枯草杆菌酶 SBT3.8 和 PSK 信号处理植物硫素 (PSK) 前体提高拟南芥的干旱胁迫耐受性,Journal of Experimental Botany

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枯草杆菌酶 SBT3.8 和 PSK 信号处理植物硫素 (PSK) 前体提高拟南芥的干旱胁迫耐受性
Journal of Experimental Botany ( IF 5.6 ) Pub Date : 2021-01-17 , DOI: 10.1093/jxb/erab017
Nils Stührwohldt ₁ , Eric Bühler ₁ , Margret Sauter ₂ , Andreas Schaller ₁

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日益严重的干旱压力对农业生产力构成严重威胁。然而，植物已经进化出许多机制来应对这种环境压力。在这里，我们报告压力诱导的肽信号产生有助于压力耐受性。发现植物硫素 (PSK) 肽前体基因的表达和三种枯草杆菌蛋白酶样丝氨酸蛋白酶 SBT1.4、SBT3.7 和 SBT3.8 的转录本在响应渗透胁迫时上调。压力症状在 sbt3.8 功能丧失突变体中更为明显，并且可以通过 PSK 治疗得到缓解。与野生型植物相比，过表达 PSK1 前体 (proPSK1) 或 SBT3.8 的植物的渗透胁迫耐受性得到改善，从而导致转基因植物的鲜重更高，侧根发育得到改善。我们进一步证明了 SBT3。8 参与生物活性 PSK 肽的生物发生。ProPSK1 在 PSK 五肽的 C 末端被 SBT3.8 切割。SBT3.8 的处理依赖于切割位点之后的天冬氨酸残基。ProPSK1 加工在 sbt3.8 突变体中受损。数据表明，proPSK1 响应渗透胁迫的表达增加，随后 SBT3.8 对 proPSK1 进行翻译后加工，导致 PSK 作为缓解压力的肽信号产生。

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Phytosulfokine (PSK) precursor processing by subtilase SBT3.8 and PSK signaling improve drought stress tolerance in Arabidopsis

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.

更新日期：2021-01-17

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