Rotenone-induced reactive oxygen species signal the recruitment of STAT3 to mitochondria.

Abstract:

:STAT3, a transcription factor involved in various physiological and pathological processes, is also present in mitochondria. Mitochondrial STAT3 regulates complex I activity and reactive oxygen species (ROS) production, yet the mechanisms governing its translocation to mitochondria remain poorly understood. In this study, we show that rotenone-induced ROS triggers the Ser727 phosphorylation of STAT3 and its increased mitochondrial localisation. Furthermore, we show that STAT3-depleted cells display increased ROS levels during rotenone treatment. Targeted expression in mitochondria of wild-type STAT3 - but not S727A mutant - lowers ROS levels, indicating the importance of Ser727 phosphorylation, both in rotenone-induced mitochondrial targeting and quenching of ROS levels. Together, our results demonstrate a novel STAT3-mediated feedback mechanism to maintain redox homeostasis during stress.

journal_name

FEBS Lett

journal_title

FEBS letters

authors

Mohammed F,Gorla M,Bisoyi V,Tammineni P,Sepuri NBV

doi

10.1002/1873-3468.13741

subject

Has Abstract

pub_date

2020-05-01 00:00:00

pages

1403-1412

issue

9

eissn

0014-5793

issn

1873-3468

journal_volume

594

pub_type

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