Transfer of the Septin Ring to Cytokinetic Remnants in ER Stress Directs Age-Sensitive Cell-Cycle Re-entry.
Journal Article (Journal Article)
During cell division, the inheritance of a functional endoplasmic reticulum (ER) is ensured by the endoplasmic reticulum stress surveillance (ERSU) pathway. Activation of ERSU causes the septin ring to mislocalize, which blocks ER inheritance and cytokinesis. Here, we uncover that the septin ring in fact translocates to previously utilized cell division sites called cytokinetic remnants (CRMs). This unconventional translocation requires Nba1, a negative polarity regulator that normally prevents repolarization and re-budding at CRMs. Furthermore, septin ring translocation relies on the recruitment and activation of a key ERSU component Slt2 by Bem1, without activating Cdc42. Failure to transfer all septin subunits to CRMs delays the cell's ability to re-enter the cell cycle when ER homeostasis is restored and hinders cell growth after ER stress recovery. Thus, these deliberate but unprecedented rearrangements of cell polarity factors during ER stress safeguard cell survival and the timely cell-cycle re-entry upon ER stress recovery.
Full Text
Duke Authors
Cited Authors
- Chao, JT; Piña, F; Onishi, M; Cohen, Y; Lai, Y-S; Schuldiner, M; Niwa, M
Published Date
- October 2019
Published In
Volume / Issue
- 51 / 2
Start / End Page
- 173 - 191.e5
PubMed ID
- 31564614
Pubmed Central ID
- PMC7085932
Electronic International Standard Serial Number (EISSN)
- 1878-1551
International Standard Serial Number (ISSN)
- 1534-5807
Digital Object Identifier (DOI)
- 10.1016/j.devcel.2019.08.017
Language
- eng