Bacterial polysaccharides suppress induced innate immunity by calcium chelation.
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.
Aslam
Shazia N
SN
Department of Biology & Biochemistry, University of Bath, Bath BA2 7AY, UK.
Newman
Mari-Anne
MA
Erbs
Gitte
G
Morrissey
Kate L
KL
Chinchilla
Delphine
D
Boller
Thomas
T
Jensen
Tina Tandrup
TT
De Castro
Cristina
C
Ierano
Teresa
T
Molinaro
Antonio
A
Jackson
Robert W
RW
Knight
Marc R
MR
Cooper
Richard M
RM
D017360:Arabidopsis / Q000276:immunology / Q000382:microbiology; D001419:Bacteria / Q000472:pathogenicity; D020013:Calcium Signaling / Q000187:drug effects / Q000276:immunology; D007113:Immunity, Innate / Q000187:drug effects; D010935:Plant Diseases / Q000276:immunology / Q000382:microbiology; D010944:Plants / Q000187:drug effects / Q000276:immunology* / Q000382:microbiology*; D011135:Polysaccharides, Bacterial / Q000633:toxicity*; D014774:Virulence / Q000276:immunology; D016959:Xanthomonas campestris / Q000472:pathogenicity
D011135:Polysaccharides, Bacterial