Tabei S Mohammed B, Hitchen Paul G, Day-Williams Michaela J, Merino Susana, Vart Richard, Pang Poh-Choo, Horsburgh Gavin J, Viches Silvia, Wilhelms Markus, Tomás Juan M, Dell Anne, Shaw Jonathan G
Unit of Infection and Immunity, School of Medicine and Biomedical Sciences, University of Sheffield, Sheffield S10 2RX, United Kingdom.
J Bacteriol. 2009 Apr;191(8):2851-63. doi: 10.1128/JB.01406-08. Epub 2009 Feb 13.
Aeromonas caviae Sch3N possesses a small genomic island that is involved in both flagellin glycosylation and lipopolysaccharide (LPS) O-antigen biosynthesis. This island appears to have been laterally acquired as it is flanked by insertion element-like sequences and has a much lower G+C content than the average aeromonad G+C content. Most of the gene products encoded by the island are orthologues of proteins that have been shown to be involved in pseudaminic acid biosynthesis and flagellin glycosylation in both Campylobacter jejuni and Helicobacter pylori. Two of the genes, lst and lsg, are LPS specific as mutation of them results in the loss of only a band for the LPS O-antigen. Lsg encodes a putative Wzx flippase, and mutation of Lsg affects only LPS; this finding supports the notion that flagellin glycosylation occurs within the cell before the flagellins are exported and assembled and not at the surface once the sugar has been exported. The proteins encoded by flmA, flmB, neuA, flmD, and neuB are thought to make up a pseudaminic acid biosynthetic pathway, and mutation of any of these genes resulted in the loss of motility, flagellar expression, and a band for the LPS O-antigen. Furthermore, pseudaminic acid was shown to be present on both flagellin subunits that make up the polar flagellum filament, to be present in the LPS O-antigen of the A. caviae wild-type strain, and to be absent from the A. caviae flmD mutant strain.
豚鼠气单胞菌Sch3N拥有一个小的基因组岛，该岛参与鞭毛蛋白糖基化和脂多糖（LPS）O抗原生物合成。这个岛似乎是通过侧向获得的，因为它两侧是类似插入元件的序列，并且其G+C含量比气单胞菌的平均G+C含量低得多。该岛编码的大多数基因产物是在空肠弯曲菌和幽门螺杆菌中已被证明参与假氨基糖生物合成和鞭毛蛋白糖基化的蛋白质的直系同源物。其中两个基因，lst和lsg，是LPS特异性的，因为它们的突变仅导致LPS O抗原的一条带缺失。Lsg编码一种假定的Wzx翻转酶，Lsg的突变仅影响LPS；这一发现支持了这样一种观点，即鞭毛蛋白糖基化发生在鞭毛蛋白输出和组装之前的细胞内，而不是在糖输出后在表面发生。flmA、flmB、neuA、flmD和neuB编码的蛋白质被认为构成假氨基糖生物合成途径，这些基因中的任何一个发生突变都会导致运动性丧失、鞭毛表达丧失以及LPS O抗原的一条带缺失。此外，假氨基糖在构成极鞭毛丝的两个鞭毛蛋白亚基上均有存在，在豚鼠气单胞菌野生型菌株的LPS O抗原中也有存在，而在豚鼠气单胞菌flmD突变株中则不存在。
