnormal ovum substance reacts with the normal substance in sperm from other strains to produce a factor lethal to the embryo. Combinations of normal sperm with normal ovum, mutant sperm with mutant ovum, or mutant sperm with normal ovum substances are not lethal. Heterozygous females (Om/+) are thought to produce normal and mutant ovum substances in equal amounts, with one or the other at random interacting irreversibly with the sperm in any given fertilized egg (J:5498). Sapienza et al. (J:2175)) find data that make this proposed action of the Om mutation untenable, and propose an imprinting explanation for the phenomenon. On the basis of this hypothesis, Om is an imprinted locus, with the maternal allele only expressed. Imprinting in the DDK strain is, however, reversed, and only the paternal allele is expressed.
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References |
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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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last database update 11/12/2024 MGI 6.24 |
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