Changes in flagellin glycosylation affect Campylobacter autoagglutination and virulence
Changes in flagellin glycosylation affect Campylobacter autoagglutination and virulence
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DOI：
10.1111/j.1365-2958.2006.05100.x
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发表时间：
2006-04-01
影响因子：
3.6
通讯作者：
Logan, S
中科院分区：
文献类型：
--
作者：
Guerry, P;Ewing, CP;Logan, S
对空肠弯曲菌81-176株鞭毛蛋白糖基化位点的分析表明，与该基因组株的相应区域相比，空肠弯曲菌NCTC 11168的基因组结构没有那么复杂。在NCTC 11168中发现的Cj1293和Cj1337之间的45个基因中，有24个基因在81-176中缺失。除了先前报道的3个基因外，还有6个新基因的突变导致了一种非运动性表型，这与合成伪氨基酸(PseAc)或将PseAc转移到鞭毛蛋白中的作用一致。Cj1316c或PSEA的突变已被证明导致伪氨基酸(PseAm)的乙酰氨基形式丢失。第二个基因的突变也导致PseAm的丢失，以及一个微小的修饰，似乎是用N-乙酰-谷氨酸延长的PseAm。之前在空肠弯曲菌81-176和弯曲杆菌VC167中描述的突变株产生的鞭毛缺乏PseAm或PseAc，不能自我凝集。这表明，自身凝集需要相邻鞭毛细丝上的修饰之间的相互作用。自身凝集缺陷的突变体(81-176)显示INT407细胞的黏附和侵袭能力略有下降。然而，使用GFP标记的81-176和缺乏PseAm的突变体与INT407细胞的结合模式存在质的差异。在雪貂腹泻病模型中，一个缺乏PseAM的突变体被减弱。
Analysis of the complete flagellin glycosylation locus of Campylobacter jejuni strain 81-176 revealed a less complex genomic organization than the corresponding region in the genome strain, C. jejuni NCTC 11168. Twenty-four of the 45 genes found between Cj1293 and Cj1337 in NCTC 11168 are missing in 81-176. Mutation of six new genes, in addition to three previously reported, resulted in a non-motile phenotype, consistent with a role in synthesis of pseudaminic acid (PseAc) or transfer of PseAc to flagellin. Mutation of Cj1316c or pseA had been shown to result in loss of the acetamidino form of pseudaminic acid (PseAm). Mutation of a second gene also resulted in loss of PseAm, as well as a minor modification that appears to be PseAm extended with N-acetyl-glutamic acid. Previously described mutants in C. jejuni 81-176 and Campylobacter coli VC167 that produced flagella lacking PseAm or PseAc failed to autoagglutinate. This suggests that interactions between modifications on adjacent flagella filaments are required for autoagglutination. Mutants (81-176) defective in autoagglutination showed a modest reduction in adherence and invasion of INT407 cells. However, there was a qualitative difference in binding patterns to INT407 cells using GFP-labelled 81-176 and mutants lacking PseAm. A mutant lacking PseAm was attenuated in the ferret diarrhoeal disease model.