Institute of Physiological Chemistry, Technische Universität Dresden, Medizinische Fakultät Carl Gustav Carus, Fetscherstrasse 74, 01307, Dresden, Germany.
Luxembourg Institute of Health, 1a Rue Thomas Edison, 1445, Strassen, Luxembourg.
Sci Rep. 2022 Oct 27;12(1):18084. doi: 10.1038/s41598-022-21414-x.
Hexokinase 2 (Hxk2) of Saccharomyces cerevisiae is a dual function hexokinase, acting as a glycolytic enzyme and being involved in the transcriptional regulation of glucose-repressible genes. Relief from glucose repression is accompanied by phosphorylation of Hxk2 at serine 15, which has been attributed to the protein kinase Tda1. To explore the role of Tda1 beyond Hxk2 phosphorylation, the proteomic consequences of TDA1 deficiency were investigated by difference gel electrophoresis (2D-DIGE) comparing a wild type and a Δtda1 deletion mutant. To additionally address possible consequences of glucose repression/derepression, both were grown at 2% and 0.1% (w/v) glucose. A total of eight protein spots exhibiting a minimum twofold enhanced or reduced fluorescence upon TDA1 deficiency was detected and identified by mass spectrometry. Among the spot identities are-besides the expected Hxk2-two proteoforms of hexokinase 1 (Hxk1). Targeted proteomics analyses in conjunction with 2D-DIGE demonstrated that TDA1 is indispensable for Hxk2 and Hxk1 phosphorylation at serine 15. Thirty-six glucose-concentration-dependent protein spots were identified. A simple method to improve spot quantification, approximating spots as rotationally symmetric solids, is presented along with new data on the quantities of Hxk1 and Hxk2 and their serine 15 phosphorylated forms at high and low glucose growth conditions. The Δtda1 deletion mutant exhibited no altered growth under high or low glucose conditions or on alternative carbon sources. Also, invertase activity, serving as a reporter for glucose derepression, was not significantly altered. Instead, an involvement of Tda1 in oxidative stress response is suggested.
酿酒酵母己糖激酶 2(Hxk2)是一种双功能己糖激酶,既是糖酵解酶,又参与葡萄糖可诱导基因的转录调控。解除葡萄糖抑制伴随着 Hxk2 丝氨酸 15 的磷酸化,这归因于蛋白激酶 Tda1。为了探究 Tda1 在 Hxk2 磷酸化之外的作用,通过比较野生型和Δtda1 缺失突变体的差异凝胶电泳(2D-DIGE),研究了 TDA1 缺失的蛋白质组学后果。为了进一步探讨葡萄糖抑制/去抑制的可能后果,两者均在 2%和 0.1%(w/v)葡萄糖下生长。通过质谱鉴定,共检测到并鉴定了 8 个蛋白质斑点,它们在 TDA1 缺乏时荧光至少增强或降低了两倍。除了预期的 Hxk2 之外,这些斑点的身份还包括两种己糖激酶 1(Hxk1)的蛋白形式。与 2D-DIGE 相结合的靶向蛋白质组学分析表明,TDA1 对于 Hxk2 和 Hxk1 丝氨酸 15 的磷酸化是不可或缺的。鉴定了 36 个葡萄糖浓度依赖性蛋白质斑点。本文提出了一种改进斑点定量的简单方法,即将斑点近似为旋转对称的固体,并提供了在高、低葡萄糖生长条件下关于 Hxk1 和 Hxk2 及其丝氨酸 15 磷酸化形式的数量的新数据。Δtda1 缺失突变体在高或低葡萄糖条件下或替代碳源上的生长没有改变。此外,作为葡萄糖去抑制报告的转化酶活性没有明显改变。相反,Tda1 可能参与了氧化应激反应。