Abstract：
Salt stress negatively affects rice growth, development and yield. Metabolic adjustments contribute to the adaptation of rice under salt stress. Branched-chain amino acids (BCAA) are three essential amino acids that cannot be synthesized by humans or animals. However, little is known about the role of BCAA in response to salt stress in plants. Here, we showed that BCAAs may function as scavengers of reactive oxygen species (ROS) to provide protection against damage caused by salinity. We determined that branched-chain aminotransferase 2 (OsBCAT2), a protein responsible for the degradation of BCAA, positively regulates salt tolerance. Salt significantly induces the expression of OsBCAT2 rather than BCAA synthesis genes, which indicated that salt mainly promotes BCAA degradation and not de novo synthesis. Metabolomics analysis revealed that vitamin B5 (VB5) biosynthesis pathway intermediates were higher in the OsBCAT2-overexpressing plants but lower in osbcat2 mutants under salt stress. The salt stress-sensitive phenotypes of the osbcat2 mutants are rescued by exogenous VB5, indicating that OsBCAT2 affects rice salt tolerance by regulating VB5 synthesis. Our work provides new insights into the enzymes involved in BCAAs degradation and VB5 biosynthesis and sheds light on the molecular mechanism of BCAAs in response to salt stress.
摘要：
盐胁迫对水稻生长产生负面影响，发展和产量。代谢调节有助于水稻在盐胁迫下的适应。支链氨基酸（BCAA）是人类或动物无法合成的三种必需氨基酸。然而,对植物中BCAA在盐胁迫反应中的作用知之甚少。这里,我们表明，BCAAs可以作为活性氧（ROS）的清除剂，以提供保护免受盐度造成的损害。我们确定支链氨基转移酶2（OsBCAT2），一种负责BCAA降解的蛋白质，积极调节耐盐性。盐显着诱导OsBCAT2而不是BCAA合成基因的表达，这表明盐主要促进BCAA降解，而不是从头合成。代谢组学分析表明，在盐胁迫下，OsBCAT2过表达植物中维生素B5（VB5）生物合成途径中间体较高，而osbcat2突变体中维生素B5生物合成途径中间体较低。外源VB5拯救了osbcat2突变体的盐胁迫敏感性表型，表明OsBCAT2通过调节VB5合成影响水稻耐盐性。我们的工作为参与BCAAs降解和VB5生物合成的酶提供了新的见解，并阐明了BCAAs响应盐胁迫的分子机制。
