| First Author | Gawriluk TR | Year | 2014 |
| Journal | Proc Natl Acad Sci U S A | Volume | 111 |
| Issue | 40 | Pages | E4194-203 |
| PubMed ID | 25246579 | Mgi Jnum | J:216461 |
| Mgi Id | MGI:5608837 | Doi | 10.1073/pnas.1409323111 |
| Citation | Gawriluk TR, et al. (2014) Beclin-1 deficiency in the murine ovary results in the reduction of progesterone production to promote preterm labor. Proc Natl Acad Sci U S A 111(40):E4194-203 |
| abstractText | Autophagy is an important cellular process that serves as a companion pathway to the ubiquitin-proteasome system to degrade long-lived proteins and organelles to maintain cell homeostasis. Although initially characterized in yeast, autophagy is being realized as an important regulator of development and disease in mammals. Beclin1 (Becn1) is a putative tumor suppressor gene that has been shown to undergo a loss of heterozygosity in 40-75% of human breast, ovarian, and prostate cancers. Because Becn1 is a key regulator of autophagy, we sought to investigate its role in female reproduction by using a conditional knockout approach in mice. We find that pregnant females lacking Becn1 in the ovarian granulosa cell population have a defect in progesterone production and a subsequent preterm labor phenotype. Luteal cells in this model exhibit defective autophagy and a failure to accumulate lipid droplets needed for steroidogenesis. Collectively, we show that Becn1 provides essential functions in the ovary that are essential for mammalian reproduction. |
