Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Suto, J. et al.

Genetic analysis of neonatal death with growth retardation in F(1) male Dh/+ mice.

Nearly all F(1) male mice with Dh/+ genotype between DDD female and DH-Dh/+ male die within a few days after birth; however, this is not observed in the reciprocal cross. The F(1) Dh/+ males usually exhibit growth retardation prior to death. To identify the putative genetic locus or loci in DDD genome that cause the abnormalities in the presence of the Dh, a linkage analysis was carried out in backcross progeny of a cross of (DDD female x DH-+/+ male) F(1) female x DH-Dh/+ male. Appearance of growth retardation was examined from the day of birth, and both growth-retarded and normally weaned Dh/+ males were genotyped for microsatellite marker loci spanning autosomes and the X Chromosome (Chr). Significant evidence for linkage was identified on the distal edge of the X Chr, near the microsatellite marker of DXMit135. Furthermore, among mice from DDD female x reciprocal F(1)Dh/+ male produced between DH-Dh/+ and progenitor strains (C57BL/6J, C3H/HeJ and BALB/cA), only the progeny from female DDD x male (female DH-Dh/+ x male C3H/HeJ) F(1) Dh/+ male did not show any lethality and/or growth retardation. Thus, the lethality in F(1) Dh/+ males accompanied by growth retardation is caused by the interactions between the Dh gene, X Chr, and Y Chr. Based on the CAG repeat sequence length polymorphism among Mus musculus musculus Sry gene, C3H/HeJ was different from C57BL/6J, BALB/cA, and DH. These data suggest that there are at least two functional types of Y Chr in Mus musculus musculus.[1]

References

Genetic analysis of neonatal death with growth retardation in F(1) male Dh/+ mice. Suto, J., Yamanaka, H., Sekikawa, K. Mamm. Genome (1999) [Pubmed]

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