Abstract
The aim of this study was to explore whether application of BRs could alleviate drought-induced photoinhibition in pepper leaves by improving the photosynthetic electron transport via up-regulation of alternative oxidase (AOX) pathway, we examined the effects of 24-epibrassinolide (EBR, 0.1 μM) and salicylhydroxamic acid (SHAM, 1 mM) on the AOX pathway capacity, matale/oxaloacetate (OAA) shuttle, and chlorophyll fluorescence in pepper (Capsicum annuum L.) leaves under drought condition (treated by 15% polyethylene glycol, PEG). In this study, the leaf relative water content (LRWC) decreased from 92.0% to 47.0% by drought treatment for 4 d. Drought induced the up-regulation of AOX pathway and increased the activities of NADP-malate dehydrogenase (MDH) and NAD-MDH. Inhibition of AOX pathway decreased NADP-MDH and NAD-MDH activities and enhanced the increases of NADPH and NADPH/NADP+ ratio in leaves under drought condition. Meanwhile, inhibition of AOX pathway aggravated the decreases of maximal quantum efficiency of PSII (Fv/Fm), quantum efficiency of PSII (ФPSII), photochemical quenching coefficient (qP), and photosynthetic electron transport rate (ETR) in leaves under drought condition. These results indicated that up-regulation of AOX pathway could activate malate/OAA shuttle and dissipate the excess reducing equivalents in chloroplast, resulting in an optimization of PSII efficiency and photosynthetic electron transport. EBR treatment up-regulated the activity of AOX pathway in leaves under well-watered and drought conditions. EBR treatment also significantly alleviated the decreases of Fv/Fm, ФPSII, qP, and ETR in leaves with/without SHAM treatment under drought condition, however, the improvement degree was more efficiently in leaves with SHAM treatment. Furthermore, EBR increased the activities of NADP-MDH and NAD-MDH, and significantly decreased NADPH/NADP+ ratio in leaves with/without SHAM treatment under drought condition. These results suggested that EBR-induced protection against photoinhibition was partly related to the up-regulation of AOX pathway by dissipating excess reducing equivalents.
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