Institute of Plant Genetics and Developmental Biology, College of Chemistry and Life Sciences, Zhejiang Normal University, Jinhua 321004, China.
Zhejiang Provincial Key Laboratory of Biotechnology on Specialty Economic Plants, Zhejiang Normal University, Jinhua 321004, China.
Int J Mol Sci. 2023 Mar 25;24(7):6240. doi: 10.3390/ijms24076240.
E3 ubiquitin ligases play important roles in plant immunity, but their role in soybean has not been investigated previously. Here, we used (BPMV)-mediated virus-induced gene silencing (VIGS) to investigate the function of SAUL1 (Senescence-Associated E3 Ubiquitin Ligase 1) homologs in soybean. When two closely related homologs were silenced simultaneously, the soybean plants displayed autoimmune phenotypes, which were significantly alleviated by high temperature, suggesting that SAUL1a/1b might be guarded by an R protein. Interestingly, silencing resulted in the decreased activation of MPK6, but increased activation of MPK3 in response to flg22, suggesting that the activation of MPK3 is most likely responsible for the activated immunity observed in the SAUL1a/1b-silenced plants. Furthermore, we provided evidence that SAUL1a is a bona fide E3 ligase. Collectively, our results indicated that SAUL1 plays a negative role in regulating cell death and immunity in soybean.
E3 泛素连接酶在植物免疫中发挥重要作用，但它们在大豆中的作用尚未被研究过。在这里，我们使用 (BPMV)-介导的病毒诱导基因沉默 (VIGS) 来研究大豆中 SAUL1（衰老相关 E3 泛素连接酶 1）同源物的功能。当同时沉默两个密切相关的 同源物时，大豆植物表现出自免疫表型，高温显著缓解了这种表型，表明 SAUL1a/1b 可能受到 R 蛋白的保护。有趣的是，沉默 导致 MPK6 的激活减少，但对 flg22 的反应中 MPK3 的激活增加，这表明 MPK3 的激活很可能是 SAUL1a/1b 沉默植物中观察到的激活免疫的原因。此外，我们提供了证据表明 SAUL1a 是一种真正的 E3 连接酶。总之，我们的结果表明，SAUL1 在调节大豆细胞死亡和免疫中发挥负作用。
