Niu Canfang, Luo Huiying, Shi Pengjun, Huang Huoqing, Wang Yaru, Yang Peilong, Yao Bin
Key Laboratory for Feed Biotechnology of the Ministry of Agriculture, Feed Research Institute, Chinese Academy of Agricultural Sciences, Beijing, People's Republic of China.
Key Laboratory for Feed Biotechnology of the Ministry of Agriculture, Feed Research Institute, Chinese Academy of Agricultural Sciences, Beijing, People's Republic of China
Appl Environ Microbiol. 2015 Dec 4;82(4):1004-1014. doi: 10.1128/AEM.02881-15. Print 2016 Feb 15.
N-Glycosylation can modulate enzyme structure and function. In this study, we identified two pepsin-resistant histidine acid phosphatase (HAP) phytases from Yersinia kristensenii (YkAPPA) and Yersinia rohdei (YrAPPA), each having an N-glycosylation motif, and one pepsin-sensitive HAP phytase from Yersinia enterocolitica (YeAPPA) that lacked an N-glycosylation site. Site-directed mutagenesis was employed to construct mutants by altering the N-glycosylation status of each enzyme, and the mutant and wild-type enzymes were expressed in Pichia pastoris for biochemical characterization. Compared with those of the N-glycosylation site deletion mutants and N-deglycosylated enzymes, all N-glycosylated counterparts exhibited enhanced pepsin resistance. Introduction of the N-glycosylation site into YeAPPA as YkAPPA and YrAPPA conferred pepsin resistance, shifted the pH optimum (0.5 and 1.5 pH units downward, respectively) and improved stability at acidic pH (83.2 and 98.8% residual activities at pH 2.0 for 1 h). Replacing the pepsin cleavage sites L197 and L396 in the immediate vicinity of the N-glycosylation motifs of YkAPPA and YrAPPA with V promoted their resistance to pepsin digestion when produced in Escherichia coli but had no effect on the pepsin resistance of N-glycosylated enzymes produced in P. pastoris. Thus, N-glycosylation may improve pepsin resistance by enhancing the stability at acidic pH and reducing pepsin's accessibility to peptic cleavage sites. This study provides a strategy, namely, the manipulation of N-glycosylation, for improvement of phytase properties for use in animal feed.
N-糖基化可以调节酶的结构和功能。在本研究中,我们从克氏耶尔森菌(YkAPPA)和罗德耶尔森菌(YrAPPA)中鉴定出两种耐胃蛋白酶的组氨酸酸性磷酸酶(HAP)植酸酶,它们各自具有一个N-糖基化基序,以及一种来自小肠结肠炎耶尔森菌(YeAPPA)的对胃蛋白酶敏感的HAP植酸酶,该酶缺乏N-糖基化位点。采用定点诱变通过改变每种酶的N-糖基化状态来构建突变体,并将突变体和野生型酶在毕赤酵母中表达以进行生化特性分析。与N-糖基化位点缺失突变体和N-去糖基化酶相比,所有N-糖基化的对应物均表现出增强的胃蛋白酶抗性。将N-糖基化位点引入YeAPPA中使其成为YkAPPA和YrAPPA后赋予了胃蛋白酶抗性,使最适pH分别向下移动了0.5和1.5个pH单位,并提高了在酸性pH下的稳定性(在pH 2.0下1小时的残留活性分别为83.2%和98.8%)。将YkAPPA和YrAPPA的N-糖基化基序紧邻处的胃蛋白酶切割位点L197和L396替换为V,可促进它们在大肠杆菌中产生时对胃蛋白酶消化的抗性,但对在毕赤酵母中产生的N-糖基化酶的胃蛋白酶抗性没有影响。因此,N-糖基化可能通过增强在酸性pH下的稳定性并减少胃蛋白酶对蛋白水解切割位点的可及性来提高胃蛋白酶抗性。本研究提供了一种策略,即操纵N-糖基化,以改善用于动物饲料的植酸酶特性。