Mitochondrial fission complex, SLOH5/ELM1, DRP3A, and DRP3B are required for long-term heat tolerance of Arabidopsis
Plants are often exposed not only to short-term (S-) heat-stress but also to long-term (L-) one over several consecutive days. A few Arabidopsis mutants defective in L-heat tolerance had been identified, however, the molecular mechanism in L-heat tolerance is poorly understood compared to it in S-heat tolerance. To elucidate the mechanism, we newly isolated the sensitive to long-term heat5 (sloh5) mutant from EMS-mutagenized Col-0 seeds, which is a L-heat tolerant accession among Arabidopsis. The mutant was hypersensitive to L-heat but not to S-heat, osmo-shock, salt-shock, and oxidative stresses. The causal gene, SLOH5 was identical to ELONGATED MITOCHONDRIA1 (ELM1) that plays an important role in mitochondrial fission with dynamin-related proteins, DRP3A and DRP3B. We found that the transcript levels of ELM1, DRP3A, and DRP3B were induced by L-heat stress in a time-dependent manner, and drp3a drp3b double mutant exhibited hypersensitivity to L-heat stress as well as sloh5. The sloh5 mutant has massive elongated mitochondria and interconnected network with some beaded structures. Furthermore, a mitochondrial myosin ATPase inhibitor, BDM-treated plants exhibited hypersensitivity to L-heat stress, and mitochondrial dysfunctions and cell death were occurred in sloh5 under L-heat stress. These findings suggest that the mitochondrial fission and homeostasis of mitochondrial function were important in L-heat tolerance of Arabidopsis.