The autophagy gene AtG16L1 is necessary for endometrial decidualization

Arin K. Oestreich, Sangappa B. Chadchan, Pooja Popli, Alexandra Medvedeva, Marina N. Rowen, Claire S. Stephens, Ran Xu, John P. Lydon, Francesco J. Demayo, Emily S. Jungheim, Kelle H. Moley*, Ramakrishna Kommagani

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

24 Scopus citations


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.

Original languageEnglish (US)
JournalEndocrinology (United States)
Issue number1
StatePublished - Jan 1 2020


  • Fertility
  • Implantation
  • Pregnancy

ASJC Scopus subject areas

  • Endocrinology


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