帮我把下面这段英文从用词、语法、结构上修改一下。Rab GTPases serve as master regulators of membrane trafficking. They can be activated by guanine nucleotide exchange factors (GEF) and be inactivated by GTPase-activating proteins (GAPs). The roles of some GAPs have been explored in Saccharomyces cerevisiae, but are largely unknown in filamentous fungi. Here, we investigated the role of GAP Gyp3 gene, an ortholog of S. cerevisiae Gyp3, in an entomopathogenic fungus, Metarhizium acridum. We found that MaGyp3 is mainly localized to the endoplasmic reticulum (ER) of vegetative hyphae, nuclei of mature conidia, and both ER and nuclei in invasive hyphae. Lack of MaGyp3 caused a decreased tolerance to hyperosmotic stress, heat-shock and UV-B radiation. Moreover, the ΔMaGyp3 mutant showed a significantly decreased pathogenicity owing to delayed germination, reduced appressorium-mediated penetration and impaired invasive growth. Loss of MaGyp3 also caused impaired fungal growth, advanced conidiation and defects in utilization of carbon and nitrogen sources, while overexpression of MaGyp3 exhibited delayed conidiation on nutrient-rich medium and conidiation pattern shift from microcycle conidiation to normal conidiation on nutrient-limited medium. Mavib-1, a tanscription factor invloved in conidiation by affecting nutrient utilizaiton, can directly bind to the promoter of MaGyp3. ΔMaGyp3 and ΔMavib-1 mutants shared similar phenotypes, and overexpression mutants of MaGyp3 and Mavib-1 (Mavib-1-OE) exhibited similar phenotypes in growth, conidiation and pathogenicity. Reintroduction of the Magyp3 driven by strong promoter gpd in ΔMavib-1 mutant recovered the defects in growth and conidiation for dysfunction of Mavib1. Taken together, our findings uncovered the role of GAP3 in a filamentous pathogenic fungus and and illustrated the upstream regulatory mechanism by direct interaction with Mavib-1.

我们研究了捕食性真菌Metarhizium acridum中GAP Gyp3基因的作用，它是酵母菌Saccharomyces cerevisiae Gyp3的同源基因。我们发现MaGyp3主要定位于营养生长期的内质网、成熟孢子的细胞核以及侵染性菌丝的内质网和细胞核。缺乏MaGyp3导致对高渗应激、热冲击和紫外线B辐射的耐受性降低。此外，由于孢子萌发延迟、趾状体介导的侵入减弱和侵染性生长受阻，ΔMaGyp3突变体的致病性显著降低。MaGyp3的缺失还导致菌丝生长受阻、孢子形成加速以及碳和氮源利用缺陷，而MaGyp3的过表达则导致营养丰富培养基上的孢子形成延迟，以及从微周期孢子形成转变为正常孢子形成的模式变化。M

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Rab GTPases serve as master regulators of membrane trafficking. They can be activated by guanine nucleotide exchange factors (GEF) and be inactivated by GTPase-activating proteins (GAPs). The roles of some GAPs have been explored in Saccharomyces cerevisiae, but are largely unknown in filamentous fungi. Here, we investigated the role of GAP Gyp3 gene, an ortholog of S. cerevisiae Gyp3, in an entomopathogenic fungus, Metarhizium acridum. We found that MaGyp3 is mainly localized to the endoplasmic reticulum (ER) of vegetative hyphae, nuclei of mature conidia, and both ER and nuclei in invasive hyphae. Lack of MaGyp3 caused a decreased tolerance to hyperosmotic stress, heat-shock and UV-B radiation. Moreover, the ΔMaGyp3 mutant showed a significantly decreased pathogenicity owing to delayed germination, reduced appressorium-mediated penetration and impaired invasive growth. Loss of MaGyp3 also caused impaired fungal growth, advanced conidiation and defects in utilization of carbon and nitrogen sources, while overexpression of MaGyp3 exhibited delayed conidiation on nutrient-rich medium and conidiation pattern shift from microcycle conidiation to normal conidiation on nutrient-limited medium. Mavib-1, a tanscription factor invloved in conidiation by affecting nutrient utilizaiton, can directly bind to the promoter of MaGyp3. ΔMaGyp3 and ΔMavib-1 mutants shared similar phenotypes, and overexpression mutants of MaGyp3 and Mavib-1 (Mavib-1-OE) exhibited similar phenotypes in growth, conidiation and pathogenicity. Reintroduction of the Magyp3 driven by strong promoter gpd in ΔMavib-1 mutant recovered the defects in growth and conidiation for dysfunction of Mavib1. Taken together, our findings uncovered the role of GAP3 in a filamentous pathogenic fungus and and illustrated the upstream regulatory mechanism by direct interaction with Mavib-1.

研究表明，GAP Gyp3基因（与酵母菌S. cerevisiae Gyp3的同源基因）在害虫真菌Metarhizium acridum中发挥着重要作用。MaGyp3主要分布于营养菌丝的内质网，成熟孢子的细胞核以及侵染性菌丝的内质网和细胞核。缺乏MaGyp3导致抗高渗应激，热激和UV-B辐射能力降低，并且由于孢子萌发延迟，贴附体介导的侵入受损以及侵染性生长受限，而导致病原性大幅度降低。此外，MaGyp3缺失还导致营养菌丝生长受限，孢子产量增加以及碳氮源利用能力受损。研究发现，Mavib-1，一种参与孢子形成的转录因子，可以直接结合MaGyp3的启动子。综上所述，我们揭示了GAP3在菌丝性病原真菌中的作用，并阐明了Mavib-1通过直接与MaGyp3的互作来调节MaGyp3的上游调控机制。

翻译Rab GTPases serve as master regulators of membrane trafficking. They can be activated by guanine nucleotide exchange factors (GEF) and be inactivated by GTPase-activating proteins (GAPs). The roles of some GAPs have been explored in Saccharomyces cerevisiae, but are largely unknown in filamentous fungi. Here, we investigated the role of GAP Gyp3 gene, an ortholog of S. cerevisiae Gyp3, in an entomopathogenic fungus, Metarhizium acridum.

结合素GTP酶是膜货运的主要调节因子，它们可以通过环腺苷酸交换因子（GEF）激活，并被GTP酶激活蛋白（GAP）抑制。在酵母菌中，一些GAP的作用已经被探索，但在丝状真菌中却大多未知。在这里，我们研究了昆虫病原真菌Metarhizium acridum中GAP Gyp3基因的作用，它是酵母菌Gyp3的同源基因。