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Sci. Signal., 3 August 2010
Vol. 3, Issue 133, p. ec236
[DOI: 10.1126/scisignal.3133ec236]

EDITORS' CHOICE

Stress Signaling Inherit the ER

Wei Wong

Science Signaling, AAAS, Washington, DC 20005, USA

During mitosis, the endoplasmic reticulum (ER) is not created de novo, but rather is subdivided between mother and daughter cells. Different mechanisms exist for the inheritance of perinuclear ER (which is located near the nucleus) compared with cortical ER (which is located near the plasma membrane). In Saccharomyces cerevisiae, ER stress causes a defect in cytokinesis that delays the cell cycle, and Babour et al. sought to uncover the mechanisms involved in this process (which the authors called ER stress surveillance). Cytokinesis requires the assembly of septins into a ringlike structure at the mother cell-bud neck. The authors found that the septin ring had an abnormal morphology and did not disperse in cells undergoing ER stress, whether due to treatment with tunicamycin or dithiothreitol (DTT) or to expression of ero-1-1, a temperature-sensitive version of the gene encoding ERO-1 (ER oxidoreductin I) that induces ER stress at the nonpermissive temperature. Tunicamycin stabilized the septin ring and rescued the septin ring disassembly defect in cdc12-6 cells, which express a temperature-sensitive version of a gene encoding a septin subunit. Imaging of cells expressing an ER marker showed that cortical ER was transmitted to daughter cells early in the cell cycle in unstressed cells, whereas delivery of cortical ER was delayed in stressed cells. In contrast, delivery of perinuclear ER to daughter cells was unaffected by ER stress. In cells lacking the mitogen-activated protein kinase (MAPK) Slt2, cytokinesis defects were not apparent after ER stress, morphology of the septin ring was normal, and inheritance of cortical ER was less delayed than in wild-type cells. Rescue of this phenotype required Slt2 phosphorylation and its kinase activity, as well as the Slt2 upstream activator Pkc1 and the cell surface receptor Wsc1. Although Wsc1 is involved in the cell wall integrity pathway and can be activated in response to excess turgor pressure, cell wall stress did not induce alterations in septin ring morphology. Furthermore, endocytosis of Wsc1 is required for its role in the cell wall integrity pathway, but cells expressing a form of Wsc1 that cannot be endocytosed did not show growth defects in the presence of tunicamycin. Thus, a MAPK pathway delays inheritance of cortical ER when cells are undergoing ER stress, which the authors postulate acts to ensure that daughter cells receive functional ER.

A. Babour, A. A. Bicknell, J. Tourtellotte, M. Niwa, A surveillance pathway monitors the fitness of the endoplasmic reticulum to control its inheritance. Cell 142, 256–269 (2010). [PubMed]

Citation: W. Wong, Inherit the ER. Sci. Signal. 3, ec236 (2010).



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