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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, CD81(null/null) mice grew at the same rate as CD81(+/+) and CD81(+/null) mice. Because of an inhibition in sperm-egg fusion, CD81(null/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-Cd81(tm1) N7) female mice and male mice with CD81(+/null), CD81(+/+), or CD81(null/null) genotypes. The survival and development of CD81(+/null), CD81(+/+), and CD81(null/null) offspring were monitored and compared. Compared with those of heterozygous male breeders, CD81(null/null) pups were born at a less-than-expected ratio from CD81(null/null) males. Sex distribution did not differ among pups sired by CD81(null/null) compared with CD81(+/null) mice. The data suggest that the effect of the CD81(null/null) paternal genotype on offspring is manifested early in development or in utero.

SUBMITTER: Mordica WJ

PROVIDER: S-EPMC2890394 | biostudies-literature | 2010 Jun

REPOSITORIES: biostudies-literature

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Male CD81 knockout genotype disrupts Mendelian distribution of offspring.

Mordica Whitney J WJ Gallagher Ryan J RJ Kennedy Jenna L JL Chapes Stephen K SK

Comparative medicine 20100601 3

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, CD81(null/null) mice grew at the same rate as CD81(+/+) and CD81(+/null) mice. Because of an inhibition in sperm-egg fusion, CD81(null/null) female mice are much less fertile than CD81(+/+) and CD81(+/null) mice. However, no pub ...[more]

PMID: 20579434

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Project description:BACKGROUND: Vitamin D deficiency is associated with increased cardiovascular disease risk in observational studies. Whether these associations are causal is not clear. Loss-of-function mutations in the filaggrin gene result in up to 10% higher serum vitamin D concentrations, supposedly due to a decreased UV-protection of the keratinocytes. We used a Mendelian randomization approach to estimate the causal effect of vitamin D status on serum lipids, blood pressure, body mass index, waist circumference, and the metabolic syndrome. METHODS: Three population based studies were included, Monica10 (2,656 individuals aged 40-71 years), Inter99 (6,784 individuals aged 30-60 years), and Health2006 (3,471 individuals aged 18-69 years) conducted in 1993-94, 1999-2001, and 2006-2008, respectively. Participants were genotyped for the two most common filaggrin gene mutations in European descendants R501X and 2282del4, in all three studies and further for the R2447X mutation in the Inter99 and Health2006 studies. Filaggrin genotype was used as instrumental variable for vitamin D status. Baseline measurements of serum 25-hydroxyvitamin D were performed in all three studies. RESULTS: Instrumental variable analyses showed a 23.8% (95% confidence interval, CI 3.0, 48.6) higher HDL cholesterol level and a 30.5% (95% CI: 0.8, 51.3) lower serum level of triglycerides per doubling of vitamin D. These associations were, however, not statistically significant when applying the Bonferroni adjusted significance level. The remaining lipids showed non-significant changes in a favorable direction. Doubling of vitamin D gave a non-significantly lower odds ratio = 0.26 (95% CI: 0.06, 1.17) of the metabolic syndrome. There were no statistically significant causal effects of vitamin D status on blood pressure, body mass index, or waist circumference. CONCLUSION: Our results support a causal effect of higher vitamin D status on a more favorable lipid profile, although more studies in other populations are needed to confirm our results.

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Male CD81 knockout genotype disrupts Mendelian distribution of offspring.

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Male CD81 knockout genotype disrupts Mendelian distribution of offspring.

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