Abstract
Low egg-producing turkeys reduce the profitability of a flock by limiting the number of poults that can be hatched. Understanding the biological mechanics behind egg-production rates will greatly benefit the industry. Two lines with vastly different egg production rates are the Ohio State University E line, and its unselected counterpart, the random-bred control one (RBC1). Differences between E Line and RBC1 hens (n = 4 per line) were investigated by measuring egg production traits, ovarian and follicle anatomical characteristics, and gene expression for reproductively important genes within different follicle types. Data were analyzed by an ANOVA mixed model procedure in SAS. The E line hens produced 20% more eggs than the RBC1 hens, even though they had similar numbers of preovulatory follicles in their ovaries. This was accomplished by increasing clutch length and keeping the pause length the same. On the gene expression side small white follicles (SWF) within E line hens had less LHCGR expression which coincided with downregulation of CYP11A1 and CYP17A1. Along with an upregulation of PRLR in small yellow follicles (SYF) which also coincided with downregulation of CYP17A1. In both cases changes in pituitary hormone receptor transcription levels appeared to affect the steroid hormone synthesis pathway. In SWF from E line hens ESR2 was downregulated, however in the large white follicles and selected follicles ESR1 was the estradiol receptor which was downregulated. The similarity in preovulatory numbers suggests that E line hens aren't selecting more follicles to grow, but instead, follicles are growing faster. Based on the gene expression patterns, the reduction of steroid hormone synthesis might hint at the follicles putting more energy into growth and differentiation. At the same time, the decrease in estradiol receptor might limit the negative effects of estradiol on granulosa cells and allow for more rapid growth, suggesting a possible mechanism for the higher egg production trait of the E line.