|  Help  |  About  |  Contact Us

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

First Author  Suto J Year  1999
Journal  Mamm Genome Volume  10
Issue  8 Pages  777-83
PubMed ID  10430663 Mgi Jnum  J:56501
Mgi Id  MGI:1341472 Doi  10.1007/s003359901091
Citation  Suto J, et al. (1999) Genetic analysis of neonatal death with growth retardation in F(1) male Dh/+ mice. Mamm Genome 10(8):777-83
abstractText  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.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

11 Bio Entities

Trail: Publication

0 Expression