Heat Shock Factor HSFA6b Mediates Mitochondrial Unfolded Protein Response in <i>Arabidopsis thaliana</i>
Guolong Yu,
Zhuoran Huang,
Chaocheng Guo,
Jiahao Li,
Xinyuan Wang,
Yudong Wang,
Xu Wang
Affiliations
Guolong Yu
Shanghai Collaborative Innovation Center of Agri-Seeds, Joint Center for Single Cell Biology, School of Agriculture and Biology, Shanghai Jiao Tong University, Shanghai 200240, China
Zhuoran Huang
Shanghai Collaborative Innovation Center of Agri-Seeds, Joint Center for Single Cell Biology, School of Agriculture and Biology, Shanghai Jiao Tong University, Shanghai 200240, China
Chaocheng Guo
Shanghai Collaborative Innovation Center of Agri-Seeds, Joint Center for Single Cell Biology, School of Agriculture and Biology, Shanghai Jiao Tong University, Shanghai 200240, China
Jiahao Li
Shanghai Collaborative Innovation Center of Agri-Seeds, Joint Center for Single Cell Biology, School of Agriculture and Biology, Shanghai Jiao Tong University, Shanghai 200240, China
Xinyuan Wang
Shanghai Collaborative Innovation Center of Agri-Seeds, Joint Center for Single Cell Biology, School of Agriculture and Biology, Shanghai Jiao Tong University, Shanghai 200240, China
Yudong Wang
Shanghai Collaborative Innovation Center of Agri-Seeds, Joint Center for Single Cell Biology, School of Agriculture and Biology, Shanghai Jiao Tong University, Shanghai 200240, China
Xu Wang
Shanghai Collaborative Innovation Center of Agri-Seeds, Joint Center for Single Cell Biology, School of Agriculture and Biology, Shanghai Jiao Tong University, Shanghai 200240, China
Mitochondria are important organelles in eukaryotes and are involved in various metabolic processes. Mitochondrial proteotoxic stress triggers the mitochondrial unfolded protein response (UPRmt) to restore mitochondrial protein homeostasis and maintain normal life activities. However, the regulatory mechanism of plant UPRmt remains to be revealed in Arabidopsis. Based on the fact that UPRmt activates heat shock protein (HSP) genes, we identified the heat shock transcription factor HSFA6b as a key regulator mediating UPRmt through reverse genetics. HSFA6b responded to mitochondrial proteotoxic stress and regulated mitochondrial heat shock proteins’ genes’ (mtHSPs) expression. HSFA6b translocated to the nuclear after treatment with doxycycline (Dox)—a mitochondrial ribosome translation inhibitor. HSFA6b binds to the mtHSPs promoters and activates mtHSPs expression. The HSFA6b mutation blocked the UPRmt signals to promote root growth under mitochondrial proteotoxic stress and accelerated leaf senescence during development. Our study reveals a novel signal-regulating mechanism in the UPRmt pathways and provides new insights regarding the regulation of plant growth and development and stress resistance by the UPRmt pathways.
