Arabidopsis Toxicos en Levadura 78 (AtATL78) mediates ABA-dependent ROS signaling in response to drought stress

被引:35
|
作者
Suh, Ji Yeon [1 ]
Kim, Soo Jin [1 ,3 ]
Oh, Tae Rin [1 ]
Cho, Seok Keun [1 ]
Yang, Seong Wook [1 ,2 ]
Kim, Woo Taek [1 ]
机构
[1] Yonsei Univ, Dept Syst Biol, Coll Life Sci & Biotechnol, Seoul 120749, South Korea
[2] Univ Copenhagen, Fac Sci, Dept Plant & Environm Sci, Sect Plant Biochem, Thorvaldsensvej 40, DK-1871 Copenhagen C, Denmark
[3] Korea Atom Energy Res Inst, Dept Radiat Biol, Daejon 305600, South Korea
基金
新加坡国家研究基金会;
关键词
Ubiquitin-proteasome system (UPS); RING-type E3 ligase (RING); Drought stress; Reactive oxygen species (ROS); Arabidopsis Toxicos en Levadura (ATL); ABA-dependent signaling; ABSCISIC-ACID; HYDROGEN-PEROXIDE; ARABIDOPSIS-THALIANA; PROTEASOME SYSTEM; COLD STRESS; UBIQUITIN; LIGASE; CATALASE; ATAIRP1; FAMILY;
D O I
10.1016/j.bbrc.2015.11.061
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Plants have developed a variety of complicated responses to cope with drought, one of the most challenging environmental stresses. As a quick response, plants rapidly inhibit stomatal opening under the control of abscisic acid (ABA) signaling pathway, in order to preserve water. Here, we report that Arabidopsis Toxicos en Levadura (ATL), a RING-type E3 ubiquitin ligase, mediates the ABA-dependent stomatal closure. In contrast to wild-type plants, the stomatal closure was fully impaired in atatl78 mutant plants even in the presence of exogenous ABA and reactive oxygen species (ROS). Besides, under high concentrations of Ca2+, a down-stream signaling molecule of ABA signaling pathway, atatl78 mutant plants successfully closed the pores. Furthermore, AtATL78 protein indirectly associated with catalases and the deficiency of AtATL78 led the reduction of catalase activity and H2O2, implying the function of AtATL78 in the modulation of ROS activity. Based on these results, we suggest that AtATL78 possibly plays a role in promoting ROS-mediated ABA signaling pathway during drought stress. (C) 2015 Elsevier Inc. All rights reserved.
引用
收藏
页码:8 / 14
页数:7
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