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A regulator of a G protein signalling (RGS) gene, cag8, from the insect-pathogenic fungus Metarhizium anisopliae is involved in conidiation, virulence and hydrophobin synthesis

机译:来自昆虫致病性真菌的G蛋白信号传导(RGS)基因,CAG8的稳压因子参与共分配,毒力和疏水蛋白合成

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Regulators of the G protein signalling (RGS) pathway have been implicated in the control of a diverse array of cellular functions, including conidiation in filamentous fungi. However, the regulatory processes involved in conidiation in insect-pathogenic fungi are poorly understood. Since conidia are the infective propagules in these fungi, an understanding of the regulatory processes involved in conidiation is essential to the development of an effective biocontrol fungus. Here, the cloning and characterization of an RGS protein gene, cag8 (conidiation-associated gene), from the insect-pathogenic fungus Metarhizium anisopliae is reported. Phylogenetic analysis showed that CAG8 was orthologous to the RGS protein FlbA from Aspergillus nidulans. Complementation of A. nidulans ΔflbA, which cannot conidiate, with M. anisopliae cag8 restored conidiation. Gene disruption of cag8 in M. anisopliae resulted in the lack of conidia on agar plates and on infected insects, reduced mycelial growth, decreased virulence, lysis during growth in liquid medium as well as lack of pigmentation and irregularly shaped blastospores. Transcript levels of ssgA (hydrophobin-encoding gene) were markedly reduced in a Δcag8 strain, while pr1A (subtilisin-like protease) transcription was unaffected. These results suggest that cag8 is involved in the modulation of conidiation, virulence and hydrophobin synthesis in M. anisopliae.
机译:G蛋白信号传导(RGS)途径的调节剂涉及控制各种细胞功能阵列,包括在丝状真菌中的结合。然而,在昆虫病原真菌中共结合的调节过程尚不清楚。由于分类以来是这些真菌中的感染繁殖,因此了解共分配所涉及的监管程序对于有效的生物控制真菌的发展至关重要。这里,报道了RGS蛋白基因,CAG8(结合相关基因)的克隆和表征来自昆虫致病性真菌性嗜尼血管卟啉基因素。系统发育分析表明,CAG8与来自Aspergillus Nidulans的RGS蛋白FLBA透明。 A.nidulansΔFLBA的互补,不能与M.Anisopliae CAG8恢复的共同分组。 CAG8在M.的基因中断癌症患者导致琼脂平板上缺乏分类,感染昆虫,减少菌丝体生长,减少毒力,液体培养基中生长期间的毒力,缺乏色素沉着和不规则形状的胚胎孢子。在ΔCag8菌株中显着降低了SSGA(疏水蛋白编码基因)的转录物水平,而PR1A(枯草杆菌蛋白酶样蛋白酶)转录不受影响。这些结果表明CAG8参与了M.AniSopliae中的结合,毒力和疏水蛋白合成的调节。

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