Fungi activate corresponding metabolic pathways in response to different carbon sources to adapt to different environments. Previous studies have shown that the glycerol kinase GlcA that phosphorylates glycerol to the intermediate glycerol-3-phosphate (G3P) is required for the growth of Aspergillus fumigatus when glycerol is used as the sole carbon source. The present study identified there were two putative glycerol kinases, GlcA and GlcB, in A. fumigatus but glycerol activated only glcA promoter but not glcB promoter, although both glcA and glcB could encode glycerol kinase. Under normal culture conditions, the absence of glcA caused no detectable colony phenotypes on glucose and other tested carbon sources except glycerol, indicating dissimilation of glucose and these tested carbon sources bypassed requirement of glcA. Notably, the oxidative stress agent H₂O₂ on the background of glucose medium clearly induced GlcA expression and promoted G3P synthesis. Deletion and overexpression of glcA elicited sensitivity and resistance to oxidative stress agent H₂O₂, respectively, accompanied by decrease and increase of G3P production. In addition, the sensitivity to oxidative stress in the glcA mutant was probably associated with dysfunction of mitochondria with a decreased mitochondrial membrane potential and an abnormal accumulation of the cellular reactive oxygen species (ROS). Furthermore, overexpressing the glycerol-3-phosphate dehydrogenase GfdA that catalyzes the reduction of dihydroxyacetone phosphate (DHAP) to G3P rescued phenotypes of the glcA null mutant to H₂O₂. Therefore, the present study suggests that GlcA-involved G3P synthesis participates in oxidative stress tolerance of A. fumigatus via regulating the cellular ROS level.

真菌响应不同的碳源激活相应的代谢途径以适应不同的环境。先前的研究表明，当使用甘油作为唯一碳源时，烟曲霉生长需要将甘油磷酸化为中间体 3-磷酸甘油 (G3P) 的甘油激酶 GlcA 。本研究发现有两个假定甘油激酶，中，GlcA和GlcB，在烟曲霉，但甘油只启动中，GlcA子但不glcB启动子，虽然两者中，GlcA和glcB可以编码甘油激酶。在正常培养条件下，glcA的缺失在葡萄糖和除甘油之外的其他测试碳源上没有引起可检测的菌落表型，表明葡萄糖的异化和这些测试碳源绕过了glcA 的要求。值得注意的是，葡萄糖培养基背景下的氧化应激剂 H ₂ O ₂明显诱导 GlcA 表达并促进 G3P 合成。glcA 的缺失和过表达分别引起对氧化应激剂 H ₂ O _{2 的}敏感性和抗性，伴随着 G3P 产生的减少和增加。此外，glcA对氧化应激的敏感性突变体可能与线粒体功能障碍、线粒体膜电位降低和细胞活性氧 (ROS) 异常积累有关。此外，过表达 催化磷酸二羟丙酮 (DHAP) 还原为 G3P的 3-磷酸甘油脱氢酶 GfdA拯救了glcA无效突变体的表型为 H ₂ O ₂。因此，本研究表明 GlcA 参与的 G3P 合成通过调节细胞 ROS 水平参与烟曲霉的氧化应激耐受。