Loss of S-nitrosoglutathione reductase disturbs phytohormone homeostasis and regulates shoot side branching and fruit growth in tomato.

This article investigates the role of endogenous nitric oxide (NO) and its regulation by S-nitrosoglutathione reductase (GSNOR) in controlling shoot architecture, fruit set, and early fruit development in tomato (Solanum lycopersicum). Silencing or knocking out the tomato GSNOR gene (SlGSNOR) leads to NO overaccumulation, which disrupts auxin biosynthesis and basipetal polar auxin transport, resulting in increased shoot branching and reduced fruit size and seed formation. These phenotypic changes are associated with altered hormonal signaling involving auxins, gibberellins, and cytokinins, as well as impaired pericarp cell proliferation, abnormal chloroplast development, and reduced carbon metabolism during early fruit growth. The study highlights the antagonistic interaction between NO and auxin in fine-tuning the hormonal network that governs tomato plant architecture and fruit productivity.