Ying Sheng-Hua, Feng Ming-Guang, Keyhani Nemat O
Institute of Microbiology, College of Life Sciences, Zhejiang University, Hangzhou 310058, China.
Department of Microbiology and Cell Science, University of Florida, Gainesville, FL, 32611, USA.
Environ Microbiol. 2013 Nov;15(11):2902-21. doi: 10.1111/1462-2920.12169. Epub 2013 Jul 1.
In fungi, G-protein coupled receptors (GPCRs) link ligand/nutrient sensing to growth, mating, developmental/life-stage activation and pathogenesis. A GPCR was characterized from the entomopathogenic fungus, Beauveria bassiana (BbGPCR3), which links nutrient sensing to stress response and development. ΔBbGPCR3 mutants grew slower on various carbohydrates and displayed increased sensitivity to osmotic, oxidative and cell wall stresses. Gene expression profiling revealed a set of heat-shock and antioxidant factors that failed to be induced under oxidative stress and aberrant regulation of compatible solute-forming enzymes and cell wall biosynthesis/remodelling proteins in ΔBbGPCR3 after osmotic stress. Glucose-specific developmental defects included reduced (> 90%) conidiation and reduced dimorphic transition to the production of yeast-like blastospores, effects suppressed in media containing trehalose or glycerol, but not by addition of cyclic AMP. Insect bioassays revealed reduced virulence in topical assays but no effect in intrahaemoceol injection assays, indicating that BbGPCR3 was important in sensing signals during the initial interaction with the host but dispensable for post-penetration events. Comparative gene expression profiling of ΔBbGPCR3 mutants grown in glucose media compared with wild-type/glucose and ΔBbGPCR3/trehalose grown cells revealed sets of genes misregulated and recovered, respectively. These data link BbGPCR3 to broad developmental and genetic networks that include the major MAP kinase pathways.
在真菌中，G蛋白偶联受体（GPCRs）将配体/营养感知与生长、交配、发育/生命阶段激活及致病机制联系起来。从昆虫病原真菌球孢白僵菌中鉴定出一种GPCR（BbGPCR3），它将营养感知与应激反应和发育联系起来。ΔBbGPCR3突变体在各种碳水化合物上生长较慢，且对渗透、氧化和细胞壁应激的敏感性增加。基因表达谱分析显示，一组热休克和抗氧化因子在氧化应激下未能被诱导，且在渗透应激后，ΔBbGPCR3中相容性溶质形成酶和细胞壁生物合成/重塑蛋白的调控异常。葡萄糖特异性发育缺陷包括分生孢子形成减少（>90%）以及向酵母样芽生孢子产生的双态转变减少，在含有海藻糖或甘油的培养基中这些影响受到抑制，但添加环磷酸腺苷则无此作用。昆虫生物测定表明，在局部测定中毒力降低，但在血腔注射测定中无影响，这表明BbGPCR3在与宿主的初始相互作用过程中感知信号方面很重要，但在穿透后事件中并非必需。与在葡萄糖培养基中生长的野生型/葡萄糖和在海藻糖中生长的ΔBbGPCR3细胞相比，对在葡萄糖培养基中生长的ΔBbGPCR3突变体进行比较基因表达谱分析，分别揭示了一组失调和恢复的基因。这些数据将BbGPCR3与包括主要丝裂原活化蛋白激酶途径在内的广泛发育和遗传网络联系起来。
