Abstract
Follicular atresia is an important cause of reproductive decline in egg-laying hens. Therefore, a better understanding of the regulation mechanism of follicle atresia in poultry is an important measure to maintain persistent high egg performance. However, how the role of the regulatory relationship between autophagy and apoptosis in the intrafollicular environment affects the follicular atresia of chickens is remain unclear. The objective of this study was to explore the regulatory molecular mechanisms in regard to follicular atresia. 20 white leghorn layers (32-wk-old) were equally divided into 2 groups. The control group was fed freely, and the experimental group induced follicular atretic by fasting for 5 d. The results showed that the expression of prolactin (PRL) levels was significantly higher in the fasted hens, while the levels of luteinizing hormone (LH) and follicle stimulating hormone (FSH) were lower. Most importantly, RNA sequencing, qPCR, and Western blotting detected significantly elevated levels of autophagy and apoptosis markers in atresia follicles. Interestingly, we found that fibromodulin (FMOD) levels was significantly lower in follicles from fasted hens and that this molecule had an important regulatory role in autophagy. FMOD silencing significantly promoted autophagy and apoptosis in granulosa cells, resulting in hormonal imbalance. FMOD was found to regulate autophagy via the transforming growth factor beta (TGF-β) signaling pathway. Our results suggest that the increase in autophagy and the imbalance in internal homeostasis cause granulosa cell apoptosis, leading to follicular atresia in the chicken ovary. This finding could provide further insight into broodiness in chicken and provide avenues for further improvements in poultry production.