The plasma membrane H(+) -ATPase FgPMA1 regulates the development, pathogenicity, and phenamacril sensitivity of Fusarium graminearum by interacting with FgMyo-5 and FgBmh2.

The plasma membrane H(+) -ATPase FgPMA1 regulates the development, pathogenicity, and phenamacril sensitivity of Fusarium graminearum by interacting with FgMyo-5 and FgBmh2.
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质膜 H -ATP 酶 FgPMA1 通过与 FgMyo-5 和 FgBmh2 相互作用来调节禾谷镰刀菌的发育、致病性和 phenamacril 敏感性

DOI:
10.1111/mpp.13173
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发表时间:
2022-04
影响因子:
4.9
通讯作者:
Hou Y
Hou Y
中科院分区:
农林科学1区
文献类型:
--
作者:
Wu L;Yuan Z;Wang P;Mao X;Zhou M;Hou Y

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禾谷镰刀菌作为小麦赤霉病的病原菌,不仅造成产量损失,还会产生脱氧雪腐镰刀菌烯醇(DON)等真菌毒素,污染小麦品质。质膜H+-ATPase在植物和酵母的许多生长阶段都起着重要的作用,但它们在植物病原真菌中的功能和调控仍不清楚。在这里,我们研究了禾谷镰刀菌的两种质膜H+-ATPase:FgPMA1和FgPMA2。FgPMA1缺失突变体(∆FgPMA1),而不是FgPMA2缺失突变体(∆FgPMA2),在营养生长、致病性、有性和无性发育方面受到损害。FgPMA1定位于质膜,∆FgPMA1表现为质膜完整性降低。∆FgPMA1不仅破坏了DON产生的毒素体的形成,而且还抑制了DON生物合成酶的表达水平,降低了DON的产量,减少了菌丝侵染量,通过在小麦穗和胚芽鞘的接种部位专一性地发生病害而导致致病性减弱。∆FgPMA1对渗透胁迫、细胞壁破坏剂(刚果红)、细胞膜破坏剂(十二烷基硫酸钠)和热休克胁迫的敏感性降低。FgMyo-5是苯那普利控制FHB的靶点。我们发现FgPMA1与FgMyo-5相互作用,∆FgPMA1显示FgMyo-5的表达水平增加,导致对苯那普利的敏感性增加,但对其他杀菌剂的敏感性增加。此外,免疫共沉淀证实FgPMA1、FgMyo-5和FgBmh2(一个14-3-3蛋白)形成一个复合体,调节对苯那普利的敏感性和生物学功能。综上所述,本研究确定了FgPMA1对禾谷镰刀菌致病性和非那普利敏感性的一种新的调控机制。FgPMA1、FgBmh2和FgMyo-5形成一个复合体,调节禾谷镰刀菌的发育、致病性和对苯那普利的敏感性。
Fusarium graminearum, as the causal agent of Fusarium head blight (FHB), not only causes yield loss, but also contaminates the quality of wheat by producing mycotoxins, such as deoxynivalenol (DON). The plasma membrane H+‐ATPases play important roles in many growth stages in plants and yeasts, but their functions and regulation in phytopathogenic fungi remain largely unknown. Here we characterized two plasma membrane H+‐ATPases: FgPMA1 and FgPMA2 in F. graminearum. The FgPMA1 deletion mutant (∆FgPMA1), but not FgPMA2 deletion mutant (∆FgPMA2), was impaired in vegetative growth, pathogenicity, and sexual and asexual development. FgPMA1 was localized to the plasma membrane, and ∆FgPMA1 displayed reduced integrity of plasma membrane. ∆FgPMA1 not only impaired the formation of the toxisome, which is a compartment where DON is produced, but also suppressed the expression level of DON biosynthetic enzymes, decreased DON production, and decreased the amount of mycelial invasion, leading to impaired pathogenicity by exclusively developing disease on inoculation sites of wheat ears and coleoptiles. ∆FgPMA1 exhibited decreased sensitivity to some osmotic stresses, a cell wall‐damaging agent (Congo red), a cell membrane‐damaging agent (sodium dodecyl sulphate), and heat shock stress. FgMyo‐5 is the target of phenamacril used for controlling FHB. We found FgPMA1 interacted with FgMyo‐5, and ∆FgPMA1 showed an increased expression level of FgMyo‐5, resulting in increased sensitivity to phenamacril, but not to other fungicides. Furthermore, co‐immunoprecipitation confirmed that FgPMA1, FgMyo‐5, and FgBmh2 (a 14‐3‐3 protein) form a complex to regulate the sensitivity to phenamacril and biological functions. Collectively, this study identified a novel regulating mechanism of FgPMA1 in pathogenicity and phenamacril sensitivity of F. graminearum. FgPMA1, FgBmh2, and FgMyo‐5 form a complex to regulate the development, pathogenicity, and phenamacril sensitivity of Fusarium graminearum.
DOI: 10.1073/pnas.83.20.7693
发表时间: 1986-10-01
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