National Key Lab for Germplasm Innovation and Utilization of Horticultural Crops, College of Horticulture and Forestry Sciences, Huazhong Agricultural University, Wuhan, Hubei Province 430070, China.
PlantStressLab, Department of Agriculture, Forestry and Food Science DISAFA, Turin University, Grugliasco, Torino10095, Italy.
Plant Physiol. 2023 Aug 3;192(4):3134-3151. doi: 10.1093/plphys/kiad279.
Gummosis is 1 of the most common and destructive diseases threatening global peach (Prunus persica) production. Our previous studies have revealed that ethylene and methyl jasmonate enhance peach susceptibility to Lasiodiplodia theobromae, a virulent pathogen inducing gummosis; however, the underlying molecular mechanisms remain obscure. Here, 2 ethylene response factors (ERFs), PpERF98 and PpERF1, were identified as negative regulators in peach response to L. theobromae infection. Expression of 2 putative paralogs, PpERF98-1/2, was dramatically induced by ethylene and L. theobromae treatments and accumulated highly in the gummosis-sensitive cultivar. Silencing of PpERF98-1/2 increased salicylic acid (SA) content and pathogenesis-related genes PpPR1 and PpPR2 transcripts, conferring peach resistance to L. theobromae, whereas peach and tomato (Solanum lycopersicum) plants overexpressing either of PpERF98-1/2 showed opposite changes. Also, jasmonic acid markedly accumulated in PpERF98-1/2-silenced plants, but reduction in PpPR3, PpPR4, and PpCHI (Chitinase) transcripts indicated a blocked signaling pathway. PpERF98-1 and 2 were further demonstrated to directly bind the promoters of 2 putative paralogous PpERF1 genes and to activate the ERF branch of the jasmonate/ethylene signaling pathway, thus attenuating SA-dependent defenses. The lesion phenotypes of peach seedlings overexpressing PpERF1-1/2 and PpERF98-1/2 were similar. Furthermore, PpERF98-1/2 formed homodimers/heterodimers and interacted with the 2 PpERF1 proteins to amplify the jasmonate/ethylene signaling pathway, as larger lesions were observed in peach plants cooverexpressing PpERF98 with PpERF1 relative to individual PpERF98 overexpression. Overall, our work deciphers an important regulatory network of ethylene-mediated peach susceptibility to L. theobromae based on a PpERF98-PpERF1 transcriptional cascade, which could be utilized as a potential target for genetic engineering to augment protection against L. theobromae-mediated diseases in crops and trees.
胶病是威胁全球桃（Prunus persica）生产的最常见和最具破坏性的疾病之一。我们之前的研究表明，乙烯和茉莉酸甲酯增强了桃对导致胶病的强毒病原体Lasiodiplodia theobromae 的易感性；然而，其潜在的分子机制尚不清楚。在这里，我们鉴定出 2 个乙烯应答因子（ERFs），即 PpERF98 和 PpERF1，它们是桃对 L. theobromae 感染反应的负调控因子。2 个假定的同源物 PpERF98-1/2 的表达被乙烯和 L. theobromae 处理显著诱导，并在胶病敏感品种中高度积累。沉默 PpERF98-1/2 增加了水杨酸（SA）含量和病程相关基因 PpPR1 和 PpPR2 的转录本，赋予了桃对 L. theobromae 的抗性，而桃和番茄（Solanum lycopersicum）植株过表达其中任何一个 PpERF98-1/2 都表现出相反的变化。此外，茉莉酸在 PpERF98-1/2 沉默植株中明显积累，但 PpPR3、PpPR4 和 PpCHI（几丁质酶）转录本的减少表明信号通路受阻。进一步证明 PpERF98-1 和 2 可直接结合 2 个假定的同源物 PpERF1 基因的启动子，并激活茉莉酸/乙烯信号通路的 ERF 分支，从而削弱了依赖 SA 的防御。过表达 PpERF1-1/2 和 PpERF98-1/2 的桃苗的损伤表型相似。此外，PpERF98-1/2 形成同源二聚体/异源二聚体，并与 2 个 PpERF1 蛋白相互作用，放大了茉莉酸/乙烯信号通路，因此在共同过表达 PpERF98 和 PpERF1 的桃植株中观察到的损伤比单独过表达 PpERF98 时更大。总的来说，我们的工作基于 PpERF98-PpERF1 转录级联，破译了一个重要的乙烯介导桃对 L. theobromae 易感性的调控网络，该网络可作为基因工程的潜在靶点，增加对作物和树木中由 L. theobromae 介导的疾病的保护。
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