PDF(Pubmed)
Abstract：
SUPPRESSOR OF MAX2-LIKE 6, 7, and 8 (SMXL6,7,8) function as repressors and transcription factors of the strigolactone (SL) signaling pathway, playing an important role in the development and stress tolerance in Arabidopsis thaliana. However, the molecular mechanism by which SMXL6,7,8 negatively regulate drought tolerance and ABA response remains largely unexplored. In the present study, the interacting protein and downstream target genes of SMXL6,7,8 were investigated. Our results showed that the substrate receptor for the CUL4-based E3 ligase DDB1-BINDING WD-REPEAT DOMAIN (DWD) HYPERSENSITIVE TO ABA DEFICIENT 1 (ABA1) (DWA1) physically interacted with SMXL6,7,8. The degradation of SMXL6,7,8 proteins were partially dependent on DWA1. Disruption of SMXL6,7,8 resulted in increased drought tolerance and could restore the drought-sensitive phenotype of the dwa1 mutant. In addition, SMXL6,7,8 could directly bind to the promoter of SUCROSE NONFERMENTING 1 (SNF1)-RELATED PROTEIN KINASE 2.3 (SnRK2.3) to repress its transcription. The mutations in SnRK2.2/2.3 significantly suppressed the hypersensitivity of smxl6/7/8 to ABA-mediated inhibition of seed germination. Conclusively, SMXL6,7,8 interact with DWA1 to negatively regulate drought tolerance and target ABA-response genes. These data provide insights into drought tolerance and ABA response in Arabidopsis via the SMXL6,7,8-mediated SL signaling pathway.
摘要：
MAX2样6、7和8的抑制因子（SMXL6,7,8）作为strigolactone（SL）信号通路的抑制因子和转录因子，在拟南芥的发育和抗逆性中起着重要作用。然而,SMXL6,7,8负调节耐旱性和ABA响应的分子机制仍未被探索。在本研究中,研究了SMXL6,7,8的相互作用蛋白和下游靶基因。我们的结果表明，基于CUL4的E3连接酶DDB1结合WD重复域（DWD）对ABA缺陷1（ABA1）（DWA1）的底物受体与SMXL6,7,8物理相互作用。SMXL6,7,8蛋白的降解部分依赖于DWA1。SMXL6,7,8的破坏导致耐旱性增加，并可以恢复dwa1突变体的干旱敏感表型。此外,SMX76,7,8可直接与蔗糖不发酵1(SNF1)相关蛋白激酶2.3(SnRK2.3)启动子结合，抑制其转录。SnRK2.2/2.3中的突变显着抑制了smxl6/7/8对ABA介导的种子萌发抑制的超敏反应。最后，SMXL6,7,8与DWA1相互作用，负调控耐旱性和靶向ABA反应基因。这些数据通过SMXL6,7,8介导的SL信号通路提供了对拟南芥耐旱性和ABA应答的见解。
