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SlSOS2 参与番茄的耐盐性。

Involvement of SlSOS2 in tomato salt tolerance.

机构信息

Department of Biochemistry, Molecular and Cellular Biology of Plants, Estación Experimental del Zaidín, Consejo Superior de Investigaciones Científicas (CSIC), Granada, Spain.

出版信息

Bioengineered. 2012 Sep-Oct;3(5):298-302. doi: 10.4161/bioe.20796. Epub 2012 Jul 24.

Abstract

The Ca(2+)-dependent SOS pathway has emerged as a key mechanism in the homeostasis of Na(+) and K(+) under saline conditions. We recently identified and functionally characterized by complementation studies in yeast and Arabidopsis the gene encoding the calcineurin-interacting protein kinase of the SOS pathway in tomato, SlSOS2.(1) We also show evidences on the biotechnological potential of SlSOS2 conferring salt tolerance to transgenic tomato. The increased salinity tolerance of SlSOS2 overexpressing plants is associated with higher sodium content in stems and leaves. SlSOS2 overexpression upregulates the Na(+)/H(+) exchange at the plasma membrane (SlSOS1) and K(+), Na(+)/H(+) antiport at the endosomal and vacuolar compartments (LeNHX2 and LeNHX4). Therefore, SlSOS2 seems to be involved in tomato salinity tolerance through regulation of Na(+) extrusion from the root, active loading of Na(+) into the xylem and Na(+) and K(+) compartmentalization.

摘要

钙依赖的 SOS 途径已成为盐胁迫条件下维持钠(Na+)和钾(K+)稳态的关键机制。我们最近通过在酵母和拟南芥中的互补研究,鉴定并功能表征了番茄中钙调神经磷酸酶相互作用蛋白激酶的 SOS 途径基因 SlSOS2。(1)我们还提供了 SlSOS2 赋予转基因番茄耐盐性的生物技术潜力的证据。SlSOS2 过表达植物的耐盐性增加与茎和叶中更高的钠离子含量有关。SlSOS2 过表达上调了质膜上的 Na+/H+交换(SlSOS1)和 K+、内体和液泡区室中的 Na+/H+反向转运(LeNHX2 和 LeNHX4)。因此,SlSOS2 似乎通过调节从根部排出 Na+、主动将 Na+装载到木质部以及 Na+和 K+区室化来参与番茄的耐盐性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5e0/3477699/719aa0b43d83/bbug-3-298-g1.jpg

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