| Résumé | Deletion of the lipooligosaccharide biosynthesis region (Cj1132c to Cj1152c) from the genome of Campylobacter jejuni NCTC11168 shows that the core is not required for viability. The mutant was attenuated for growth and has increased sensitivity to antibiotics and detergents. Natural transformation and invasion of cultured host cells was abolished. Campylobacter jejuni is the leading cause of bacterial food-borne gastroenteritis worldwide and consequently is a significant public health, social, and economic burden (1, 11). Lipooligosaccharide (LOS) is an important constituent of the bacterial outer membrane, and by acting as a barrier, it maintains cellular integrity (19). The Campylobacter LOS molecule consists of a lipid A moiety and a nonrepeating unit of inner and outer core oligosaccharides (OS) (3, 10). The outer core OS of NCTC11168 LOS mimics GM1 ganglioside (16, 22, 23). Such molecular mimicry may form a strategy for the avoidance of host immune defenses by C. jejuni and is the likely explanation for its association with the neuropathies Guillain-Barré syndrome and Miller Fisher syndrome (2, 15). The core biosynthesis genes are present in a large cluster in the genome (10, 17) (Fig. 1), and modulation of LOS structure arises due to gene content diversity, allelic variation, and high-frequency sequence variation of homopolymeric tracts (10). The function of some genes in the cluster has been elucidated, and individual mutations in waaC and waaF have yielded deep rough mutants (7, 8, 16). Here, we describe the construction and phenotype of a mutant in which the core LOS biosynthesis gene cluster has been removed. |
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