YdgG (TqsA) controls biofilm formation in Escherichia coli K-12 through autoinducer 2 transport
YdgG (TqsA) controls biofilm formation in Escherichia coli K-12 through autoinducer 2 transport
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DOI：
10.1128/jb.188.2.587-598.2006
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发表时间：
2006-01-01
影响因子：
3.2
通讯作者：
Wood, TK
中科院分区：
文献类型：
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作者：
Herzberg, M;Kaye, IK;Wood, TK
YdgG是在大肠杆菌生物膜中诱导的一种未被鉴定的蛋白。本研究表明，ydgG的缺失降低了细胞外和细胞内的自诱导剂2 （AI-2）浓度；因此，YdgG增强了AI-2的转运。与这一假设相一致，ydgG的缺失导致How细胞的生物膜厚度增加了7000倍，生物量增加了574倍。同样与假设一致的是，ydgG的缺失通过增加鞭毛基因（AI-2诱导的基因）的转录来增加细胞的运动性。通过反式表达ydgG，恢复了细胞外AI-2活性、运动性和生物膜形成的野生型表型。据预测，YdgG也是一种在许多细菌中保守的跨膜蛋白，它影响对几种抗菌剂的耐药性，包括结晶紫和链霉素（这种表型也可以补充）。正如预期的那样，ydgG的缺失也导致31%的细菌染色体在生物膜中差异表达，因为AI-2控制着数百个基因。YdgG被发现负调节鞭毛和运动相关基因的表达，以及其他已知的生物膜形成所必需的产物，包括1型菌毛的操纵子、自转运蛋白Ag43、卷曲蛋白的产生、结肠酸的产生和多糖粘附素的产生。还鉴定了80个先前与生物膜形成无关的基因，包括编码转运蛋白（yihN和yihP）、多唾液酸产生（gutM和gutQ）、CP4-57噬菌体功能（yfiR和alpA）、蛋氨酸生物合成（metR）、生物素和硫胺生物合成（bioF和thiDFH）、厌氧代谢（focB、hy-fACDR、ttdA和fumB）和功能未知的蛋白质（ybfG、yceO、yjhQ和yjbE）的基因；其中10个基因（yfjR、bioF、yccW、yjbE、yceO、ttdA、fumB、yjiP、gutQ和yihR）通过突变使生物膜形成减少40%或更多。因此，YdgG似乎控制群体感应信号AI-2的运输，因此我们建议将基因命名为tqsA。
YdgG is an uncharacterized protein that is induced in Escherichia coli biofilms. Here it is shown that deletion of ydgG decreased extracellular and increased intracellular concentrations of autoinducer 2 (AI-2); hence, YdgG enhances transport of AI-2. Consistent with this hypothesis, deletion of ydgG resulted in a 7,000-fold increase in biofilm thickness and 574-fold increase in biomass in How cells. Also consistent with the hypothesis, deletion of ydgG increased cell motility by increasing transcription of flagellar genes (genes induced by AI-2). By expressing ydgG in trans, the wild-type phenotypes for extracellular AI-2 activity, motility, and biofilm formation were restored. YdgG is also predicted to be a membrane-spanning protein that is conserved in many bacteria, and it influences resistance to several antimicrobials, including crystal violet and streptomycin (this phenotype could also be complemented). Deletion of ydgG also caused 31% of the bacterial chromosome to be differentially expressed in biofilms, as expected, since AI-2 controls hundreds of genes. YdgG was found to negatively modulate expression of flagellum- and motility-related genes, as well as other known products essential for biofilm formation, including operons for type 1 fimbriae, autotransporter protein Ag43, curli production, colanic acid production, and production of polysaccharide adhesin. Eighty genes not previously related to biofilm formation were also identified, including those that encode transport proteins (yihN and yihP), polysialic acid production (gutM and gutQ), CP4-57 prophage functions (yfiR and alpA), methionine biosynthesis (metR), biotin and thiamine biosynthesis (bioF and thiDFH), anaerobic metabolism (focB, hy-fACDR, ttdA, and fumB), and proteins with unknown function (ybfG, yceO, yjhQ, and yjbE); 10 of these genes were verified through mutation to decrease biofilm formation by 40% or more (yfjR, bioF, yccW, yjbE, yceO, ttdA, fumB, yjiP, gutQ, and yihR). Hence, it appears YdgG controls the transport of the quorum-sensing signal AI-2, and so we suggest the gene name tqsA.