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植物细胞因子信号重新开启植物免疫和水分损失中的气孔。

Phytocytokine signalling reopens stomata in plant immunity and water loss.

机构信息

Department of Biochemistry and Biophysics, Texas A&M University, College Station, TX, USA.

School of Municipal and Environmental Engineering, Shandong Jianzhu University, Jinan, China.

出版信息

Nature. 2022 May;605(7909):332-339. doi: 10.1038/s41586-022-04684-3. Epub 2022 May 4.

DOI:10.1038/s41586-022-04684-3
PMID:35508659
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9710542/
Abstract

Stomata exert considerable effects on global carbon and water cycles by mediating gas exchange and water vapour. Stomatal closure prevents water loss in response to dehydration and limits pathogen entry. However, prolonged stomatal closure reduces photosynthesis and transpiration and creates aqueous apoplasts that promote colonization by pathogens. How plants dynamically regulate stomatal reopening in a changing climate is unclear. Here we show that the secreted peptides SMALL PHYTOCYTOKINES REGULATING DEFENSE AND WATER LOSS (SCREWs) and the cognate receptor kinase PLANT SCREW UNRESPONSIVE RECEPTOR (NUT) counter-regulate phytohormone abscisic acid (ABA)- and microbe-associated molecular pattern (MAMP)-induced stomatal closure. SCREWs sensed by NUT function as immunomodulatory phytocytokines and recruit SOMATIC EMBRYOGENESIS RECEPTOR-LIKE KINASE (SERK) co-receptors to relay immune signalling. SCREWs trigger the NUT-dependent phosphorylation of ABA INSENSITIVE 1 (ABI1) and ABI2, which leads to an increase in the activity of ABI phosphatases towards OPEN STOMATA 1 (OST1)-a key kinase that mediates ABA- and MAMP-induced stomatal closure-and a reduction in the activity of S-type anion channels. After induction by dehydration and pathogen infection, SCREW-NUT signalling promotes apoplastic water loss and disrupts microorganism-rich aqueous habitats to limit pathogen colonization. The SCREW-NUT system is widely distributed across land plants, which suggests that it has an important role in preventing uncontrolled stomatal closure caused by abiotic and biotic stresses to optimize plant fitness.

摘要

气孔通过介导气体交换和水蒸气来对全球碳和水循环产生重要影响。气孔关闭可以防止水分流失,从而防止脱水,并限制病原体进入。然而,长时间的气孔关闭会降低光合作用和蒸腾作用,并形成水相细胞外基质,从而促进病原体的定植。植物如何在不断变化的气候条件下动态调节气孔重新开放尚不清楚。本文作者表明,分泌肽 SMALL PHYTOCYTOKINES REGULATING DEFENSE AND WATER LOSS (SCREWs)和同源受体激酶 PLANT SCREW UNRESPONSIVE RECEPTOR (NUT) 可以拮抗植物激素脱落酸(ABA)和微生物相关分子模式(MAMP)诱导的气孔关闭。被 NUT 识别的 SCREWs 作为免疫调节植物细胞因子发挥作用,并募集 SOMATIC EMBRYOGENESIS RECEPTOR-LIKE KINASE (SERK) 共受体来传递免疫信号。SCREWs 触发 NUT 依赖性的 ABA INSENSITIVE 1 (ABI1) 和 ABI2 的磷酸化,导致 ABI 磷酸酶对 OPEN STOMATA 1 (OST1)的活性增加,OST1 是介导 ABA 和 MAMP 诱导的气孔关闭的关键激酶,同时导致 S 型阴离子通道的活性降低。在脱水和病原体感染诱导后,SCREW-NUT 信号通路促进细胞外基质水的流失,并破坏富含微生物的水相栖息地,从而限制病原体的定植。SCREW-NUT 系统在陆生植物中广泛分布,这表明它在防止由生物和非生物胁迫引起的失控的气孔关闭方面发挥着重要作用,从而优化植物的适应性。

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