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Cell. 2017 Jan 12;168(1-2):172-185.e15. doi: 10.1016/j.cell.2016.12.019. Epub 2017 Jan 12.

A Periplasmic Polymer Curves Vibrio cholerae and Promotes Pathogenesis.

Author information

1
Department of Molecular Biology, Princeton University, Princeton, NJ 08544, USA.
2
Department of Molecular Biology, Princeton University, Princeton, NJ 08544, USA; Lewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, NJ 08544, USA.
3
Department of Bioengineering, Stanford University, Stanford, CA 94305, USA.
4
Department of Microbiology, Nanjing Agricultural University, Nanjing 210014, China.
5
Lewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, NJ 08544, USA.
6
Department of Chemistry, Indiana University, Bloomington, Bloomington, IN 47405, USA.
7
Department of Bioengineering, Stanford University, Stanford, CA 94305, USA; Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.
8
Department of Microbiology, Nanjing Agricultural University, Nanjing 210014, China; Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
9
Department of Molecular Biology, Princeton University, Princeton, NJ 08544, USA. Electronic address: zgitai@princeton.edu.

Abstract

Pathogenic Vibrio cholerae remains a major human health concern. V. cholerae has a characteristic curved rod morphology, with a longer outer face and a shorter inner face. The mechanism and function of this curvature were previously unknown. Here, we identify and characterize CrvA, the first curvature determinant in V. cholerae. CrvA self-assembles into filaments at the inner face of cell curvature. Unlike traditional cytoskeletons, CrvA localizes to the periplasm and thus can be considered a periskeletal element. To quantify how curvature forms, we developed QuASAR (quantitative analysis of sacculus architecture remodeling), which measures subcellular peptidoglycan dynamics. QuASAR reveals that CrvA asymmetrically patterns peptidoglycan insertion rather than removal, causing more material insertions into the outer face than the inner face. Furthermore, crvA is quorum regulated, and CrvA-dependent curvature increases at high cell density. Finally, we demonstrate that CrvA promotes motility in hydrogels and confers an advantage in host colonization and pathogenesis.

KEYWORDS:

bacterial cytoskeleton; cell shape; fluorescent D-amino acids; pathogenesis; peptidoglycan; periskeleton; quantitative cell biology

PMID:
28086090
PMCID:
PMC5287421
DOI:
10.1016/j.cell.2016.12.019
[Indexed for MEDLINE]
Free PMC Article

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