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Original Research ARTICLE Provisionally accepted The full-text will be published soon. Notify me

Front. Plant Sci. | doi: 10.3389/fpls.2019.01032

Arabidopsis GAAP1 to GAAP3 Play Redundant Role in Cell Death Inhibition by Suppressing the Upregulation of Salicylic Acid Pathway under Endoplasmic Reticulum Stress

 Wei Wang1, Xin Li1, Manli Zhu1, Xiaohan Tang1, Zhiying Wang1,  Kun Guo1, Yan Zhou1,  Yue Sun1, Wei Zhang1 and  Xiaofang Li1*
  • 1East China Normal University, China

The unfolded protein response (UPR) is activated to sustain cell survival by reducing misfolded protein accumulation in the endoplasmic reticulum (ER). The UPR also promotes cell death when the ER stress is severe. However, the underlying molecular mechanisms of UPR activity regulation and cell death transition are less understood in plants. Arabidopsis GAAP1 and GAAP3 are involved in the regulation of UPR and cell death. Five GAAP gene members are found in Arabidopsis. Here, we analyzed the function of GAAP2 in addition to GAAP1 and GAAP3 in ER stress response using single, double, and triple mutants. Results showed that single or double or triple mutants reduced plant survival and enhanced cell death under ER stress. And the sensitivity increased with the number of mutation genes increase. Quantitative real-time polymerase chain reaction analysis showed that mutation in triple genes promoted UPR signaling when confronted with mild ER stress, advanced SA target genes upregulation when confronted with severe stress. Moreover, Quantitative detection by UPLC-ESI-MS/MS showed that ER stress upregulated salicylic acid (SA) content in plants. These data suggest that GAAP1 to GAAP3 played redundant roles in cell death resistance and fine tuning UPR activation. And the anti-cell death function of GAAPs might be achieved by impairing the up-regulation of the SA pathway under ER stress.

Keywords: Arabidopsis thaliana, GAAP, Endoplasmic Reticulum Stress, Cell Death, Salicylic Acid, unfolded-protein response

Received: 22 May 2019; Accepted: 24 Jul 2019.

Copyright: © 2019 Wang, Li, Zhu, Tang, Wang, Guo, Zhou, Sun, Zhang and Li. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Dr. Xiaofang Li, East China Normal University, Shanghai, 200062, Shanghai Municipality, China, xfli@bio.ecnu.edu.cn