植物积累类黄酮作为UV-B适应的一部分,而高水平的UV-B照射会诱导DNA损伤并导致基因组不稳定。这里,我们表明,MYB4是MYB转录因子的R2R3亚家族的成员,通过直接抑制类黄酮生物合成和DNA双链断裂(DSBs)修复的关键基因,在调节植物对UV-B暴露的反应中起重要作用。我们的结果表明,MYB4在UV-B暴露后抑制拟南芥的种子萌发和幼苗建立。atmyb4-1单突变体系以及uvr8-6/atmyb4-1,cop1-6/atmyb4-1和hy5-215/atmyb4-1双突变体的表型分析表明,MYB4在UVR8介导的信号通路下游起作用,并对UV-B适应和子叶扩展产生负面影响。我们的结果表明,MYB4作为两个关键的类黄酮生物合成基因的转录抑制因子,包括4CL和FLS,通过直接结合它们的启动子,从而减少类黄酮的积累。另一方面,AtMYB4过表达导致更高的DSB积累水平以及几个关键DSB修复基因的表达被抑制。包括AtATM,分别为AtKU70、AtLIG4、AtXRCC4、AtBRCA1、AtSOG1、AtRAD51和AtRAD54。我们的结果进一步表明,MYB4蛋白抑制了两个关键的DSB修复基因的表达,AtKU70和AtXRCC4通过与其启动子直接结合。一起,我们的结果表明,MYB4是调节植物对UV-B反应的重要协调因子,通过转录调节黄酮类化合物生物合成和修复UV-B诱导的DNA损伤的关键基因。
Plants accumulate flavonoids as part of UV-B acclimation, while a high level of UV-B irradiation induces DNA damage and leads to genome instability. Here, we show that MYB4, a member of the R2R3-subfamily of MYB transcription factor plays important role in regulating plant response to UV-B exposure through the direct repression of the key genes involved in flavonoids biosynthesis and repair of DNA double-strand breaks (DSBs). Our results demonstrate that MYB4 inhibits seed germination and seedling establishment in Arabidopsis following UV-B exposure. Phenotype analyses of atmyb4-1 single mutant line along with uvr8-6/atmyb4-1, cop1-6/atmyb4-1, and hy5-215/atmyb4-1 double mutants indicate that MYB4 functions downstream of UVR8 mediated signaling pathway and negatively affects UV-B acclimation and cotyledon expansion. Our results indicate that MYB4 acts as transcriptional repressor of two key flavonoid biosynthesis genes, including 4CL and FLS, via directly binding to their promoter, thus reducing flavonoid accumulation. On the other hand, AtMYB4 overexpression leads to higher accumulation level of DSBs along with repressed expression of several key DSB repair genes, including AtATM, AtKU70, AtLIG4, AtXRCC4, AtBRCA1, AtSOG1, AtRAD51, and AtRAD54, respectively. Our results further suggest that MYB4 protein represses the expression of two crucial DSB repair genes, AtKU70 and AtXRCC4 through direct binding with their promoters. Together, our results indicate that MYB4 functions as an important coordinator to regulate plant response to UV-B through transcriptional regulation of key genes involved in flavonoids biosynthesis and repair of UV-B induced DNA damage.