Arabidopsis ERdj3B coordinates with ERECTA-family receptor kinases to regulate ovule development and the heat stress response

Author:

Leng Ya-Jun1ORCID,Yao Ya-Sen1ORCID,Yang Ke-Zhen23ORCID,Wu Pei-Xiang1ORCID,Xia Yu-Xin1ORCID,Zuo Chao-Ran23ORCID,Luo Jing-Hong1ORCID,Wang Pu1ORCID,Liu Yang-Yang1ORCID,Zhang Xue-Qin1ORCID,Ye De1ORCID,Le Jie23ORCID,Chen Li-Qun1ORCID

Affiliation:

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

2. Key Laboratory of Plant Molecular Physiology, CAS Center for Excellence in Molecular Plant Sciences, Institute of Botany, Chinese Academy of Sciences , Beijing 100093, China

3. University of Chinese Academy of Sciences , Beijing 100049, China

Abstract

Abstract The endoplasmic reticulum-localized DnaJ family 3B (ERdj3B), is a component of the stromal cell-derived factor 2 (SDF2)–ERdj3B–binding immunoglobulin protein (BiP) chaperone complex, which functions in protein folding, translocation, and quality control. We found that ERdj3B mutations affected integument development in the Ler ecotype but not in the Col-0 ecotype of Arabidopsis (Arabidopsis thaliana). Map-based cloning identified the ERECTA (ER) gene as a natural modifier of ERdj3B. The double mutation of ERdj3B and ER caused a major defect in the inner integument under heat stress. Additional mutation of the ER paralog ERECTA-LIKE 1 (ERL1) or ERL2 to the erdj3b er double mutant exacerbated the defective integument phenotype. The double mutation of ER and SDF2, the other component of the SDF2–ERdj3B–BiP complex, resulted in similar defects in the inner integument. Furthermore, both the protein abundance and plasma membrane partitioning of ER, ERL1, and ERL2 were markedly reduced in erdj3b plants, indicating that the SDF2–ERdj3B–BiP chaperone complex might control the translocation of ERECTA-family proteins from the endoplasmic reticulum to the plasma membrane. Our results suggest that the SDF2–ERdj3B–BiP complex functions in ovule development and the heat stress response in coordination with ERECTA-family receptor kinases.

Funder

National Natural Science Foundation of China

Publisher

Oxford University Press (OUP)

Subject

Cell Biology,Plant Science

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