Department of Geosciences and Natural Resource Management, University of Copenhagen, Frederiksberg, Denmark.
Department of Biotechnology and Biomedicine, Technical University of Denmark, Lyngby, Denmark.
J Biol Chem. 2021 Jan-Jun;296:100504. doi: 10.1016/j.jbc.2021.100504. Epub 2021 Mar 3.
Lytic polysaccharide monooxygenases (LPMOs) are known to act synergistically with glycoside hydrolases in industrial cellulolytic cocktails. However, a few studies have reported severe impeding effects of C1-oxidizing LPMOs on the activity of reducing-end cellobiohydrolases. The mechanism for this effect remains unknown, but it may have important implications as reducing-end cellobiohydrolases make up a significant part of such cocktails. To elucidate whether the impeding effect is general for different reducing-end cellobiohydrolases and study the underlying mechanism, we conducted a comparative biochemical investigation of the cooperation between a C1-oxidizing LPMO from Thielavia terrestris and three reducing-end cellobiohydrolases; Trichoderma reesei (TrCel7A), T. terrestris (TtCel7A), and Myceliophthora heterothallica (MhCel7A). The enzymes were heterologously expressed in the same organism and thoroughly characterized biochemically. The data showed distinct differences in synergistic effects between the LPMO and the cellobiohydrolases; TrCel7A was severely impeded, TtCel7A was moderately impeded, while MhCel7A was slightly boosted by the LPMO. We investigated effects of C1-oxidations on cellulose chains on the activity of the cellobiohydrolases and found reduced activity against oxidized cellulose in steady-state and pre-steady-state experiments. The oxidations led to reduced maximal velocity of the cellobiohydrolases and reduced rates of substrate complexation. The extent of these effects differed for the cellobiohydrolases and scaled with the extent of the impeding effect observed in the synergy experiments. Based on these results, we suggest that C1-oxidized chain ends are poor attack sites for reducing-end cellobiohydrolases. The severity of the impeding effects varied considerably among the cellobiohydrolases, which may be relevant to consider for optimization of industrial cocktails.
溶细胞多糖单加氧酶(LPMOs)已知与糖苷水解酶在工业纤维素酶制剂中协同作用。然而,一些研究报道了 C1 氧化 LPMO 对还原端纤维二糖水解酶活性的严重阻碍作用。这种影响的机制尚不清楚,但它可能具有重要意义,因为还原端纤维二糖水解酶构成了这些酶制剂的重要组成部分。为了阐明这种阻碍作用是否普遍适用于不同的还原端纤维二糖水解酶,并研究其潜在机制,我们对来自土曲霉的 C1 氧化 LPMO 与三种还原端纤维二糖水解酶(里氏木霉(TrCel7A)、土曲霉(TtCel7A)和异核侧耳(MhCel7A))之间的合作进行了比较生化研究。这些酶在同一生物体内异源表达,并进行了彻底的生化特性分析。数据显示,LPMO 与纤维二糖水解酶之间的协同作用存在明显差异;TrCel7A 受到严重阻碍,TtCel7A 受到中度阻碍,而 MhCel7A 则受到轻微促进。我们研究了 C1 氧化对纤维素链的影响对纤维二糖水解酶活性的影响,发现氧化纤维素在稳态和预稳态实验中活性降低。这些氧化作用导致纤维二糖水解酶的最大速度降低,并且降低了底物络合的速率。这些影响的程度因纤维二糖水解酶而异,并与协同实验中观察到的阻碍效应的程度成正比。基于这些结果,我们建议 C1 氧化的链末端是还原端纤维二糖水解酶的不良攻击位点。阻碍效应的严重程度在纤维二糖水解酶之间差异很大,这在优化工业酶制剂时可能需要考虑。