Key Laboratory of Plant Molecular Physiology, Institute of Botany, the Chinese Academy of Sciences, Beijing 100093, China.
University of the Chinese Academy of Sciences, Beijing 100049, China.
J Integr Plant Biol. 2018 Oct;60(10):924-937. doi: 10.1111/jipb.12669. Epub 2018 Jul 30.
The small ubiquitin-related modifier (SUMO) modification plays an important role in the regulation of abscisic acid (ABA) signaling, but the function of the SUMO protease, in ABA signaling, remains largely unknown. Here, we show that the SUMO protease, ASP1 positively regulates ABA signaling. Mutations in ASP1 resulted in an ABA-insensitive phenotype, during early seedling development. Wild-type ASP1 successfully rescued, whereas an ASP1 mutant (C577S), defective in SUMO protease activity, failed to rescue, the ABA-insensitive phenotype of asp1-1. Expression of ABI5 and MYB30 target genes was attenuated in asp1-1 and our genetic analyses revealed that ASP1 may function upstream of ABI5 and MYB30. Interestingly, ASP1 accumulated upon ABA treatment, and ABA-induced accumulation of ABI5 (a positive regulator of ABA signaling) was abolished, whereas ABA-induced accumulation of MYB30 (a negative regulator of ABA signaling) was increased in asp1-1. These findings support the hypothesis that increased levels of ASP1, upon ABA treatment, tilt the balance between ABI5 and MYB30 towards ABI5-mediated ABA signaling.
小泛素相关修饰物 (SUMO) 修饰在脱落酸 (ABA) 信号转导的调节中起着重要作用，但 SUMO 蛋白酶在 ABA 信号转导中的功能在很大程度上仍是未知的。在这里，我们表明 SUMO 蛋白酶 ASP1 正向调控 ABA 信号转导。ASP1 中的突变导致在早期幼苗发育过程中 ABA 不敏感表型。野生型 ASP1 成功地挽救了表型，而 ASP1 突变体 (C577S) ，其 SUMO 蛋白酶活性有缺陷，不能挽救 asp1-1 的 ABA 不敏感表型。ABI5 和 MYB30 靶基因的表达在 asp1-1 中减弱，我们的遗传分析表明 ASP1 可能在 ABI5 和 MYB30 上游发挥作用。有趣的是，ASP1 在 ABA 处理后积累，而 ABA 诱导的 ABI5 （ABA 信号的正调节剂）积累被消除，而 ABA 诱导的 MYB30 （ABA 信号的负调节剂）积累在 asp1-1 中增加。这些发现支持这样一种假设，即在 ABA 处理后，ASP1 水平的增加会使 ABI5 和 MYB30 之间的平衡向 ABI5 介导的 ABA 信号转导倾斜。
