Fig. 8.

A schematic summary of the role of Sse1 during ER stress. A schematic model summarizing the role of Sse1 during ER stress. The upper box represents the physiological condition when there is no stress to ER. The lower left box summarizes the condition of WT cells during Tm-mediated ER stress where polysomes are majorly reorganized into monosomes, and in this process Sse1 plays an important role. There is UPR induction by activation of Ire1-Hac1 pathway, which restores homeostasis up to a tolerable level of stress. The lower right box summarizes the condition of sse1Δ cells during ER stress with tunicamycin. Polysome to monosome conversion is inefficient in absence of Sse1 which leads to faster production of UPR-responsive proteins which in turn restores the homeostasis faster. Additionally, the ER stress induced cell cycle-arrest is evaded in sse1Δ cells leading to fitness advantage during tunicamycin stress and more cell viability.