Department of Agriculture, Abdul Wali Khan University Mardan, Khyber-Pakhtunkhwa, Pakistan.
Institute of Molecular Plant Sciences, School of Biological Sciences, University of Edinburgh, Edinburgh, UK.
J Exp Bot. 2019 Sep 24;70(18):4877-4886. doi: 10.1093/jxb/erz234.
Nitric oxide (NO) is emerging as a key signalling molecule in plants. The chief mechanism for the transfer of NO bioactivity is thought to be S-nitrosylation, the addition of an NO moiety to a protein cysteine thiol to form an S-nitrosothiol (SNO). The enzyme S-nitrosoglutathione reductase (GSNOR) indirectly controls the total levels of cellular S-nitrosylation, by depleting S-nitrosoglutathione (GSNO), the major cellular NO donor. Here we show that depletion of GSNOR function impacts tomato (Solanum lycopersicum. L) fruit development. Thus, reduction of GSNOR expression through RNAi modulated both fruit formation and yield, establishing a novel function for GSNOR. Further, depletion of S. lycopersicum GSNOR (SlGSNOR) additionally impacted a number of other developmental processes, including seed development, which also has not been previously linked with GSNOR activity. In contrast to Arabidopsis, depletion of GSNOR function did not influence root development. Further, reduction of GSNOR transcript abundance compromised plant immunity. Surprisingly, this was in contrast to previous data in Arabidopsis that reported that reducing Arabidopsis thaliana GSNOR (AtGSNOR) expression by antisense technology increased disease resistance. We also show that increased SlGSNOR expression enhanced pathogen protection, uncovering a potential strategy to enhance disease resistance in crop plants. Collectively, our findings reveal, at the genetic level, that some but not all GSNOR activities are conserved outside the Arabidopsis reference system. Thus, manipulating the extent of GSNOR expression may control important agricultural traits in tomato and possibly other crop plants.
一氧化氮（NO）正在成为植物中的一种关键信号分子。NO 生物活性的主要传递机制被认为是 S-亚硝基化，即将 NO 部分添加到蛋白质半胱氨酸硫醇上形成 S-亚硝基硫醇（SNO）。酶 S-亚硝基谷胱甘肽还原酶（GSNOR）通过耗尽 S-亚硝基谷胱甘肽（GSNO），间接控制细胞内 S-亚硝基化的总水平，GSNO 是主要的细胞内 NO 供体。在这里，我们表明 GSNOR 功能的耗竭会影响番茄（Solanum lycopersicum. L）果实发育。因此，通过 RNAi 降低 GSNOR 的表达既调节了果实的形成和产量，也确立了 GSNOR 的新功能。此外，番茄 SlGSNOR 的耗竭还影响了其他一些发育过程，包括种子发育，这也与 GSNOR 活性以前没有联系过。与拟南芥不同的是，GSNOR 功能的耗竭并不影响根的发育。此外，降低 GSNOR 转录丰度会损害植物免疫力。令人惊讶的是，这与以前在拟南芥中的数据形成对比，该数据报告通过反义技术降低拟南芥 GSNOR（AtGSNOR）的表达增加了对疾病的抗性。我们还表明，增加 SlGSNOR 的表达增强了对病原体的保护，揭示了一种在作物植物中增强抗病性的潜在策略。总之，我们的研究结果从遗传水平上揭示，GSNOR 的某些但不是所有活性在拟南芥参考系统之外是保守的。因此，操纵 GSNOR 表达的程度可能会控制番茄和可能其他作物植物的重要农业性状。
