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ROS Induces Anthocyanin Production Via Late Biosynthetic Genes and Anthocyanin Deficiency Confers the Hypersensitivity to ROS-Generating Stresses in Arabidopsis

Authors :
Steven J. Rothstein
Zhenhua Xu
Kashif Mahmood
Source :
Plantcell physiology. 58(8)
Publication Year :
2016

Abstract

Anthocyanins are known to have antioxidant activities. Their accumulation can be triggered by many chemical and environmental factors, including reactive oxygen species (ROS). However, the mechanism of ROS-induced anthocyanin accumulation and the role of anthocyanins in the response of Arabidopsis (Arabidopsis thaliana) to different stresses are largely unknown. Here, we study the cross-regulation between ROS and anthocyanin production. Ten Arabidopsis mutants covering the main anthocyanin regulatory and biosynthetic genes are systematically analyzed under ROS-generating stresses. We find that ROS triggers anthocyanin accumulation by up-regulating the anthocyanin late biosynthetic and the corresponding regulatory genes. The anthocyanin-deficient mutants have more endogenous ROS and are more sensitive to ROS-generating stresses while having decreased antioxidant capacity. Supplementation with cyanidin makes them less susceptible to ROS, with increased anthocyanin and reduced ROS accumulation. In contrast, pap1-D, which overaccumulates anthocyanins, shows the opposite responses. Gene expression analysis reveals that photosynthetic capacity is more impaired in anthocyanin-deficient mutants under high-light stress. Expression levels of ROS-scavenging enzyme genes are not correlated with the radical-scavenging activity in different mutants. We conclude that ROS are an important source signal to induce anthocyanin accumulation by up-regulating late biosynthetic and the corresponding regulatory genes and, as a feed-back regulation, anthocyanins modulate the ROS level and the sensitivity to ROS-generating stresses in maintaining photosynthetic capacity.

Details

ISSN :
14719053
Volume :
58
Issue :
8
Database :
OpenAIRE
Journal :
Plantcell physiology
Accession number :
edsair.doi.dedup.....02ba35f8dd1b950915835a4394d6f68d