Departamento de Genética, Campus de Excelencia Internacional Agroalimentario ceiA3, Universidad de Córdoba, Córdoba, Spain.
Department of Applied Genetics and Cell Biology, Institute of Microbial Genetics, BOKU University, Vienna, Austria.
PLoS Pathog. 2024 Nov 4;20(11):e1012671. doi: 10.1371/journal.ppat.1012671. eCollection 2024 Nov.
Plant pathogenic fungi provoke devastating agricultural losses and are difficult to control. How these organisms acquire micronutrients during growth in the host environment remains poorly understood. Here we show that efficient regulation of copper acquisition mechanisms is crucial for plant colonization and virulence in the soilborne ascomycete Fusarium oxysporum, the causal agent of vascular wilt disease in more than 150 different crops. Using a combination of RNA-seq and ChIP-seq, we establish a direct role of the transcriptional regulator Mac1 in activation of copper deficiency response genes, many of which are induced during plant infection. Loss of Mac1 impaired growth of F. oxysporum under low copper conditions and abolishes pathogenicity on tomato plants and on the invertebrate animal host Galleria mellonella. Importantly, overexpression of two Mac1 target genes encoding a copper reductase and a copper transporter was sufficient to restore virulence in the mac1 mutant background. Our results establish a previously unrecognized role of copper reduction and uptake in fungal infection of plants and reveal new ways to protect crops from phytopathogens.
植物病原真菌引发严重的农业损失，难以控制。这些生物体在宿主环境中生长时如何获取微量元素，目前仍知之甚少。本文中，我们发现，在土传子囊菌尖孢镰刀菌（引起超过 150 种不同作物维管束萎蔫病的病原菌）中，高效调控铜吸收机制对于其在土壤中的定植和毒力至关重要。通过 RNA-seq 和 ChIP-seq 的联合使用，我们确定了转录调控因子 Mac1 在激活铜缺乏响应基因中的直接作用，其中许多基因在植物感染过程中被诱导。Mac1 缺失会损害尖孢镰刀菌在低铜条件下的生长，并使其丧失对番茄植株和无脊椎动物宿主地中海实蝇的致病性。重要的是，过表达 Mac1 两个靶基因（编码铜还原酶和铜转运蛋白）足以恢复 Mac1 突变体背景下的毒力。本研究结果确立了铜还原和摄取在真菌感染植物过程中的一个新作用，为保护作物免受植物病原菌侵害提供了新途径。
