RhoA/ROCK1 signaling regulates stress granule formation and apoptosis

Nien Pei Tsai, Li-Na Wei

Research output: Contribution to journalArticle

60 Scopus citations

Abstract

Cells form stress granules (SGs), in response to unfavorable environments, to avoid apoptosis, but it is unclear whether and how SG formation and cellular apoptosis are coordinately regulated. In this study we detected the small GTPase, Ras homolog gene family member A (RhoA), and its downstream kinase, Rho-associated, coiled-coil containing protein kinase 1 (ROCK1), in SG, and found that their stress-induced activities were important for SG formation and subsequent global translational repression. Importantly, only activated RhoA and ROCK1 were sequestered into SG. Sequestration of activated ROCK1 into SG prevented ROCK1 from interacting with JNK-interacting protein 3 (JIP-3) and its activation of c-Jun N-terminal kinase (JNK), a pathway triggering apoptosis, thereby protecting cells from apoptosis. This study identifies a specific signaling pathway, mediated by RhoA and ROCK1, which determines cell fate by promoting SG formation or initiating apoptosis during stress.

Original languageEnglish (US)
Pages (from-to)668-675
Number of pages8
JournalCellular Signalling
Volume22
Issue number4
DOIs
StatePublished - Apr 1 2010

Keywords

  • Apoptosis
  • JIP-3
  • JNK
  • P19
  • ROCK1
  • RhoA
  • Stress granules

Fingerprint Dive into the research topics of 'RhoA/ROCK1 signaling regulates stress granule formation and apoptosis'. Together they form a unique fingerprint.

  • Cite this