干旱胁迫造成全球每年作物产量的重大损失,威胁全球粮食安全。鉴定植物耐旱性的遗传成分非常重要。在这项研究中,我们报道了染色质重塑因子PICKLE(PKL)的功能丧失,参与转录的抑制,提高拟南芥的耐旱性。起初,我们发现PKL与ABI5相互作用以调节种子萌发,但PKL独立于ABI5调节耐旱性。然后,我们发现PKL对于抑制耐旱基因AFL1是必需的,AFL1负责pkl突变体的耐旱表型。遗传互补测试表明,PKL调节耐旱性的功能需要Chromo域和ATPase域,而不是PHD域。有趣的是,我们发现DNA结合域(DBD)对于PKL的蛋白质稳定性至关重要。此外,我们证明SUMOE3连接酶MMS21与PKL相互作用并增强其蛋白质稳定性。遗传互作分析表明,MMS21和PKL对植物的耐旱性有加性调控作用。总的来说,我们的发现揭示了调节植物耐旱性的MMS21-PKL-AFL1模块,并提供了提高作物耐旱性的新策略的见解。
Drought stress causes substantial losses in crop production per year worldwide, threatening global food security. Identification of the genetic components underlying drought tolerance in plants is of great importance. In this study, we report that loss-of-function of the chromatin-remodeling factor PICKLE (
PKL), which is involved in repression of transcription, enhances drought tolerance of Arabidopsis. At first, we find that
PKL interacts with ABI5 to regulate seed germination, but
PKL regulates drought tolerance independently of ABI5. Then, we find that
PKL is necessary for repressing the drought-tolerant gene AFL1, which is responsible for the drought-tolerant phenotype of
pkl mutant. Genetic complementation tests demonstrate that the Chromo domain and ATPase domain but not the PHD domain are required for the function of PKL in regulating drought tolerance. Interestingly, we find that the DNA-binding domain (DBD) is essential for the protein stability of PKL. Furthermore, we demonstrate that the SUMO E3 ligase MMS21 interacts with and enhances the protein stability of PKL. Genetic interaction analysis shows that MMS21 and
PKL additively regulate plant drought tolerance. Collectively, our findings uncover a MMS21-PKL-AFL1 module in regulating plant drought tolerance and offer insights into a novel strategy to improve crop drought tolerance.