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Title

A nitrogen response pathway regulates virulence in plant pathogenic fungi

Other TitlesRole of TOR and the bZIP protein MeaB
AuthorsLópez-Berges, Manuel S.; Rispail, Nicolas ; Prados-Rosales, Rafael C.; Pietro, Antonio D.
KeywordsNitrogen
Virulence
MAPK
TOR
MeaB
Rapamycin
Issue Date2010
PublisherTaylor & Francis
CitationPlant Signaling and Behavior 5(12): 1623-1625 (2010)
AbstractVirulence in plant pathogenic fungi is controlled through a variety of cellular pathways in response to the host environment. Nitrogen limitation has been proposed to act as a key signal to trigger the in planta expression of virulence genes. Moreover, a conserved Pathogenicity mitogen activated protein kinase (MAPK) cascade is strictly required for plant infection in a wide range of pathogens. We investigated the relationship between nitrogen signaling and the Pathogenicity MAPK cascade in controlling infectious growth of the vascular wilt fungus Fusarium oxysporum. Several MAPK-activated virulence functions such as invasive growth, vegetative hyphal fusion and host adhesion were strongly repressed in the presence of the preferred nitrogen source ammonium. Repression of these functions by ammonium was abolished by L-Methionine sulfoximine (MSX) or rapamycin, two specific inhibitors of Gln synthetase and the protein kinase TOR (Target Of Rapamycin), respectively, and was dependent on the bZIP protein MeaB. Supplying tomato plants with ammonium rather than nitrate resulted in a significant delay of vascular wilt symptoms caused by the F. oxysporum wild type strain, but not by the ΔmeaB mutant. Ammonium also repressed invasive growth in two other pathogens, the rice blast fungus Magnaporthe oryzae and the wheat head blight pathogen Fusarium graminearum. Our results suggest the presence of a conserved nitrogen-responsive pathway that operates via TOR and MeaB to control infectious growth in plant pathogenic fungi.
Publisher version (URL)https://doi.org/10.4161/psb.5.12.13729
URIhttp://hdl.handle.net/10261/160655
DOI10.4161/psb.5.12.13729
ISSN1559-2316
E-ISSN1559-2324
Appears in Collections:(IAS) Artículos
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