Abstract:
:Many race- or isolate-specific disease resistance responses of plants toward pathogens (incompatible interactions) invoke hypersensitive response (HR)-like programmed cell death (PCD) and the coordinated activation of mitogen-activated protein kinases homologous with Arabidopsis (Arabidopsis thaliana) AtMPK6 and AtMPK3 (or tobacco [Nicotiana tabacum] SIPK and WIPK), respectively. Resistance of wheat (Triticum aestivum) leaves to the necrotrophic fungal pathogen Mycosphaerella graminicola can also operate at an isolate/cultivar-specific level. We confirm here that resistance is achieved without any sign of HR-like PCD during the incompatible interaction. Instead, PCD is strictly associated with the compatible interaction and is triggered during disease symptom expression. A strong transcriptional activation of TaMPK3, the wheat homolog of Arabidopsis AtMPK3, was observed immediately preceding PCD and symptom development in the compatible interaction. Generation and use of TaMPK3- and TaMPK6-specific antibodies on western blots and in coupled immunoprecipitation-protein kinase assays demonstrated that the TaMPK3 protein also accumulated, and was subsequently posttranslationally activated, during the compatible interaction in parallel to PCD. In contrast, no increase in expression, protein levels, or posttranslational activation of TaMPK6 was observed at any stage of either compatible or incompatible interactions. However, the protein levels of TaMPK6 became markedly reduced during the compatible interaction coincident with the onset of TaMPK3 protein accumulation. These data highlight the emerging similarity between the signaling pathways triggered in a host plant during successful infection by a necrotrophic fungal pathogen and the resistance responses normally effective against biotrophs.
journal_name
Plant Physioljournal_title
Plant physiologyauthors
Rudd JJ,Keon J,Hammond-Kosack KEdoi
10.1104/pp.108.119511subject
Has Abstractpub_date
2008-06-01 00:00:00pages
802-15issue
2eissn
0032-0889issn
1532-2548pii
pp.108.119511journal_volume
147pub_type
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