The molecular chaperone mtHSC70‐1 interacts with DjA30 to regulate female gametophyte development and fertility in Arabidopsis

Author:

Zhai Xiaoting1234,Bai Jiaoteng123,Xu Wenyan123,Yang Xiujuan123,Jia Zichao123,Xia Wenxuan123,Wu Xiaoqing123,Liang Qi123,Li Bing123ORCID,Jia Ning5

Affiliation:

1. Ministry of Education Key Laboratory of Molecular and Cellular Biology, College of Life Sciences Hebei Normal University Shijiazhuang 050024 China

2. Hebei Research Center of the Basic Discipline of Cell Biology Hebei Normal University Shijiazhuang 050024 China

3. Hebei Collaboration Innovation Center for Cell Signaling and Environmental Adaptation Hebei Normal University Shijiazhuang 050024 China

4. College of Agriculture and Forestry Hebei North University Zhangjiakou 075000 China

5. National Key Laboratory of Plant Molecular Genetics, CAS Center for Excellence in Molecular Plant Sciences Shanghai Institute of Plant Physiology and Ecology, Chinese Academy of Sciences Shanghai 200032 China

Abstract

SUMMARYArabidopsis mitochondria‐targeted heat shock protein 70 (mtHSC70‐1) plays important roles in the establishment of cytochrome c oxidase‐dependent respiration and redox homeostasis during the vegetative growth of plants. Here, we report that knocking out the mtHSC70‐1 gene led to a decrease in plant fertility; the fertility defect of the mutant was completely rescued by introducing the mtHSC70‐1 gene. mtHSC70‐1 mutants also showed defects in female gametophyte (FG) development, including delayed mitosis, abnormal nuclear position, and ectopic gene expression in the embryo sacs. In addition, we found that an Arabidopsis mitochondrial J‐protein gene (DjA30) mutant, j30+/−, had defects in FG development and fertility similar to those of mtHSC70‐1 mutant. mtHSC70‐1 and DjA30 had similar expression patterns in FGs and interacted in vivo, suggesting that these two proteins might cooperate during female gametogenesis. Further, respiratory chain complex IV activity in mtHSC70‐1 and DjA30 mutant embryo sacs was markedly downregulated; this led to the accumulation of mitochondrial reactive oxygen species (ROS). Scavenging excess ROS by introducing Mn‐superoxide dismutase 1 or catalase 1 gene into the mtHSC70‐1 mutant rescued FG development and fertility. Altogether, our results suggest that mtHSC70‐1 and DjA30 are essential for the maintenance of ROS homeostasis in the embryo sacs and provide direct evidence for the roles of ROS homeostasis in embryo sac maturation and nuclear patterning, which might determine the fate of gametic and accessory cells.

Funder

National Natural Science Foundation of China

Publisher

Wiley

Subject

Cell Biology,Plant Science,Genetics

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