In pathogenic filamentous fungi, conidial germination not only is fundamental for propagation in the environment but is also a critical step of infection. In the insect mycopathogen Beauveria bassiana, we genetically characterized the role of the basic leucine zipper (bZIP) transcription factor HapX (BbHapX) in conidial nutrient reserves and pathogen-host interaction. Ablation of BbHapX resulted in an almost complete loss of virulence in the topical inoculation and intrahemocoel injection assays. Comparative transcriptomic analysis revealed that BbHapX is required for fatty acid (FA)/lipid metabolism, and biochemical analyses indicated that BbHapX loss caused a significant reduction in conidial FA contents. Exogenous oleic acid could partially or completely restore the impaired phenotypes of the ΔBbHapX mutant, including germination rate, membrane integrity, vegetative growth, and virulence. BbHapX mediates fungal iron acquisition which is not required for desaturation of stearic acid. Additionally, inactivation of the Δ9-fatty acid desaturase gene (BbOle1) generated defects similar to those of the ΔBbHapX mutant; oleic acid also had significant restorative effects on the defective phenotypes of the ΔBbOle1 mutant. A gel retarding assay revealed that BbHapX directly regulated the expression of BbOle1. Lipidomic analyses indicated that both BbHapX and BbOle1 contributed to the homeostasis of phospholipids with nonpolar tails derived from oleic acid; therefore, exogenous phospholipids could significantly restore membrane integrity. These data reveal that the HapX-Ole1 pathway contributes to conidial fatty acid/lipid reserves and that there are important links between the lipid biology and membrane functionality involved in the early stages of infection caused by B. bassiana.

中文翻译：

---

HapX 是一种必不可少的铁获取 bZIP 转录因子，通过协调分生孢子油酸稳态和细胞膜功能来调节真菌病原体白僵菌的感染起始

在病原丝状真菌中，分生孢子萌发不仅是在环境中繁殖的基础，而且还是感染的关键步骤。在昆虫真菌病原体白僵菌中，我们对碱性亮氨酸拉链 (bZIP) 转录因子 HapX ( BbHapX ) 在分生孢子营养储备和病原体-宿主相互作用中的作用进行了遗传表征。BbHapX 的消融导致在局部接种和血细胞腔内注射试验中毒力几乎完全丧失。比较转录组学分析显示BbHapX是脂肪酸 (FA)/脂质代谢所必需的，生化分析表明BbHapX损失导致分生孢子 FA 含量显着减少。外源油酸可以部分或完全恢复 Δ BbHapX突变体受损的表型，包括萌发率、膜完整性、营养生长和毒力。BbHapX介导真菌铁的获取，这是硬脂酸去饱和所不需要的。此外，Δ9-脂肪酸去饱和酶基因 ( BbOle1 ) 的失活会产生与 Δ BbHapX突变体相似的缺陷；油酸对 Δ BbOle1突变体的缺陷表型也具有显着的修复作用。凝胶阻滞测定显示BbHapX直接调节的表达BbOle1. 脂质组学分析表明，BbHapX和BbOle1 都有助于具有来自油酸的非极性尾部的磷脂的稳态；因此，外源性磷脂可以显着恢复膜的完整性。这些数据揭示，HapX-OLE1通路有助于分生孢子脂肪酸/脂质储备和有脂质生物学和参与引起感染的早期阶段，膜的功能之间重要的联系B. 白僵菌。