Beclin-1 deficiency in the murine ovary results in the reduction of progesterone production to promote preterm labor.

TitleBeclin-1 deficiency in the murine ovary results in the reduction of progesterone production to promote preterm labor.
Publication TypeJournal Article
Year of Publication2014
JournalProceedings of the National Academy of Sciences of the United States of America
Volume111
Issue40
PaginationE4194-203
Date Published2014
ISSN0027-8424
Abstract

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.

URLhttp://www.pnas.org/cgi/pmidlookup?view=long&pmid=25246579
DOI10.1073/pnas.1409323111
Short TitleProc Natl Acad Sci U S A
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