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对质子根毒性敏感 1 通过 CIPK23 的转录调控调控拟南芥的耐盐耐旱性。

Sensitive to Proton Rhizotoxicity1 Regulates Salt and Drought Tolerance of Arabidopsis thaliana through Transcriptional Regulation of CIPK23.

机构信息

Faculty of Applied Biological Sciences, Gifu University, 1-1 Yanagido, Gifu, Japan.

Research Faculty of Agriculture, Hokkaido University, Kita-9, Nishi-9, Kitaku, Sapporo, Japan.

出版信息

Plant Cell Physiol. 2019 Sep 1;60(9):2113-2126. doi: 10.1093/pcp/pcz120.

DOI:10.1093/pcp/pcz120
PMID:31241160
Abstract

The transcription factor sensitive to proton rhizotoxicity 1 (STOP1) regulates multiple stress tolerances. In this study, we confirmed its involvement in NaCl and drought tolerance. The root growth of the T-DNA insertion mutant of STOP1 (stop1) was sensitive to NaCl-containing solidified MS media. Transcriptome analysis of stop1 under NaCl stress revealed that STOP1 regulates several genes related to salt tolerance, including CIPK23. Among all available homozygous T-DNA insertion mutants of the genes suppressed in stop1, only cipk23 showed a NaCl-sensitive root growth phenotype comparable to stop1. The CIPK23 promoter had a functional STOP1-binding site, suggesting a strong CIPK23 suppression led to NaCl sensitivity of stop1. This possibility was supported by in planta complementation of CIPK23 in the stop1 background, which rescued the short root phenotype under NaCl. Both stop1 and cipk23 exhibited a drought tolerant phenotype and increased abscisic acid-regulated stomatal closure, while the complementation of CIPK23 in stop1 reversed these traits. Our findings uncover additional pleiotropic roles of STOP1 mediated by CIPK23, which regulates various ion transporters including those regulating K+-homeostasis, which may induce a trade-off between drought tolerance and other traits.

摘要

对质子根毒性敏感的转录因子 1(STOP1)调节多种胁迫耐受性。在本研究中,我们证实了它参与了耐盐和耐旱性。STOP1(stop1)的 T-DNA 插入突变体的根生长对含 NaCl 的固化 MS 培养基敏感。NaCl 胁迫下 stop1 的转录组分析表明,STOP1 调节与耐盐性相关的几个基因,包括 CIPK23。在 stop1 中被抑制的所有可用的纯合 T-DNA 插入突变体中,只有 cipk23 表现出与 stop1 相当的 NaCl 敏感的根生长表型。CIPK23 启动子具有功能性 STOP1 结合位点,表明强烈的 CIPK23 抑制导致 stop1 的 NaCl 敏感性。这种可能性得到了在 stop1 背景下体内 CIPK23 互补的支持,该互补挽救了 NaCl 下短根表型。stop1 和 cipk23 均表现出耐旱表型和增加脱落酸调节的气孔关闭,而 CIPK23 在 stop1 中的互补则逆转了这些特征。我们的发现揭示了 STOP1 通过 CIPK23 介导的额外的多效性作用,该作用调节各种离子转运体,包括调节 K+稳态的离子转运体,这可能导致耐旱性和其他特征之间的权衡。

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