美国加州大学栾升研究团队的研究发现钙(Ca2+)平衡机制调控植物生长和免疫。该研究于2024年2月28日发表于国际学术期刊《自然》杂志。
研究人员揭示了拟南芥中的两种信号通路,它们在液泡Ca2+/H+交换器(CAXs)激活处汇聚,以清除植物体内过量的细胞膜Ca2+。其中一条通路在外部Ca2+水平升高时激活,其需要类钙调素B(CBL)Ca2+传感器和与CBL有相互作用的蛋白激酶(CIPKs),它们通过磷酸化自动抑制结构域中的丝氨酸(S)簇来激活CAXs。
第二种途径由与微生物相关的分子模式触发,免疫受体复合物FLS2-BAK1以及相关的细胞质激酶BIK1和PBL1参与该过程,它们调控CAXs中相同S簇的磷酸化,从而调节免疫过程中Ca2+信号。这种依赖Ca2+(CBL-CIPK)和不依赖Ca2+的机制(FLS2-BAK1-BIK1/PBL1)通过调节细胞膜处Ca2+的平衡,共同平衡植物生长和免疫。
研究人员表示,钙是植物必需的营养物质,也是一种细胞信号,但过量的钙会产生毒性并抑制生长。为了在动态环境中茁壮成长,植物必须通过调节大量Ca2+转运蛋白来监控和维持细胞膜Ca2+平衡。
附:英文原文
Title: Mechanisms of calcium homeostasis orchestrate plant growth and immunity
Author: Wang, Chao, Tang, Ren-Jie, Kou, Senhao, Xu, Xiaoshu, Lu, Yi, Rauscher, Kenda, Voelker, Angela, Luan, Sheng
Issue&Volume: 2024-02-28
Abstract: Calcium (Ca2+) is an essential nutrient for plants and a cellular signal, but excessive levels can be toxic and inhibit growth1,2. To thrive in dynamic environments, plants must monitor and maintain cytosolic Ca2+ homeostasis by regulating numerous Ca2+ transporters3. Here we report two signalling pathways in Arabidopsis thaliana that converge on the activation of vacuolar Ca2+/H+ exchangers (CAXs) to scavenge excess cytosolic Ca2+ in plants. One mechanism, activated in response to an elevated external Ca2+ level, entails calcineurin B-like (CBL) Ca2+ sensors and CBL-interacting protein kinases (CIPKs), which activate CAXs by phosphorylating a serine (S) cluster in the auto-inhibitory domain. The second pathway, triggered by molecular patterns associated with microorganisms, engages the immune receptor complex FLS2–BAK1 and the associated cytoplasmic kinases BIK1 and PBL1, which phosphorylate the same S-cluster in CAXs to modulate Ca2+ signals in immunity. These Ca2+-dependent (CBL–CIPK) and Ca2+-independent (FLS2–BAK1–BIK1/PBL1) mechanisms combine to balance plant growth and immunity by regulating cytosolic Ca2+ homeostasis.
DOI: 10.1038/s41586-024-07100-0
Source: https://www.nature.com/articles/s41586-024-07100-0
Nature:《自然》,创刊于1869年。隶属于施普林格·自然出版集团,最新IF:69.504
官方网址:http://www.nature.com/
投稿链接:http://www.nature.com/authors/submit_manuscript.html