ARS | Publication request: VALIDATION OF QTL FOR REPRODUCTIVE TRAITS IN ADVANCED GENERATIONS OF A MEISHAN CROSS POPULATION

Submitted to: Plant and Animal Genome VX Conference Abstracts
Publication Type: Abstract Only
Publication Acceptance Date: January 10, 2006
Publication Date: January 13, 2006
Citation: Rohrer, G.A., Nonneman, D.J., Wise, T.H., Ford, J.J. 2006. Validation of QTL for reproductive traits in advanced generations of a Meishan cross population. Proc., Plant and Animal Genome XIV, 1/14-18/2006. San Diego, CA, Poster #P577, p. 245.

Technical Abstract: A QTL scan of a backcross, F3 and F4 generations of a Meishan-White composite resource population identified a genome-wide significant QTL for ovulation rate on SSC 8 along with suggestive QTL for ovulation rate on SSC 3 and 10 and for age at puberty on SSC 1 and 10. The F4 generation was crossed to a Yorkshire-Landrace composite population to yield a F5 generation with only 25% Meishan germplasm. This population has remained closed since that time. F8 females were phenotyped for age at puberty and ovulation rate and ovulation rate was also measured on F10 females. Single nucleotide polymorphism (SNP) markers were developed that spanned the confidence intervals for the 5 QTL regions and genotyped across the F8 and F10 phenotyped females. SAS PROC GLM was used to analyze the data where the model fitted for age at puberty included SNP genotype, sire and maternal grandsire as fixed effects. Ovulation rate analyses included an additional fixed effect for method of measurement. Each SNP marker was analyzed separately. Significant genotypic associations with phenotypes were detected on SSC 8 and 10 for ovulation rate, but no significant associations were detected for age at puberty. These results validate the segregation of QTL for ovulation rate on SSC 8 and 10 in this Meishan cross population. Lack of associations for the other three locations may indicate the absence of a real QTL; however, the introduction of new germplasm or recombination may have disrupted the linkage disequilibrium between the SNP markers and the causative polymorphisms.