Using Paleogenomics to Study the Evolution of Gene Families: Origin and Duplication History of the Relaxin Family Hormones and Their Receptors

Recent progress in the analysis of whole genome sequencing data has resulted in the emergence of paleogenomics, a field devoted to the reconstruction of ancestral genomes. Ancestral karyotype reconstructions have been used primarily to illustrate the dynamic nature of genome evolution. In this paper, we demonstrate how they can also be used to study individual gene families by examining the evolutionary history of relaxin hormones (RLN/INSL) and relaxin family peptide receptors (RXFP). Relaxin family hormones are members of the insulin superfamily, and are implicated in the regulation of a variety of primarily reproductive and neuroendocrine processes. Their receptors are G-protein coupled receptors (GPCR's) and include members of two distinct evolutionary groups, an unusual characteristic. Although several studies have tried to elucidate the origins of the relaxin peptide family, the evolutionary origin of their receptors and the mechanisms driving the diversification of the RLN/INSL-RXFP signaling systems in non-placental vertebrates has remained elusive. Here we show that the numerous vertebrate RLN/INSL and RXFP genes are products of an ancestral receptor-ligand system that originally consisted of three genes, two of which apparently trace their origins to invertebrates. Subsequently, diversification of the system was driven primarily by whole genome duplications (WGD, 2R and 3R) followed by almost complete retention of the ligand duplicates in most vertebrates but massive loss of receptor genes in tetrapods. Interestingly, the majority of 3R duplicates retained in teleosts are potentially involved in neuroendocrine regulation. Furthermore, we infer that the ancestral AncRxfp3/4 receptor may have been syntenically linked to the AncRln-like ligand in the pre-2R genome, and show that syntenic linkages among ligands and receptors have changed dynamically in different lineages. This study ultimately shows the broad utility, with some caveats, of incorporating paleogenomics data into understanding the evolution of gene families

Combining Maternal and Post-Hatch Dietary 25-Hydroxycholecalciferol Supplementation on Broiler Chicken Growth Performance and Carcass Characteristics

Dietary inclusion of the vitamin D3 (D3) metabolite, 25-hydroxycholecalciferol (25OHD3), was demonstrated to improve broiler growth performance and breast meat yield. To assess the effect of combined maternal (MDIET) and post-hatch (PDIET) dietary 25OHD3 inclusion on broiler growth performance and carcass characteristics, a randomized complete block design experiment with a 2 × 2 factorial treatment structure was conducted. From 25 to 38 weeks of age, broiler breeder hens were provided with 1 of 2 MDIET formulated to contain: 5000 IU D3 (MCTL), or 2240 IU of D3 + 2760 IU of 25OHD3 per kg of feed (M25OHD3). Their chick offspring (n = 448; 224 per MDIET) hatched from eggs collected from 37 to 38 weeks of age were reared in 16 replicate pens with 7 birds per pen and fed 1 of 2 PDIET in 3 phases up to day 40 formulated to contain: 5000 IU of D3 per kg of feed (PCTL), or 2240 IU of D3 + 2760 IU of 25OHD3 per kg of feed (P25OHD3). No additive or synergistic effects of combining 25OHD3 inclusion in MDIET and PDIET were observed. Broilers from 25OHD3-fed hens (M25OHD3) were heavier on day 40 than those from hens fed only D3 (MCTL; 2.911 vs. 2.834 kg; p = 0.040). Tender weight (123 vs. 117 g) and yield (5.63 vs. 5.44%) were greater in the M25OHD3 broilers than the MCTL broilers (p = 0.006). Broilers fed 25OHD3 (P25OHD3) tended to have heavier breasts (637 vs. 615 g; p = 0.050), bone-in wings (215 vs. 210 g; p = 0.070), and boneless thighs (279 vs. 270 g; p = 0.078) compared with those fed only D3 (PCTL). Neither MDIET nor PDIET altered the severity of Wooden Breast and White Striping (p ≥ 0.106). Overall, including 25OHD3 in either the maternal or broiler diet increased broiler meat yield