Streptococcus mutans (S. mutans) effectively utilizes dietary sucrose for the exopolysaccharide productions, which are mostly synthesized by the effects of glucosyltransferases (Gtfs). In the present study, the acetylome of S. mutans was identified and quantitative acetylome analysis of the bacterial biofilm growth (SMB) was compared with that of planktonic growth (SMP). The dynamic changes of protein acetylation were quantified using the integrated approach involving TMT labeling and Kac affinity enrichment followed by high‐resolution mass spectrometry‐based quantitative proteomics. In total, 973 acetylation sites in 445 proteins were identified, among which 617 acetylation sites in 302 proteins were quantitated. The overall analysis indicated that 22.7% of proteins were acetylated. Among the quantified proteins in SMB, the acetylation degree of lysine in 56 sites increased, while that of lysine decreased in 52 sites. In the acetylome of S. mutans, six significantly enriched motifs were identified and obtained including Kac****K, KacF, Kac****R, KacY, KacH, F*Kac. In addition, KEGG pathway‐based enrichment analysis indicated significant enrichments in glycolysis/gluconeogenesis, and RNA degradation. Particularly, most downregulated acetylated lysine proteins were glucosyltransferase‐SI, glucosyltransferase‐I, and glucosyltransferase‐S in S. mutans biofilm, which probably reveals a switch‐off mechanism for the regulation of glucosyltransferases function during the biofilm development.

中文翻译：

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定量乙酰组分析揭示了葡糖基转移酶乙酰化参与变形链球菌生物膜形成

变形链球菌( S. mutans ) 有效地利用膳食蔗糖生产胞外多糖，其主要由葡糖基转移酶 (Gtfs) 的作用合成。在本研究中，变形链球菌的乙酰组被鉴定并将细菌生物膜生长（SMB）的定量乙酰组分析与浮游生长（SMP）的定量乙酰组分析进行了比较。使用涉及 TMT 标记和 Kac 亲和富集的综合方法，以及基于高分辨率质谱的定量蛋白质组学，对蛋白质乙酰化的动态变化进行量化。共鉴定出 445 个蛋白质中的 973 个乙酰化位点，其中对 302 个蛋白质中的 617 个乙酰化位点进行了定量。总体分析表明 22.7% 的蛋白质被乙酰化。在SMB的定量蛋白中，56个位点的赖氨酸乙酰化程度升高，而52个位点的赖氨酸乙酰化程度降低。在S. mutans 的乙酰组中，鉴定并获得了六个显着丰富的基序，包括 Kac****K、KacF、Kac****R、KacY、KacH、F*Kac。此外，基于 KEGG 通路的富集分析表明糖酵解/糖异生和 RNA 降解显着富集。特别是，大多数下调的乙酰化赖氨酸蛋白是变形链球菌生物膜中的葡萄糖基转移酶-SI、葡萄糖基转移酶-I和葡萄糖基转移酶-S ，这可能揭示了在生物膜发育过程中调节葡萄糖基转移酶功能的关闭机制。