Feeding level is associated with altered liver transcriptome and follicle selection in hen†.

Genetic selection for particular traits in domestic animals may have altered the optimal feedback regulation among systems regulating appetite, growth, and reproduction. Broiler breeder chickens have been selected for fast and efficient growth and, unless feed restricted, consume excessively resulting in poor reproductive efficiency. We examined the effect of dietary treatment in full-fed and restricted-fed broiler breeder hens on ovarian responses, liver morphology, and transcriptome associated with reproductive function. Although full-fed broiler breeder hens had lower egg production (P < 0.01), the total number of ovarian follicles >8 mm (P < 0.01), 6-8 mm (P < 0.03), and 3-5 mm (P < 0.04) were greater in full-fed hens compared to restricted-fed hens. There was a large amount of lipid accumulation in the liver of full-fed hens and differential gene analysis yielded 120 genes that were differentially expressed >2-fold in response to feeding level (P < 0.01; false discovery rate < 0.05). Elevated T3 may indicate that general metabolism was affected by diet and GHR (P < 0.01) and insulin like growth factor 1 (IGF1) (P < 0.04) mRNA expression were both greater in the liver of full-fed hens as compared to restricted-fed hens. It is likely that selection for increased growth, associated with enhanced activity of the IGF1 system, has altered nutritional coupling of feed intake to follicle development.

Ad Libitum Feeding in Broiler Breeder Hens Alters the Transcriptome of Granulosa Cells of Pre-Hierarchal Follicles.

Intense selective breeding of chickens has resulted in suboptimal egg production in broiler breeder hens. This reproductive phenotype is exacerbated by ad libitum feeding, which leads to excessive and disorganized follicular growth. One strategy used to improve broiler breeder hens' reproductive efficiency is restricted feeding. In this study, we sought to identify transcriptional changes, which translate the level of dietary intake into increased follicle selection. Broiler breeder hens (n = 16 per group) were raised according to commercial guidelines until 28 weeks of age and then randomly assigned to an ad libitum diet (FF) or continued on a restricted diet (RF) for 6 weeks. Following dietary treatment, FF hens (n = 2) with excessive follicle selection and RF hens (n = 3) with normal follicle selection were selected for RNA-sequencing. Transcriptomes of granulosa cells from 6-8-mm follicles were sequenced to identify transcriptional differences in the follicle population from which selection was made for the preovulatory stage. Differential expression analysis identified several genes known to play a role in follicle development (CYP11A1, STAR, INHA, and INHBB) that are upregulated in FF hens. These changes in gene expression suggest earlier granulosa cell differentiation and steroidogenic competency in the granulosa layer from FF hens.

The Autophagy Gene Atg16L1 is Necessary for Endometrial Decidualization.

Uterine receptivity is critical for establishing and maintaining pregnancy. For the endometrium to become receptive, stromal cells must differentiate into decidual cells capable of secreting factors necessary for embryo survival and placental development. Although there are multiple reports of autophagy induction correlated with endometrial stromal cell (ESC) decidualization, the role of autophagy in decidualization has remained elusive. To determine the role of autophagy in decidualization, we utilized 2 genetic models carrying mutations to the autophagy gene Atg16L1. Although the hypomorphic Atg16L1 mouse was fertile and displayed proper decidualization, conditional knockout in the reproductive tract of female mice reduced fertility by decreasing the implantation rate. In the absence of Atg16L1, ESCs failed to properly decidualize and fewer blastocysts were able to implant. Additionally, small interfering RNA knock down of Atg16L1 was detrimental to the decidualization response of human ESCs. We conclude that Atg16L1 is necessary for decidualization, implantation, and overall fertility in mice. Furthermore, considering its requirement for human endometrial decidualization, these data suggest Atg16L1 may be a potential mediator of implantation success in women.