Citrus Research and Education Center, Department of Plant Pathology, Institute of Food and Agricultural Sciences (IFAS), University of Florida, 700 Experiment Station Road, Lake Alfred, Florida 33850, USA.
Fungal Genet Biol. 2010 Apr;47(4):381-91. doi: 10.1016/j.fgb.2009.12.009. Epub 2009 Dec 29.
Alternaria alternata, the fungus that causes citrus brown spot, invades its hosts primarily through the production and action of a host-selective ACT toxin that kills citrus cells prior to invasion. In this study, we show that, in the tangerine pathotype of A. alternata, a mitogen-activated protein kinase (MAPK)-mediated signaling pathway governs a number of biological functions, either separately or in a cooperative manner, with the AaAP1 gene encoding a transcription regulator. The reported MAPK is encoded by the AaFUS3 gene, which we show to be necessary for conidial development, resistance to copper fungicides, melanin biosynthesis, and particularly, for elaboration of the penetration process. In contrast, AaFUS3 negatively controls salt tolerance and production of several hydrolytic enzymes. AaFUS3 has no apparent role in the biosynthesis of host-selective toxin or in resistance to oxidative stress. Both AaAP1 and AaFUS3 are required for fungal resistance to 2,3,5-triiodobenzoic acid (TIBA), 2-chloro-5-hydroxypyridine (CHP), diethyl maleate (DEM), and many pyridine-containing compounds. A strain with mutations in both AaAP1 and AaFUS3 displayed an increased sensitivity to these compounds. Expression of the AaAP1 and AaFUS3 genes and phosphorylation of AaFUS3 were also induced by CHP, DEM, or TIBA. Expression of two genes coding for a putative MFS transporter was coordinately regulated by AaAP1 and AaFUS3. The AaAP1::sGFP (synthetic green fluorescent protein) fusion protein became localized in the nucleus in response to CHP or TIBA. Inactivation of the AaAP1 gene, however, promoted phosphorylation of AaFUS3. Taken together, our results indicate that A. alternata utilizes specialized or synergistic regulatory interactions between the AP1 and MAPK signaling pathways for diverse physiological functions.
交链格孢菌，导致柑橘褐斑病的真菌，主要通过产生和作用于一种宿主选择性的 ACT 毒素来入侵其宿主，该毒素在入侵前杀死柑橘细胞。在这项研究中，我们表明，在柑橘病原菌交链格孢菌中，一种丝裂原活化蛋白激酶（MAPK）介导的信号通路通过与编码转录调节剂的 AaAP1 基因，分别或以协同方式控制多种生物学功能。报告的 MAPK 由 AaFUS3 基因编码，我们发现该基因对于分生孢子的发育、对铜杀菌剂的抗性、黑色素生物合成以及特别是穿透过程的形成是必需的。相比之下，AaFUS3 负调控盐耐受性和几种水解酶的产生。AaFUS3 在宿主选择性毒素的生物合成或对氧化应激的抗性中没有明显作用。AaAP1 和 AaFUS3 都需要真菌对 2,3,5-三碘苯甲酸（TIBA）、2-氯-5-羟基吡啶（CHP）、马来酸二乙酯（DEM）和许多含吡啶化合物的抗性。在同时突变 AaAP1 和 AaFUS3 的菌株中，对这些化合物的敏感性增加。AaAP1 和 AaFUS3 基因的表达以及 AaFUS3 的磷酸化也被 CHP、DEM 或 TIBA 诱导。两个编码假定 MFS 转运蛋白的基因的表达也被 AaAP1 和 AaFUS3 协调调控。AaAP1::sGFP（合成绿色荧光蛋白）融合蛋白响应 CHP 或 TIBA 而定位于细胞核。然而，AaAP1 基因的失活促进了 AaFUS3 的磷酸化。总之，我们的结果表明，交链格孢菌利用 AP1 和 MAPK 信号通路之间的专门或协同调节相互作用来实现多种生理功能。
