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- Title
Mitochondrial Fission Complex Is Required for Long-Term Heat Tolerance of Arabidopsis.
- Authors
Tsukimoto, Ryo; Isono, Kazuho; Kajino, Takuma; Iuchi, Satoshi; Shinozawa, Akihisa; Yotsui, Izumi; Sakata, Yoichi; Taji, Teruaki
- Abstract
Plants are often exposed not only to short-term (S) heat stress but also to long-term (L) heat stress over several consecutive days. A few Arabidopsis mutants defective in L-heat tolerance have been identified, but the molecular mechanisms involved are less well understood than those involved in S-heat tolerance. To elucidate the mechanisms, we isolated the new s ensitive to lo ng-term h eat5 (sloh5) mutant from EMS-mutagenized seeds of L-heat-tolerant Col-0. The sloh5 mutant was hypersensitive to L-heat but not to S-heat, osmo-shock, salt-shock or oxidative stress. The causal gene, SLOH5 , is identical to elongated mitochondria1 (ELM1), which plays an important role in mitochondrial fission in conjunction with dynamin-related proteins DRP3A and DRP3B. Transcript levels of ELM1, DRP3A and DRP3B were time-dependently increased by L-heat stress, and drp3a drp3b double mutants were hypersensitive to L-heat stress. The sloh5 mutant contained massively elongated mitochondria. L-heat stress caused mitochondrial dysfunction and cell death in sloh5. Furthermore, WT plants treated with a mitochondrial myosin ATPase inhibitor were hypersensitive to L-heat stress. These findings suggest that mitochondrial fission and function are important in L-heat tolerance of Arabidopsis.
- Subjects
MYOSIN; MITOCHONDRIA; ARABIDOPSIS; CELL death; OXIDATIVE stress; HEAT shock proteins
- Publication
Plant & Cell Physiology, 2022, Vol 63, Issue 3, p296
- ISSN
0032-0781
- Publication type
Article
- DOI
10.1093/pcp/pcab171