Asymmetries, heterosis, and phenotypic profiles of red junglefowl, White Plymouth Rocks, and F1 and F2 reciprocal crosses.

During the domestication of farm animals, humans have manipulated genetic variation for growth and reproduction through artificial selection. Here, data are presented for growth, reproductive, and behavior traits for the red junglefowl, a line of White Plymouth Rock chickens, and their F1 and F2 reciprocal crosses. Intra- and intergenerational comparisons for growth related traits reflected considerable additive genetic variation. In contrast, those traits associated with reproduction exhibited heterosis. The role of sexual selection was seen in the evolution of prominent secondary sexual ornaments that lend to female choice and male-male competition. The large differences between parental lines in fearfulness to humans were only mitigated slightly in the intercross generations. Whereas, overall F1 generation heterosis was not transferred to the F2, there was developmental stability in the F2, as measured by relative asymmetry of bilateral traits. Through multigenerational analyses between the red junglefowl and the domestic White Plymouth Rocks, we observed plasticity and considerable residual genetic variation. These factors likely facilitated the adaptability of the chicken to a broad range of husbandry practices throughout the world.

Genomic regions associated with antibody response to sheep red blood cells in the chicken.

F(1) and F(2) populations were generated by crossing two lines of chickens divergently selected from a common founder population for 32 generations for either high or low antibody response 5 days post-injection of a non-pathogenic antigen, sheep red blood cells (SRBCs). The number of loci with major effects on day 5 SRBC titers was estimated to be more than 7 in this population. There was a significant association between MHC haplotype and day 5 antibody titers as well as body weight at sexual maturity. A significant difference between reciprocal F(2) crosses for both 5- and 12-day antibody titers suggests that sex chromosome and/or parent of origin effects on autosomal loci have an important role in immune response. A single marker-trait association analysis on 1024 genetic markers and 128 F(2) individuals detected 11 genomic regions associated with antibody response traits and 17 regions associated with body weight gain. Several of the genomic regions identified as being associated with antibody response have been described previously, while novel regions associated with antibody response were identified on chromosomes 11 and 24. Based on the lack of overlap of the regions associated with body weight and antibody response, we conclude that while these phenotypes are inversely correlated in the selected lines, they are controlled by distinct genetic loci and may be reflective of intense selection pressure on loci affecting the partitioning of nutrients between the immune system and growth pathways.

Genetic mapping of the sex-linked barring gene in the chicken.

The sex-linked barring gene of the chicken (Gallus gallus), first identified in 1908, produces an alternating pattern of white and black bars in the adult plumage. More recent studies have shown that melanocytes in the developing feather follicle of the Barred Plymouth Rock experience premature cell death, whereas initially it was thought that melanocytes remained viable in the region of the feather devoid of pigmentation but were simply inhibited from synthesizing melanin. In an attempt to reconcile these 2 different hypotheses at the molecular level, we have taken a gene mapping approach to isolate the sex-linked barring gene variant. We developed a mapping population consisting of 71 F2 chickens from crossing a single Barred Plymouth Rock female with a White Crested Black Polish male. Existing and novel microsatellite markers located on the chicken chromosome Z were used to genotype all individuals in our mapping population. Single marker association analysis revealed a 2.8-Mb region of the distal q arm of chicken chromosome Z to be significantly associated with the barring phenotype (P<0.001). Further analysis suggests that the causal mutation is located within a 355-kb region showing complete association with the barring phenotype and containing 5 known genes [micro-RNA 31 (miRNA-31), methylthioadenosine phosphorylase (MTAP), cyclin-dependent kinase inhibitor 2B (CDKN2B), tripartite motif 36 (TRIM36), and protein geranylgeranyltransferase type I, beta subunit (PGGT1B)], none of which have a defined role in normal melanocyte function. Although several of these genes or their homologs are known to be involved in processes that could potentially explain the barring phenotype, our results indicate that further work directed at fine-mapping this region is necessary to identify this novel mechanism of melanocyte regulation.