College of Plant Protection, Shenyang Agricultural University, Shenyang, 110866, China.
Southern Zhejiang Key Laboratory of Crop Breeding, Wenzhou Vocational College of Science and Technology (Wenzhou Academy of Agricultural Sciences), Wenzhou, Zhejiang, 325006, China.
Biochem Biophys Res Commun. 2021 Dec 31;585:117-123. doi: 10.1016/j.bbrc.2021.11.042. Epub 2021 Nov 13.
Sheath blight (ShB) is one of the most common diseases in rice that significantly affects yield production. However, the underlying mechanisms of rice defense remain largely unknown. Our previous transcriptome analysis identified that infection with Rhizoctonia solani significantly induced the expression level of SWEET2a, a member of the SWEET sugar transporter. The sweet2a genome-editing mutants were less susceptible to ShB. Further yeast-one hybrid, ChIP, and transient assays demonstrated that WRKY53 binds to the SWEET2a promoter to activate its expression. WRKY53 is a key brassinosteroid (BR) signaling transcription factor. Similar to the BR receptor gene BRI1 and biosynthetic gene D2 mutants, the WRKY53 mutant and overexpressor were less and more susceptible to ShB compared to wild-type, respectively. Inoculation with R. solani induced expression of BRI1, D2, and WRKY53, but inhibited MPK6 (a BR-signaling regulator) activity. Also, MPK6 is known to phosphorylate WRKY53 to enhance its transcription activation activity. Transient assay results indicated that co-expression of MPK6 and WRKY53 enhanced WRKY53 trans-activation activity to SWEET2a. Furthermore, expression of WRKY53 SD (the active phosphorylated forms of WRKY53) but not WRKY53 SA (the inactive phosphorylated forms of WRKY53), enhanced WRKY53-mediated activation of SWEET2a compared to expression of WRKY53 alone. Taken together, our analyses showed that R. solani infection may activate BR signaling to induce SWEET2a expression via WRKY53 through negative regulation of ShB resistance in rice.
鞘腐病（ShB）是水稻中最常见的疾病之一，严重影响产量。然而，水稻防御的潜在机制在很大程度上仍然未知。我们之前的转录组分析表明，与立枯丝核菌的感染显著诱导 SWEET2a 的表达水平，SWEET2a 是 SWEET 糖转运蛋白的一个成员。甜 2a 基因组编辑突变体对 ShB 的敏感性降低。进一步的酵母单杂交、ChIP 和瞬时测定表明，WRKY53 结合到 SWEET2a 启动子上激活其表达。WRKY53 是一个关键的油菜素内酯（BR）信号转导转录因子。与 BR 受体基因 BRI1 和生物合成基因 D2 突变体类似，WRKY53 突变体和过表达体对 ShB 的敏感性分别比野生型低和高。接种立枯丝核菌诱导 BRI1、D2 和 WRKY53 的表达，但抑制 MPK6（BR 信号调节因子）的活性。此外，MPK6 已知磷酸化 WRKY53 以增强其转录激活活性。瞬时测定结果表明，MPK6 和 WRKY53 的共表达增强了 WRKY53 对 SWEET2a 的转录激活活性。此外，WRKY53 SD（WRKY53 的活性磷酸化形式）的表达而不是 WRKY53 SA（WRKY53 的非活性磷酸化形式）的表达增强了 WRKY53 介导的 SWEET2a 的激活，与 WRKY53 单独表达相比。综上所述，我们的分析表明，立枯丝核菌的感染可能通过 WRKY53 负调控水稻对 ShB 的抗性来激活 BR 信号，从而诱导 SWEET2a 的表达。
