Titel
The Arabidopsis MAP kinase kinase MKK1 participates in defence responses to the bacterial elicitor flagellin
Autor*in
Tamás Mészáros
Budapest University of Technology and Economics
Autor*in
Anne Helfer
Scripps Research Institute
Autor*in
László Bögre
University of London
... show all
Abstract
Plants sense pathogens through both pathogen-associated molecular patterns and recognition of race-specific virulence factors, which induce basal defence or an accelerated defence (often manifest in the form of local cell death), respectively. A mitogen-activated protein kinase (MAPK) module in Arabidopsis was previously proposed to signal from perception of the bacterial elicitor flagellin to the activation of basal defence-related genes. Here, we present evidence for a parallel MAPK-signalling pathway involved in the response to flg22, a peptide corresponding to the most conserved domain of flagellin. The endogenous Arabidopsis MAP kinase kinase MKK1 is activated in cells treated with flg22, phosphorylates the MAPK MPK4 in vitro, and activates it in vivo in protoplasts. In mkk1 mutant plants, the activation by flg22 of MPK4 and two other flg22-induced MAPKs (MPK3 and MPK6) is impaired. In the mkk1 mutant, a battery of both flg22-induced and flg22-repressed genes show altered expression, indicating that MKK1 negatively regulates the activity of flagellin-responsive genes. Intriguingly, in contrast to the mpk4 mutant, mkk1 shows no morphological anomalies and is compromised in resistance to both virulent and avirulent Pseudomonas syringae strains. Thus, the MKK1 signalling pathway modulates the expression of genes responding to elicitors and plays an important role in pathogen defence. Π2006 The Authors.
Stichwort
ArabidopsisDefence-related genesFlagellinMitogen-activated protein kinase signallingPathogen resistanceSignalling networks
Objekt-Typ
Sprache
Englisch [eng]
Persistent identifier
https://phaidra.univie.ac.at/o:243988
Erschienen in
Titel
The Plant Journal
Band
48
Ausgabe
4
Seitenanfang
485
Seitenende
498
Erscheinungsdatum
01.12.2006
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