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dc.contributor.authorTan, Kar-Chun
dc.contributor.authorOliver, Richard
dc.contributor.authorSolomon, P.
dc.contributor.authorMoffat, Caroline
dc.date.accessioned2017-01-30T10:27:12Z
dc.date.available2017-01-30T10:27:12Z
dc.date.created2014-06-29T20:00:19Z
dc.date.issued2010
dc.identifier.citationTan, K. and Oliver, R. and Solomon, P. and Moffat, C. 2010. Proteinaceous necrotrophic effectors in fungal virulence. Functional Plant Biology. 37 (10): pp. 907-912.
dc.identifier.urihttp://hdl.handle.net/20.500.11937/2936
dc.identifier.doi10.1071/FP10067
dc.description.abstract

The host–pathogen interface can be considered as a biological battlefront. Molecules produced by both the pathogen and the host are critical factors determining the outcome of the interaction. Recent studies have revealed that an increasing number of necrotrophic fungal pathogens produce small proteinaceous effectors that are able to function as virulence factors. These molecules can cause tissue death in host plants that possess dominant sensitivity genes, leading to subsequent pathogen colonisation. Such effectors are only found in necrotrophic fungi, yet their roles in virulence are poorly understood. However, several recent key studies of necrotrophic effectors from two wheat (Triticum aestivum L.) pathogens, Pyrenophora tritici-repentis (Died.) Drechs. and Stagonospora nodorum (Berk.) Castell. & Germano, have shed light upon how these effector proteins serve to disable the host from the inside out.

dc.publisherCSIRO Publishing
dc.subjectPyrenophora
dc.subjecttan spot
dc.subjectStagonospora
dc.subjectseptoria
dc.subjectnet blotch
dc.subjecthost-selective toxin
dc.titleProteinaceous necrotrophic effectors in fungal virulence
dc.typeJournal Article
dcterms.source.volume37
dcterms.source.startPage907
dcterms.source.endPage912
dcterms.source.issn14454408
dcterms.source.titleFunctional Plant Biology
curtin.note

© Copyright 2010 CSIRO

curtin.departmentAustralian Centre for Necrotrophic Fungal Pathogens, Curtin University
curtin.accessStatusOpen access


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