ABSTRACT
The mechanism that coordinates cell growth and cell cycle progression remains poorly understood; in particular, whether the cell cycle and cell wall biosynthesis are coordinated remains unclear. Recently, cell wall biosynthesis and cell cycle progression were reported to respond to wounding. Nonetheless, no genes are reported to synchronize the biosynthesis of the cell wall and the cell cycle. Here, we report that wounding induces the expression of genes associated with cell wall biosynthesis and the cell cycle, and that two genes, AtMYB46 in Arabidopsis thaliana and RrMYB18 in Rosa rugosa, are induced by wounding. We found that AtMYB46 and RrMYB18 promote the biosynthesis of the cell wall by upregulating the expression of cell wall-associated genes, and that both of them also upregulate the expression of a battery of genes associated with cell cycle progression. Ultimately, this response leads to the development of curled leaves of reduced size. We also found that the coordination of cell wall biosynthesis and cell cycle progression by AtMYB46 and RrMYB18 is evolutionarily conservative in multiple species. In accordance with wounding promoting cell regeneration by regulating the cell cycle, these findings also provide novel insight into the coordination between cell growth and cell cycle progression and a method for producing miniature plants.
Subject(s)
Arabidopsis/metabolism , Cell Cycle , Cell Wall/metabolism , Rosa/metabolism , Arabidopsis/genetics , Arabidopsis Proteins/genetics , Arabidopsis Proteins/physiology , Gene Expression Regulation, Plant , Genes, Plant/genetics , Genes, Plant/physiology , Phylogeny , Plant Leaves/metabolism , Plant Proteins/genetics , Plant Proteins/physiology , Rosa/genetics , Transcription Factors/genetics , Transcription Factors/physiology , TranscriptomeABSTRACT
Flavonoids play critical roles in plant responses to various stresses. Few studies have been reported on what the mechanism of activating flavonoid biosynthesis in plant responses to wounding and oxidation is. In this study, flavonoid metabolites and many MYB transcript factors from Rosa rugosa were verified to be induced by wounding and oxidation. RrMYB5 and RrMYB10, which belong to PA1- and TT2-type MYB TFs, respectively, showed extremely high induction. Overexpression of RrMYB5 and RrMYB10 resulted in an increased accumulation of proanthocyanidins in R. rugosa and tobacco by promoting the expression of flavonoid structural genes. Transcriptomic analysis of the transgenic plants showed that most genes, involved in wounding and oxidation response and ABA signalling modulation, were up-regulated by the overexpression of RrMYB10, which was very much similar to that observed in RrANR and RrDFR overexpression transgenics. RrMYB5 and RrMYB10 physically interacted and mutually activated each other's expressions. They solely or synergistically activated the different sets of flavonoid pathway genes in a bHLH TF EGL3-independent manner. Eventually, the accumulation of proanthocyanidins enhanced plant tolerance to wounding and oxidative stresses. Therefore, RrMYB5 and RrMYB10 regulated flavonoid synthesis in feedback loop responding to wounding and oxidation in R. rugosa. Our study provides new insights into the regulatory mechanisms of flavonoid biosynthesis by MYB TFs and their essential physiological functions in plant responses to wounding and oxidative stresses.
