Male CD81 Knockout Genotype Disrupts Mendelian Distribution of Offspring
Abstract:CD81 is an integral membrane protein in the tetraspanin superfamily that serves as an adaptor protein. CD81 is also a maternally imprinted gene that is found in a regulated cluster of genes on mouse chromosome 7. Among offspring produced from heterozygous breeding pairs, CD81null/null mice grew at the same rate as CD81+/+ and CD81+/null mice. Because of an inhibition in sperm–egg fusion, CD81null/null female mice are much less fertile than CD81+/+ and CD81+/null mice. However, no published study has detailed the effect of the male CD81 genotype on the genotype and sex distribution of offspring. We set up breeding pairs of heterozygotic (C.129-Cd81tm1 N7) female mice and male mice with CD81+/null, CD81+/+, or CD81null/null genotypes. The survival and development of CD81+/null, CD81+/+, and CD81null/null offspring were monitored and compared. Compared with those of heterozygous male breeders, CD81null/null pups were born at a less-than-expected ratio from CD81null/null males. Sex distribution did not differ among pups sired by CD81null/null compared with CD81+/null mice. The data suggest that the effect of the CD81null/null paternal genotype on offspring is manifested early in development or in utero.
Document Type: Research Article
Publication date: 2010-06-01
Comparative Medicine (CM), an international journal of comparative and experimental medicine, is the leading English-language publication in the field and is ranked by the Science Citation Index in the upper third of all scientific journals. The mission of CM is to disseminate high-quality, peer-reviewed information that expands biomedical knowledge and promotes human and animal health through the study of laboratory animal disease, animal models of disease, and basic biologic mechanisms related to disease in people and animals.
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