The Actin-Related Protein2/3 Complex Regulates Mitochondrial-Associated Calcium Signaling during Salt Stress in Arabidopsis

Author:

Zhao Yi1,Pan Zhen12,Zhang Yan1,Qu Xiaolu3,Zhang Yuguo1,Yang Yongqing1,Jiang Xiangning24,Huang Shanjin3,Yuan Ming1,Schumaker Karen S.5,Guo Yan16

Affiliation:

1. State Key Laboratory of Plant Physiology and Biochemistry, College of Biological Sciences, China Agricultural University, Beijing 100193, China

2. College of Life Sciences and Biotechnology, Beijing Forestry University, Beijing 100083, China

3. Key Laboratory of Plant Molecular Physiology, Institute of Botany, Chinese Academy of Sciences, Beijing 100093, China

4. National Engineering Laboratory of Tree Breeding, The Tree and Ornamental Plant Breeding and Biotechnology Laboratory of State Forestry Administration, Beijing 100083, China

5. School of Plant Sciences, University of Arizona, Tucson, Arizona 85721

6. National Center for Plant Gene Research, Beijing 100193, China

Abstract

Abstract Microfilament and Ca2+ dynamics play important roles in stress signaling in plants. Through genetic screening of Arabidopsis thaliana mutants that are defective in stress-induced increases in cytosolic Ca2+ ([Ca2+]cyt), we identified Actin-Related Protein2 (Arp2) as a regulator of [Ca2+]cyt in response to salt stress. Plants lacking Arp2 or other proteins in the Arp2/3 complex exhibited enhanced salt-induced increases in [Ca2+]cyt, decreased mitochondria movement, and hypersensitivity to salt. In addition, mitochondria aggregated, the mitochondrial permeability transition pore opened, and mitochondrial membrane potential Ψm was impaired in the arp2 mutant, and these changes were associated with salt-induced cell death. When opening of the enhanced mitochondrial permeability transition pore was blocked or increases in [Ca2+]cyt were prevented, the salt-sensitive phenotype of the arp2 mutant was partially rescued. These results indicate that the Arp2/3 complex regulates mitochondrial-dependent Ca2+ signaling in response to salt stress.

Publisher

Oxford University Press (OUP)

Subject

Cell Biology,Plant Science

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