A fungal pathogen secretes plant alkalinizing peptides to increase infection

Plant infections caused by fungi are often associated with an increase in the pH of the surrounding host tissue(1). Extracellular alkalinization is thought to contribute to fungal pathogenesis, but the underlying mechanisms are poorly understood. Here, we show that the root-infecting fungus Fusarium oxysporum uses a functional homologue of the plant regulatory peptide RALF (rapid alkalinization factor)(2,3) to induce alkalinization and cause disease in plants. An upshift in extracellular pH promotes infectious growth of Fusariumby stimulating phosphorylation of a conserved mitogen-activated protein kinase essential for pathogenicity(4,5). Fungal mutants lacking a functional Fusarium (F)-RALF peptide failed to induce host alkalinization and showed markedly reduced virulence in tomato plants, while eliciting a strong host immune response. Arabidopsis plants lacking the receptor-like kinase FERONIA, which mediates the RALF-triggered alkalinization response(6), displayed enhanced resistance against Fusarium. RALF homologues are found across a number of phylogenetically distant groups of fungi, many of which infect plants. We propose that fungal pathogens use functional homologues of alkalinizing peptides found in their host plants to increase their infectious potential and suppress host immunity.

由真菌引起的植物感染通常与周围宿主组织的pH值升高有关（1）。细胞外碱化被认为有助于真菌的致病性，但其潜在机制知之甚少。在此，我们表明根部感染真菌尖孢镰刀菌（Fusarium oxysporum）利用植物调节肽RALF（快速碱化因子）的一种功能同源物（2,3）来诱导碱化并在植物中引发疾病。细胞外pH值的升高通过刺激一种对致病性至关重要的保守的丝裂原活化蛋白激酶的磷酸化来促进尖孢镰刀菌的侵染性生长（4,5）。缺乏功能性尖孢镰刀菌（F）-RALF肽的真菌突变体无法诱导宿主碱化，并且在番茄植株中致病性显著降低，同时引发强烈的宿主免疫反应。缺乏受体样激酶FERONIA（其介导RALF触发的碱化反应（6））的拟南芥植株对尖孢镰刀菌表现出增强的抗性。RALF同源物在许多系统发育上距离较远的真菌类群中都有发现，其中许多会感染植物。我们提出真菌病原体利用其宿主植物中发现的碱化肽的功能同源物来增加其感染潜力并抑制宿主免疫。