Brassinosteroid-mediated apoplastic H2 O2 -glutaredoxin 12/14 cascade regulates antioxidant capacity in response to chilling in tomato.

Abstract

Brassinosteroids (BRs) regulate plant development and stress response. Although much has been learned about their roles in plant development, the mechanisms by which BRs regulate plant stress tolerance remain unclear. Chilling is a major stress that adversely affects plant growth. Here, we report that BR positively regulates chilling tolerance in tomato. BR partial deficiency aggravated chilling-induced oxidized protein accumulation, membrane lipid peroxidation, and decrease of maximum quantum efficiency of photosystem II (Fv/Fm). By contrast, overexpression of BR biosynthetic gene Dwarf or treatment with 24-epibrassinolide (EBR) attenuated chilling-induced oxidative damages and resulted in an increase of Fv/Fm. BR increased transcripts of RESPIRATORY BURST OXIDASE HOMOLOG1 (RBOH1) and GLUTAREDOXIN (GRX) genes, and BR-induced chilling tolerance was associated with an increase in the ratio of reduced/oxidized 2-cysteine peroxiredoxin (2-Cys Prx) and activation of antioxidant enzymes. However, RBOH1-RNAi plants failed to respond to EBR as regards to the induction of GRX genes, activation of antioxidant capacity, and attenuation of chilling-induced oxidative damages. Furthermore, silencing of GRXS12 and S14 compromised EBR-induced increases in the ratio of reduced/oxidized 2-Cys Prx and activities of antioxidant enzymes. Our study suggests that BR enhances chilling tolerance through a signalling cascade involving RBOH1, GRXs, and 2-Cys Prx in tomato.