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首页> 外文期刊>Eukaryotic cell >Trichoderma atroviride G-Protein α-Subunit Gene tga1 Is Involved in Mycoparasitic Coiling and Conidiation
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Trichoderma atroviride G-Protein α-Subunit Gene tga1 Is Involved in Mycoparasitic Coiling and Conidiation

机译：木霉阿troviride G蛋白α亚基基因tga1参与霉菌寄生性卷曲和分生。

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摘要

The soil fungus Trichoderma atroviride, a mycoparasite, responds to a number of external stimuli. In the presence of a fungal host, T. atroviride produces hydrolytic enzymes and coils around the host hyphae. In response to light or nutrient depletion, asexual sporulation is induced. In a biomimetic assay, different lectins induce coiling around nylon fibers; coiling in the absence of lectins can be induced by applying cyclic AMP (cAMP) or the heterotrimeric G-protein activator mastoparan. We isolated a T. atroviride G-protein α-subunit (Gα) gene (tga1) belonging to the fungal subfamily with the highest similarity to the Gαi class. Generated transgenic lines that overexpress Gα show very delayed sporulation and coil at a higher frequency. Furthermore, transgenic lines that express an activated mutant protein with no GTPase activity do not sporulate and coil at a higher frequency. Lines that express an antisense version of the gene are hypersporulating and coil at a much lower frequency in the biomimetic assay. The loss of Tga1 in these mutants correlates with the loss of GTPase activity stimulated by the peptide toxin Mas-7. The application of Mas-7 to growing mycelial colonies raises intracellular cAMP levels, suggesting that Tga1 can activate adenylyl cyclase. In contrast, cAMP levels and cAMP-dependent protein kinase activity drop when diffusible host signals are encountered and the mycoparasitism-related genes ech42 and prb1 are highly expressed. Mycoparasitic signaling is unlikely to be a linear pathway from host signals to increased cAMP levels. Our results demonstrate that the product of the tga1 gene is involved in both coiling and conidiation.
机译：土壤真菌 Trichoderma atroviride 是一种真菌寄生虫，对许多外部刺激有反应。在存在真菌宿主的情况下， T 。 atroviride 在宿主菌丝周围产生水解酶和卷曲。响应于光或营养的消耗，会引起无性孢子形成。在仿生分析中，不同的凝集素会引起尼龙纤维的卷曲。在不存在凝集素的情况下，卷曲可以通过应用环状AMP（cAMP）或异三聚体G蛋白激活剂马索帕兰来诱导。我们隔离了 T 。属于真菌亚科的 atroviride G蛋白α-亚基（ tga1 ）基因与Gα i 类具有最高的相似性。产生的过表达Gα的转基因品系显示出非常延迟的孢子形成和较高频率的卷曲。此外，表达没有GTPase活性的活化突变蛋白的转基因品系不会以更高的频率形成孢子和卷曲。在仿生分析中，表达该基因反义序列的品系超形成并以较低的频率卷曲。这些突变体中Tga1的丢失与肽毒素Mas-7刺激的GTPase活性的丢失有关。 Mas-7在生长的菌丝体菌落中的应用提高了细胞内cAMP的水平，表明Tga1可以激活腺苷酸环化酶。相反，当遇到可扩散的宿主信号并且与副寄生虫相关的基因 ech42 和 prb1 高表达时，cAMP水平和cAMP依赖性蛋白激酶活性下降。真菌寄生信号不大可能是从宿主信号到增加cAMP水平的线性途径。我们的结果表明 tga1 基因的产物参与卷曲和分生孢子。

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