Department of Plant Breeding and Genetics, Faculty of Crop and Food Sciences, PMAS Arid Agriculture University Rawalpindi, Rawalpindi, 46300, Pakistan.
RLP AgroScience GmbH, AlPlanta - Institute for Plant Research, Neustadt, Germany.
J Plant Physiol. 2021 Jun;261:153433. doi: 10.1016/j.jplph.2021.153433. Epub 2021 Apr 30.
The pervasive presence of nitric oxide (NO) in cells and its role in modifying cystein residues through protein S-nitrosylation is a remarkable redox based signalling mechanism regulating a variety of cellular processes. S-NITROSOGLUTATHIONE REDUCTASE (GSNOR) governs NO bioavailability by the breakdown of S-nitrosoglutathione (GSNO), fine-tunes NO signalling and controls total cellular S-nitrosylated proteins. Most of the published data on GSNOR functional analysis is based on the model plant Arabidopsis with no previous report for its effect on in vitro regeneration of tissue cultured plants. Moreover, the effect of GSNOR overexpression (O.E) on tomato growth, development and disease resistance remains enigmatic. Here we show that SlGSNOR O.E in tomato alters multiple developmental programs from in vitro culture establishment to plant growth and fruit set. Moreover, constitutive SlGSNOR O.E in tomato showed enhanced resistance against early blight (EB) disease caused by Alternaria solani and reduction in hypersensitive response (HR)-mediated cell death after Pseudomonas syringae pv. tomato DC3000 (Pst DC3000) infiltrations. High GSNOR transcript levels led to the inhibition of in vitro shoot proliferation in transformed explants as revealed by the fluorescence microscopy after YFP labelling. Transgenic tomato lines overexpressing SlGSNOR showed defective phenotypes exhibiting stunted plant growth and bushy-type plants due to loss of apical dominance, along with reduced seed germination and delayed flowering. Furthermore, SlGSNOR O.E plants exhibited altered leaf arrangement, fruit shape and modified locules number in tomato fruit. These findings give a novel insight into a multifaceted regulatory role of SlGSNOR in tomato plant development, reproduction and response to pathogens.
一氧化氮（NO）在细胞中的普遍存在及其通过蛋白质 S-亚硝基化修饰半胱氨酸残基的作用是一种显著的基于氧化还原的信号转导机制，调节各种细胞过程。S-亚硝基谷胱甘肽还原酶（GSNOR）通过分解 S-亚硝基谷胱甘肽（GSNO）来控制 NO 的生物利用度，精细调节 NO 信号转导并控制总细胞 S-亚硝基化蛋白。关于 GSNOR 功能分析的大部分已发表数据基于模式植物拟南芥，而没有关于其对组织培养植物体外再生影响的先前报告。此外，GSNOR 过表达（O.E）对番茄生长、发育和抗病性的影响仍然是一个谜。在这里，我们表明番茄中的 SlGSNOR O.E 改变了从体外培养建立到植物生长和结实的多个发育程序。此外，番茄中组成型 SlGSNOR O.E 表现出对早疫病（EB）的增强抗性，由Alternaria solani引起，并且在 Pseudomonas syringae pv. tomato DC3000（Pst DC3000）浸润后，降低了过敏反应（HR）介导的细胞死亡。高 GSNOR 转录水平导致转化外植体中体外芽增殖的抑制，如 YFP 标记后的荧光显微镜所示。过表达 SlGSNOR 的转基因番茄品系表现出缺陷表型，由于顶端优势丧失，植物生长矮小，植株呈丛生状，同时种子发芽率降低，开花时间延迟。此外，SlGSNOR O.E 植物表现出叶片排列、果实形状和番茄果实中修改的腔室数量的改变。这些发现为 SlGSNOR 在番茄植物发育、繁殖和对病原体的反应中的多方面调节作用提供了新的见解。
