{"title":"拟南芥保卫细胞脱落酸信号传导过程中,保卫细胞过氧化氢抗原1(Guard Cell HYDROGEN PEROXIDE-RESISTANT1)在活性羰基物种产生的上游发挥作用。","authors":"Oumayma Shaiek, Huifei Yin, Nodoka Uesako, Md Moshiul Islam, Mohammad Saidur Rhaman, Toshiyuki Nakamura, Yoshimasa Nakamura, Shintaro Munemasa, Jun'ichi Mano, Yoshiyuki Murata","doi":"10.1093/bbb/zbae135","DOIUrl":null,"url":null,"abstract":"<p><p>GUARD CELL HYDROGEN PEROXIDE-RESISTANT1 (GHR1), a leucine-rich repeat receptor-like kinase, is involved in abscisic acid (ABA)-induced stomatal closure. We investigated the role of GHR1 in reactive oxygen species (ROS) signaling for ABA-induced stomatal closure. ABA induced ROS production in wild type (WT) and the ghr1 of Arabidopsis thaliana. Hydrogen peroxide induced stomatal closure, accompanying the generation of acrolein in guard cells. The reactive carbonyl species (RCS) scavengers inhibited the ABA- and H2O2-induced stomatal closure in WT. In the ghr1, H2O2 failed to induce acrolein production and stomatal closure while RCS induced stomatal closure. Thus, GHR1 functions downstream of ROS and is required for the generation of RCS in guard-cell ABA signaling. In the ghr1, Ca2+ induced stomatal closure but RCS did not activate ICa channels. The GHR1 may be also involved in a Ca2+-independent pathway for ABA-induced stomatal closure.</p>","PeriodicalId":9175,"journal":{"name":"Bioscience, Biotechnology, and Biochemistry","volume":" ","pages":"1403-1410"},"PeriodicalIF":1.4000,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"GUARD CELL HYDROGEN PEROXIDE-RESISTANT1 functions upstream of reactive carbonyl species production in Arabidopsis guard-cell abscisic acid signaling.\",\"authors\":\"Oumayma Shaiek, Huifei Yin, Nodoka Uesako, Md Moshiul Islam, Mohammad Saidur Rhaman, Toshiyuki Nakamura, Yoshimasa Nakamura, Shintaro Munemasa, Jun'ichi Mano, Yoshiyuki Murata\",\"doi\":\"10.1093/bbb/zbae135\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>GUARD CELL HYDROGEN PEROXIDE-RESISTANT1 (GHR1), a leucine-rich repeat receptor-like kinase, is involved in abscisic acid (ABA)-induced stomatal closure. We investigated the role of GHR1 in reactive oxygen species (ROS) signaling for ABA-induced stomatal closure. ABA induced ROS production in wild type (WT) and the ghr1 of Arabidopsis thaliana. Hydrogen peroxide induced stomatal closure, accompanying the generation of acrolein in guard cells. The reactive carbonyl species (RCS) scavengers inhibited the ABA- and H2O2-induced stomatal closure in WT. In the ghr1, H2O2 failed to induce acrolein production and stomatal closure while RCS induced stomatal closure. Thus, GHR1 functions downstream of ROS and is required for the generation of RCS in guard-cell ABA signaling. In the ghr1, Ca2+ induced stomatal closure but RCS did not activate ICa channels. The GHR1 may be also involved in a Ca2+-independent pathway for ABA-induced stomatal closure.</p>\",\"PeriodicalId\":9175,\"journal\":{\"name\":\"Bioscience, Biotechnology, and Biochemistry\",\"volume\":\" \",\"pages\":\"1403-1410\"},\"PeriodicalIF\":1.4000,\"publicationDate\":\"2024-11-22\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Bioscience, Biotechnology, and Biochemistry\",\"FirstCategoryId\":\"5\",\"ListUrlMain\":\"https://doi.org/10.1093/bbb/zbae135\",\"RegionNum\":4,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Bioscience, Biotechnology, and Biochemistry","FirstCategoryId":"5","ListUrlMain":"https://doi.org/10.1093/bbb/zbae135","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0
摘要
护卫细胞过氧化氢抗原1(GHR1)是一种富亮氨酸重复受体样激酶,参与脱落酸(ABA)诱导的气孔关闭。我们研究了 GHR1 在活性氧(ROS)信号转导 ABA 诱导的气孔关闭中的作用。脱落酸诱导拟南芥野生型(WT)和ghr1产生ROS。过氧化氢诱导气孔关闭,同时在保卫细胞中产生丙烯醛。活性碳酰物种(RCS)清除剂抑制了 WT 的 ABA 和 H2O2 诱导的气孔关闭。在 ghr1 中,H2O2 不能诱导丙烯醛的产生和气孔关闭,而 RCS 能诱导气孔关闭。因此,GHR1 在 ROS 的下游发挥作用,并且在保卫细胞 ABA 信号转导中需要 RCS 的产生。在 ghr1 中,Ca2+ 能诱导气孔关闭,但 RCS 不能激活 ICa 通道。GHR1 可能也参与了 ABA 诱导气孔关闭的 Ca2+ 非依赖性途径。
GUARD CELL HYDROGEN PEROXIDE-RESISTANT1 functions upstream of reactive carbonyl species production in Arabidopsis guard-cell abscisic acid signaling.
GUARD CELL HYDROGEN PEROXIDE-RESISTANT1 (GHR1), a leucine-rich repeat receptor-like kinase, is involved in abscisic acid (ABA)-induced stomatal closure. We investigated the role of GHR1 in reactive oxygen species (ROS) signaling for ABA-induced stomatal closure. ABA induced ROS production in wild type (WT) and the ghr1 of Arabidopsis thaliana. Hydrogen peroxide induced stomatal closure, accompanying the generation of acrolein in guard cells. The reactive carbonyl species (RCS) scavengers inhibited the ABA- and H2O2-induced stomatal closure in WT. In the ghr1, H2O2 failed to induce acrolein production and stomatal closure while RCS induced stomatal closure. Thus, GHR1 functions downstream of ROS and is required for the generation of RCS in guard-cell ABA signaling. In the ghr1, Ca2+ induced stomatal closure but RCS did not activate ICa channels. The GHR1 may be also involved in a Ca2+-independent pathway for ABA-induced stomatal closure.
期刊介绍:
Bioscience, Biotechnology, and Biochemistry publishes high-quality papers providing chemical and biological analyses of vital phenomena exhibited by animals, plants, and microorganisms, the chemical structures and functions of their products, and related matters. The Journal plays a major role in communicating to a global audience outstanding basic and applied research in all fields subsumed by the Japan Society for Bioscience, Biotechnology, and Agrochemistry (JSBBA).