학술논문

Bacterial Polysaccharides Suppress Induced Innate Immunity by Calcium Chelation
Document Type
Report
Author
Source
Current Biology. July 22, 2008, Vol. 18 Issue 14, p1078, 6 p.
Subject
Polysaccharides
Alkaline earth metal compounds
Oxides
Language
English
ISSN
0960-9822
Abstract
To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.cub.2008.06.061 Byline: Shazia N. Aslam (1), Mari-Anne Newman (2), Gitte Erbs (2), Kate L. Morrissey (1), Delphine Chinchilla (3), Thomas Boller (3), Tina Tandrup Jensen (2), Cristina De Castro (4), Teresa Ierano (4), Antonio Molinaro (4), Robert W. Jackson (1)(5), Marc R. Knight (6), Richard M. Cooper (1) Keywords: SIGNALING; MICROBIO Abstract: Bacterial pathogens and symbionts must suppress or negate host innate immunity. However, pathogens release conserved oligomeric and polymeric molecules or MAMPs (Microbial Associated Molecular Patterns), which elicit host defenses . Extracellular polysaccharides (EPSs) are key virulence factors in plant and animal pathogenesis, but their precise function in establishing basic compatibility remains unclear . Here, we show that EPSs suppress MAMP-induced signaling in plants through their polyanionic nature and consequent ability to chelate divalent calcium ions . In plants, Ca.sup.2+ ion influx to the cytosol from the apoplast (where bacteria multiply) is a prerequisite for activation of myriad defenses by MAMPs . We show that EPSs from diverse plant and animal pathogens and symbionts bind calcium. EPS-defective mutants or pure MAMPs, such as the flagellin peptide flg22, elicit calcium influx, expression of host defense genes, and downstream resistance. Furthermore, EPSs, produced by wild-type strains or purified, suppress induced responses but do not block flg22-receptor binding in Arabidopsis cells. EPS production was confirmed in planta, and the amounts in bacterial biofilms greatly exceed those required for binding of apoplastic calcium. These data reveal a novel, fundamental role for bacterial EPS in disease establishment, encouraging novel control strategies. Author Affiliation: (1) Department of Biology & Biochemistry, University of Bath, Bath BA2 7AY, UK (2) Faculty of Life Sciences, Department of Plant Biology and Biotechnology, University of Copenhagen, Thorvaldsensvej 40,, 1871 Frederiksberg, Denmark (3) Zurich-Basel Plant Science Center, Botanical Institute, University of Basel, Hebelstrasse, 4056 Basel, Switzerland (4) Dipartimento di Chimica Organica e Biochimica, Universita di Napoli, Complesso Universitario Monte SantAngelo, Via Cintia 4, 80126 Napoli, Italy (5) School of Biological Sciences, University of Reading, Whiteknights, Reading, Berks RG6 6AJ, UK (6) Plant Stress Signalling Laboratory, Institute of Plant and Microbial Sciences, School of Biological and Biomedical Sciences, Durham University, South Road, Durham DH1 3LE, UK Article History: Received 25 April 2008; Revised 18 June 2008; Accepted 19 June 2008 Article Note: (miscellaneous) Published online: July 17, 2008