Genomic variations leading to alterations in cell morphology of Campylobacter spp
Campylobacter cell shape SciRep revised Oct 2016.docx (86.66Kb) Campylobacter cell shape SciRep Supplemental Information revised Oct 2016 .docx (6.140Mb) FIG 1.tif (14.08Mb) FIG 2.tif (2.821Mb) FIG 3.tiff (1005.Kb) FIG 4.tif (11.49Mb) FIG 5.tiff (228.5Kb) FIG 6.tiff (438.9Kb) Table S7.xls (85Kb)Show MoreShow Less
de Vries, SPW
Nature Publishing Group
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Campylobacter jejuni, the most common cause of bacterial diarrhoeal disease, is normally helical. However, it can also adopt straight rod, elongated helical and coccoid forms. Studying how helical morphology is generated, and how it switches between its different forms, is an important objective for understanding this pathogen. Here, we aimed to determine the genetic factors involved in generating the helical shape of Campylobacter. A C. jejuni transposon (Tn) mutant library was screened for non-helical mutants with inconsistent results. Whole genome sequence variation and morphological trends within this Tn library, and in various C. jejuni wild type strains, were compared and correlated to detect genomic elements associated with helical and rod morphologies. All rod-shaped C. jejuni Tn mutants and all rod-shaped laboratory, clinical and environmental C. jejuni and Campylobacter coli contained genetic changes within the pgp1 or pgp2 genes, which encode peptidoglycan modifying enzymes. We therefore confirm the importance of Pgp1 and Pgp2 in the maintenance of helical shape and extended this to a wide range of C. jejuni and C. coli isolates. Genome sequence analysis revealed variation in the sequence and length of homopolymeric tracts found within these genes, providing a potential mechanism of phase variation of cell shape.
Scanning Electron Microscopy was kindly performed by Dr Jeremy Skepper (Cambridge Advanced Imaging Centre). This work was funded by The Wellcome Trust through a PhD training studentship awarded to DE, and was supported by an Isaac Newton Trust/Wellcome Trust ISSF/University of Cambridge joint research grant awarded to AJG. SG and SPWDV were funded by BBSRC grant BB/K004514/1. AEM, SH, NRT and JP were supported by the Wellcome Trust grant number 098051. AEM was also supported by BBSRC grant BB/M014088/1. SKS was funded by Biotechnology and Biological Sciences Research Council grant BB/I02464X/1, Medical Research Council grant MR/L015080/1 and Wellcome Trust grant 088786/C/09/Z. GM was supported by a National Institute for Social Care and Health Research Fellowship (HF-14-13).
This is the author accepted manuscript. The final version is available from Nature Publishing Group via the DOI in this record.
Vol. 6, article 38303
Place of publication