Key Laboratory of National Forestry and Grassland Administration on Control of Artificial Forest Diseases and Pests in South China, Central South University of Forestry and Technology, Changsha, China.
Hunan Provincial Key Laboratory for Control of Forest Diseases and Pests, Central South University of Forestry and Technology, Changsha, China.
Virulence. 2024 Dec;15(1):2413851. doi: 10.1080/21505594.2024.2413851. Epub 2024 Oct 18.
Anthracnose, caused by species, induces significant economic damages to crop plants annually, especially for . During infection, the counter-defence mechanisms of plant pathogens against ROS-mediated resistance, however, remain poorly understood. By employing Weighted Gene Co-expression Network Analysis (WGCNA), we identified ACTIVATOR PROTEIN-1 (AP-1), a bZIP transcription factor, as significant to infection. And deletion of inhibited aerial hyphae formation and growth under oxidative stress. Furthermore, RNA-seq analysis post HO treatment revealed 33 significantly down-regulated genes in the AP-1 deficient strain, including A12032, a dual specificity phosphatase (DSP) homologous to MSG5 from . This Δ strain showed enhanced oxidative tolerance, reduced ROS scavenging, and negative regulation of the CWI MAPK cascade under oxygen stress, suggesting its involvement in oxidative signal transduction. Importantly, we provide evidence that CfMsg5 regulates growth, endoplasmic reticulum stress, and several unfolded protein response genes upregulated in Δ. Collectively, this study identified core components during infection and highlights a potential regulatory module involving CfAp1 and CfMsg5 in response to host ROS bursts. It provides new insights into fungal infection mechanisms and potential targets like and for managing anthracnose diseases.
炭疽病由 物种引起,每年给农作物造成巨大的经济损失,尤其是 。在感染过程中,植物病原体对 ROS 介导的抗性的反击防御机制仍知之甚少。通过采用加权基因共表达网络分析(WGCNA),我们鉴定出激活蛋白 1(AP-1),一种 bZIP 转录因子,对感染至关重要。并且缺失 抑制了气生菌丝在氧化应激下的形成和生长。此外,HO 处理后的 RNA-seq 分析显示,在 AP-1 缺失菌株中,有 33 个基因显著下调,包括 A12032,它是一种双特异性磷酸酶(DSP),与来自 的 MSG5 同源。该 Δ 菌株表现出增强的氧化耐受性、减少 ROS 清除和 CWI MAPK 级联的负调控,表明其参与氧化信号转导。重要的是,我们提供的证据表明 CfMsg5 调节 CfAp1 和 CfMsg5 对宿主 ROS 爆发的反应中涉及的生长、内质网应激和几个未折叠蛋白响应基因的表达。该研究鉴定了 感染过程中的核心组件,并强调了一个涉及 CfAp1 和 CfMsg5 的潜在调节模块,以响应宿主 ROS 爆发。它为真菌感染机制提供了新的见解,并为管理炭疽病等疾病提供了像 和 这样的潜在靶标。