Erebosis, a new cell death mechanism during homeostatic turnover of gut enterocytes

PLoS Biol. 2022 Apr 25;20(4):e3001586. doi: 10.1371/journal.pbio.3001586. eCollection 2022 Apr.

Abstract

Many adult tissues are composed of differentiated cells and stem cells, each working in a coordinated manner to maintain tissue homeostasis during physiological cell turnover. Old differentiated cells are believed to typically die by apoptosis. Here, we discovered a previously uncharacterized, new phenomenon, which we name erebosis based on the ancient Greek word erebos ("complete darkness"), in the gut enterocytes of adult Drosophila. Cells that undergo erebosis lose cytoskeleton, cell adhesion, organelles and fluorescent proteins, but accumulate Angiotensin-converting enzyme (Ance). Their nuclei become flat and occasionally difficult to detect. Erebotic cells do not have characteristic features of apoptosis, necrosis, or autophagic cell death. Inhibition of apoptosis prevents neither the gut cell turnover nor erebosis. We hypothesize that erebosis is a cell death mechanism for the enterocyte flux to mediate tissue homeostasis in the gut.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis
  • Cell Death
  • Drosophila* / metabolism
  • Enterocytes* / metabolism
  • Homeostasis

Grants and funding

This work was supported by AMED-PRIME (17939907) and the JSPS KAKENHI (JP16H06220) to S.K.Y.; Cooperative Study Program (20-225) of National Institute for Physiological Sciences to S.K.Y. and M.F.; Joint research program of the Institute for Molecular and Cellular Regulation (Gunma University) to S.K.Y. and T.N. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.