SlGSNOR manipulation consequences on reactive oxygen and nitrogen species metabolism and on nitrated and nitrosylated proteins profiles along tomato fruit ripening

Abstract

S-Nitrosoglutathione (GSNO), an S-nitrosated derivative of glutathione, plays a central role in nitric oxide (NO) signaling and represents the main NO reservoir in living cells. Endogenous GSNO levels are controlled by the enzyme S-nitrosoglutathione reductase (GSNOR), which catalyzes the reduction of GSNO to oxidized glutathione and ammonium and consequently influences protein S-nitrosylation and cell redox homeostasis. Accumulating evidence indicates that components of the nitroxidative and oxidative metabolisms, cell redox status, as well as S-nitrosylation and nitration events, are involved in the signaling cascades controlling the development and ripening of fleshy fruits. In this context, this project aims to evaluate the impacts of modulating GSNO levels via fruit-specific SlGSNOR silencing or overexpression on the nitroxidative and oxidative metabolisms and the global transcriptional profile of tomato (Solanum lycopersicum) fruits.