RhoA/ROCK1 signaling regulates stress granule formation and apoptosis |
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| Authors: | Nien-Pei Tsai Li-Na Wei |
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| Institution: | 1. Department of Biotechnology and Biological Sciences, Hannam University, Daejeon, Korea;2. Department of Life Science, Chung-Ang University, Seoul, Korea;3. Department of Medicine and Microbiology, Chungbuk National University, Cheongju, Korea;4. Department of Applied Biology, Kyungpook National University, Kyungbuk, Korea;1. Department of Chemistry and Biochemistry, University of Colorado, Boulder, CO, USA;2. Howard Hughes Medical Institute, University of Colorado, Boulder, CO, USA |
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| 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. |
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