Department of Plant Physiology and Biochemistry, Institute of Biology, University of Hohenheim, Stuttgart, Germany.
Plant Developmental Biology and Physiology, University of Kiel, Kiel, Germany.
J Exp Bot. 2021 Apr 13;72(9):3427-3440. doi: 10.1093/jxb/erab017.
Increasing drought stress poses a severe threat to agricultural productivity. Plants, however, have evolved numerous mechanisms to cope with such environmental stress. Here we report that the stress-induced production of a peptide signal contributes to stress tolerance. The expression of phytosulfokine (PSK) peptide precursor genes, and transcripts of three subtilisin-like serine proteases, SBT1.4, SBT3.7, and SBT3.8, were found to be up-regulated in response to osmotic stress. Stress symptoms were more pronounced in sbt3.8 loss-of-function mutants and could be alleviated by PSK treatment. Osmotic stress tolerance was improved in plants overexpressing the PSK1 precursor (proPSK1) or SBT3.8, resulting in higher fresh weight and improved lateral root development in transgenic plants compared with wild-type plants. We further showed that SBT3.8 is involved in the biogenesis of the bioactive PSK peptide. ProPSK1 was cleaved by SBT3.8 at the C-terminus of the PSK pentapeptide. Processing by SBT3.8 depended on the aspartic acid residue directly following the cleavage site. ProPSK1 processing was impaired in the sbt3.8 mutant. The data suggest that increased expression of proPSK1 in response to osmotic stress followed by the post-translational processing of proPSK1 by SBT3.8 leads to the production of PSK as a peptide signal for stress mitigation.
干旱胁迫的增加对农业生产力构成了严重威胁。然而，植物已经进化出许多机制来应对这种环境胁迫。在这里，我们报告称，胁迫诱导的肽信号的产生有助于提高胁迫耐受性。发现植物硫肽（PSK）肽前体基因的表达，以及三种枯草杆菌蛋白酶样丝氨酸蛋白酶 SBT1.4、SBT3.7 和 SBT3.8 的转录物，均响应渗透胁迫而上调。在 sbt3.8 功能丧失突变体中，胁迫症状更为明显，PSK 处理可减轻这些症状。过表达 PSK1 前体（proPSK1）或 SBT3.8 的植物对渗透胁迫的耐受性提高，导致转基因植物的鲜重增加，侧根发育得到改善，与野生型植物相比。我们进一步表明，SBT3.8 参与生物活性 PSK 肽的生物发生。SBT3.8 在 PSK 五肽的 C 末端切割 proPSK1。SBT3.8 的加工依赖于切割位点后直接的天冬氨酸残基。在 sbt3.8 突变体中，proPSK1 的加工受到损害。数据表明，渗透胁迫后 proPSK1 的表达增加，随后 SBT3.8 对 proPSK1 的翻译后加工导致 PSK 作为一种减轻胁迫的肽信号产生。
