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. Author manuscript; available in PMC: 2021 Dec 1.
Published in final edited form as: Biochim Biophys Acta Mol Cell Res. 2020 Aug 21;1867(12):118825. doi: 10.1016/j.bbamcr.2020.118825

Figure 4: ERSU checkpoint pathway.

Figure 4:

In response to ER stress, (1) the cellular levels of phytosphingosine (PHS) become elevated, initiating the hallmark events of the ERSU: (2) the initial ER tubule (IET) entry into the daughter cell is blocked and (3) the septin ring mislocalizes from the bud neck, ultimately, (4) resulting in cytokinesis cell cycle block. These events are mediated by the reticulon family proteins RTN1, RTN2, YOP1, and MAP kinase, SLT2, and SLT2’s upstream kinases such as PKC1. Levels of Rtn1 and Yop1 increase under ER stress. Currently, the detailed molecular mechanisms by which these components activate the ERSU hallmark events have not yet been investigated. Cytokinesis block continues until ER functional homeostasis is recovered by activation of the UPR, which is also activated by ER stress independent of the ERSU events. Upon recovery, ER inheritance and the cell cycle resume. Recent results revealed that septin ring mislocalization plays a critical role in timely re-entry into the cell cycle when ER functional homeostasis is re-established (Chao et al. 2019).