生物
分生组织
拟南芥
细胞生物学
离子运输机
内胚层
植物
生物化学
生物物理学
开枪
突变体
基因
膜
作者
Changxi Chen,Gefeng He,Jianfang Li,Javier Pérez-Hormaeche,Tobias Becker,Manqing Luo,Lukas Wallrad,Junping Gao,Jia Li,José M. Pardo,Jörg Kudla,Yan Guo
标识
DOI:10.15252/embj.2022113004
摘要
Abstract Soil salinity impairs plant growth reducing crop productivity. Toxic accumulation of sodium ions is counteracted by the Salt Overly Sensitive (SOS) pathway for Na + extrusion, comprising the Na + transporter SOS1, the kinase SOS2, and SOS3 as one of several Calcineurin‐B‐like (CBL) Ca 2 + sensors. Here, we report that the receptor‐like kinase GSO1/SGN3 activates SOS2, independently of SOS3 binding, by physical interaction and phosphorylation at Thr16. Loss of GSO1 function renders plants salt sensitive and GSO1 is both sufficient and required for activating the SOS2‐SOS1 module in yeast and in planta . Salt stress causes the accumulation of GSO1 in two specific and spatially defined areas of the root tip: in the endodermis section undergoing Casparian strip (CS) formation, where it reinforces the CIF‐GSO1‐SGN1 axis for CS barrier formation; and in the meristem, where it creates the GSO1‐SOS2‐SOS1 axis for Na + detoxification. Thus, GSO1 simultaneously prevents Na + both from diffusing into the vasculature, and from poisoning unprotected stem cells in the meristem. By protecting the meristem, receptor‐like kinase‐conferred activation of the SOS2‐SOS1 module allows root growth to be maintained in adverse environments.
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