Abstract

High-intensity light (HL) greatly induces the accumulation of anthocyanin, a fundamental compound in photoprotection and antioxidation. Many mechanisms regulating anthocyanin biosynthesis are well-characterized across developmental and environmental conditions; however, post-transcriptional regulation of its biosynthesis remains unclear. RNA splicing is one mechanism of post-transcriptional control and reprogramming in response to different developmental cues and stress conditions. The Arabidopsis splicing modulator SR45 regulates a number of developmental and environmental stress responses. Here, we investigated the role of SR45 and its isoforms in HL-induced anthocyanin accumulation. We found that the SR45 promoter contains light-responsive cis-elements, and that light stress significantly increases SR45 expression. Furthermore, we found that mutant plants lacking SR45 function (sr45) accumulate significantly more anthocyanin under HL. SR45 is alternatively spliced to produce two proteins, SR45.1 and SR45.2, which differ by seven amino acids. Intriguingly, these isoforms exhibited distinct functions, with only SR45.1 reversing anthocyanin accumulation in the sr45 plants. We also identified possible SR45 target genes that are involved in anthocyanin synthesis. Consistent with the antioxidant role of anthocyanin, we found that sr45 mutants and SR45.2 overexpression lines accumulate anthocyanin and better tolerate paraquat which induces oxidative stress. Collectively, our results reveal that the Arabidopsis splicing regulator SR45 inhibits anthocyanin accumulation under HL, which may negatively affect oxidative stress tolerance. This study illuminates splicing-level regulation of anthocyanin production in response to light stress and offers a possible target for genetic modification to increase plant stress tolerance.

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