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Bacterial polysaccharides suppress induced innate immunity by calcium chelation
JournalArticle (Originalarbeit in einer wissenschaftlichen Zeitschrift)
 
ID 40885
Author(s) Aslam, Shazia N; Newman, Mari-Anne; Erbs, Gitte; Morrissey, Kate L; Chinchilla, Delphine; Boller, Thomas; Jensen, Tina Tandrup; De Castro, Cristina; Ierano, Teresa; Molinaro, Antonio; Jackson, Robert W; Knight, Marc R; Cooper, Richard M
Author(s) at UniBasel Boller, Thomas
Chinchilla, Delphine
Year 2008
Title Bacterial polysaccharides suppress induced innate immunity by calcium chelation
Journal Current biology
Volume 18
Number 14
Pages / Article-Number 1078-83
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 [1], [2] and [3]. Extracellular polysaccharides (EPSs) are key virulence factors in plant and animal pathogenesis, but their precise function in establishing basic compatibility remains unclear [4], [5], [6] and [7]. Here, we show that EPSs suppress MAMP-induced signaling in plants through their polyanionic nature [4] and consequent ability to chelate divalent calcium ions [8]. In plants, Ca2+ ion influx to the cytosol from the apoplast (where bacteria multiply [4], [5] and [9]) is a prerequisite for activation of myriad defenses by MAMPs [10]. 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.

Publisher Cell Press
ISSN/ISBN 0960-9822
edoc-URL http://edoc.unibas.ch/dok/A5248780
Full Text on edoc No
Digital Object Identifier DOI 10.1016/j.cub.2008.06.061
PubMed ID http://www.ncbi.nlm.nih.gov/pubmed/18639458
ISI-Number WOS:000258378100032
Document type (ISI) Journal Article
 
   

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22/06/2024