Arabidopsis CAMTA3/SR1 is involved in drought stress tolerance and ABA signaling

文献类型： 外文期刊

第一作者： Zeng, Houqing

作者： Zeng, Houqing;Wu, Haicheng;Wang, Guoping;Dai, Senhuan;Zhu, Qiuqing;Chen, Huiying;Du, Liqun;Chen, Huiying;Yi, Keke

作者机构：

关键词： Calmodulin binding transcription activator; Drought stress; Abscisic acid response; Salicylic acid; Stomatal aperture; Water loss

期刊名称：PLANT SCIENCE （ 影响因子：5.363； 五年影响因子：5.454 ）

ISSN： 0168-9452

年卷期： 2022 年 319 卷

页码：

收录情况： SCI

摘要： Calcium/calmodulin signals are important for various cellular and physiological activities in plants. Calmodulin binding transcription activators also named Signal Responsive (SR) proteins belong to an important calcium/ calmodulin-dependent transcription factor family that plays critical roles in stress responses. However, the role of SRs in abscisic acid (ABA) regulated plant responses to drought stress is largely unknown. Here, we characterized the role of Arabidopsis SR1 in drought stress tolerance and ABA response by analyzing the phenotypes of SR1 knockout and SR1-overexpression plants. sr1 mutants which accumulate salicylic acid (SA) were found more sensitive to drought stress and showed a higher water loss rate as compared with wild-type. By contrast, SR1-overexpression lines exhibited increased drought tolerance and less water loss than wild-type. Furthermore, sr1 mutants showed reduced ABA response in seed germination, root elongation, and stomatal closure, while SR1-overexpression lines displayed more sensitive to ABA than wild-type. In addition, the drought sensitive and ABA-insensitive phenotypes of sr1 mutants were recovered by diminishing SA accumulation via knockouts of SA synthesizer ICS1 or activator PAD4, or through expression of SA-degrading enzyme NahG. Some drought/ABA-responsive genes exhibited differentially expressed in sr1 mutants and SR1-overexpression plants. These results suggest that SR1 plays a positive role in drought stress tolerance and ABA response, and drought/ ABA responses are antagonized by SA accumulation that is negatively regulated by SR1.

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