Oxidative Homeostasis Regulates the Response to Reductive Endoplasmic Reticulum Stress through Translation Control | Zendy

Shuvadeep Maity | Zendy; Asher Rajkumar | Zendy; Latika Matai | Zendy; Ajay Bhat | Zendy; Asmita Ghosh | Zendy; Ganesh Agam | Zendy; Simarjot Kaur | Zendy; Niraj Rajesh Bhatt | Zendy; Arnab Mukhopadhyay | Zendy; Shantanu Sengupta | Zendy; Kausik Chakraborty | Zendy

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Oxidative Homeostasis Regulates the Response to Reductive Endoplasmic Reticulum Stress through Translation Control

Author(s) -

Shuvadeep Maity,

Asher Rajkumar,

Latika Matai,

Ajay Bhat,

Asmita Ghosh,

Ganesh Agam,

Simarjot Kaur,

Niraj Rajesh Bhatt,

Arnab Mukhopadhyay,

Shantanu Sengupta,

Kausik Chakraborty

Publication year - 2016

Publication title -

cell reports

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 6.264

H-Index - 154

eISSN - 2639-1856

pISSN - 2211-1247

DOI - 10.1016/j.celrep.2016.06.025

Subject(s) - endoplasmic reticulum , oxidative stress , microbiology and biotechnology , homeostasis , translation (biology) , unfolded protein response , oxidative phosphorylation , chemistry , biology , biochemistry , messenger rna , gene

Reductive stress leads to the loss of disulfide bond formation and induces the unfolded protein response of the endoplasmic reticulum (UPR(ER)), necessary to regain proteostasis in the compartment. Here we show that peroxide accumulation during reductive stress attenuates UPR(ER) amplitude by altering translation without any discernible effect on transcription. Through a comprehensive genetic screen in Saccharomyces cerevisiae, we identify modulators of reductive stress-induced UPR(ER) and demonstrate that oxidative quality control (OQC) genes modulate this cellular response in the presence of chronic but not acute reductive stress. Using a combination of microarray and relative quantitative proteomics, we uncover a non-canonical translation attenuation mechanism that acts in a bipartite manner to selectively downregulate highly expressed proteins, decoupling the cell's transcriptional and translational response during reductive ER stress. Finally, we demonstrate that PERK, a canonical translation attenuator in higher eukaryotes, helps in bypassing a ROS-dependent, non-canonical mode of translation attenuation.

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