Abstract:
Although 14-3-3 proteins have been implicated in plant growth, development, and stress response, their roles in pepper immunity against R. solanacearum remain poorly understood. In this study, a 14-3-3-encoding gene in pepper, Ca16R, was found to be upregulated by R. solanacearum inoculation (RSI), its silencing significantly reduced the resistance of pepper plants to RSI, and its overexpression significantly enhanced the resistance of Nicotiana benthamiana to RSI. Consistently, its transient overexpression in pepper leaves triggered HR cell death, indicating that it acts positively in pepper immunity against RSI, and it was further found to act positively in pepper immunity against RSI by promoting SA but repressing JA signaling. Ca16R was also found to interact with CaASR1, originally using pull-down combined with a spectrum assay, and then confirmed using bimolecular fluorescence complementation (BiFC) and a pull-down assay. Furthermore, we found that CaASR1 transient overexpression induced HR cell death and SA-dependent immunity while repressing JA signaling, although this induction and repression was blocked by Ca16R silencing. All these data indicate that Ca16R acts positively in pepper immunity against RSI by interacting with CaASR1, thereby promoting SA-mediated immunity while repressing JA signaling. These results provide new insight into mechanisms underlying pepper immunity against RSI.
摘要:
尽管14-3-3蛋白与植物生长有关,发展,和应激反应,它们在辣椒对青枯菌免疫中的作用仍然知之甚少。在这项研究中,辣椒中的14-3-3编码基因,Ca16R,被发现通过青枯菌接种(RSI)上调,其沉默显着降低了辣椒植物对RSI的抗性,其过表达显著增强了烟草对RSI的抗性。始终如一,它在辣椒叶片中的短暂过表达引发了HR细胞死亡,表明它在辣椒对RSI的免疫中起积极作用,进一步发现,通过促进SA但抑制JA信号传导,在辣椒对RSI的免疫中起积极作用。还发现Ca16R与CaASR1相互作用,最初使用下拉结合光谱测定,然后使用双分子荧光互补(BiFC)和下拉测定进行确认。此外,我们发现,CaASR1瞬时过表达诱导HR细胞死亡和SA依赖性免疫,同时抑制JA信号,尽管这种诱导和抑制被Ca16R沉默所阻断。所有这些数据表明,Ca16R通过与CaASR1相互作用,在辣椒对RSI的免疫中起积极作用,从而促进SA介导的免疫,同时抑制JA信号传导。这些结果为辣椒抗RSI免疫的潜在机制提供了新的见解。