College of Bioscience and Biotechnology, Shenyang Agricultural University, Shenyang Liaoning 110866, China.
College of Horticulture, Shenyang Agricultural University, Shenyang Liaoning 110866, China.
Plant Cell Physiol. 2021 Nov 17;62(9):1387-1395. doi: 10.1093/pcp/pcab081.
Actin cytoskeleton and transcription factors play key roles in plant response to salt stress; however, little is known about the link between the two regulators in response to salt stress. Actin-depolymerizing factors (ADFs) are conserved actin-binding proteins in eukaryotes. Here, we revealed that the expression level of ADF1 was induced by salt stress. The adf1 mutants showed significantly reduced survival rate, increased percentage of actin cable and reduced density of actin filaments, while ADF1 overexpression seedlings displayed the opposite results when compared with WT under the same condition. Furthermore, biochemical assays revealed that MYB73, a R2R3 MYB transcription factor, binds to the promoter of ADF1 and represses its expression via the MYB-binding site core motif ACCTAC. Taken together, our results indicate that ADF1 participates in salt stress by regulating actin organization and may also serve as a potential downstream target of MYB73, which is a negative regulator of salt stress.
肌动蛋白细胞骨架和转录因子在植物应对盐胁迫中发挥着关键作用;然而,人们对这两种调节剂在应对盐胁迫时的联系知之甚少。肌动蛋白解聚因子(ADFs)是真核生物中保守的肌动蛋白结合蛋白。在这里,我们揭示了 ADF1 的表达水平受到盐胁迫的诱导。与 WT 相比,adf1 突变体在相同条件下表现出存活率显著降低、肌动蛋白电缆比例增加和肌动蛋白丝密度降低,而 ADF1 过表达幼苗则表现出相反的结果。此外,生化分析表明,R2R3 MYB 转录因子 MYB73 结合到 ADF1 的启动子上,并通过 MYB 结合位点核心模体 ACCTAC 抑制其表达。总之,我们的研究结果表明,ADF1 通过调节肌动蛋白的组织参与盐胁迫,也可能作为 MYB73 的一个潜在下游靶点,而 MYB73 是盐胁迫的负调控因子。