Transcriptional reprogramming of wheat and the hemibiotrophic pathogen Septoria tritici during two phases of the compatible interaction

Fen Yang, Wanshun Li, Hans Jørgen Lyngs Jørgensen

57 Citationer (Scopus)
726 Downloads (Pure)

Abstract

The disease septoria leaf blotch of wheat, caused by fungal pathogen Septoria tritici, is of worldwide concern. The fungus exhibits a hemibiotrophic lifestyle, with a long symptomless, biotrophic phase followed by a sudden transition to necrotrophy associated with host necrosis. Little is known about the systematic interaction between fungal pathogenicity and host responses at specific growth stages and the factors triggering the transition. In order to gain some insights into global transcriptome alterations in both host and pathogen during the two phases of the compatible interaction, disease transition was monitored using pathogenesis-related gene markers and H2O 2 signature prior to RNA-Seq. Transcriptome analysis revealed that the slow symptomless growth was accompanied by minor metabolic responses and slightly suppressed defences in the host, whereas necrotrophic growth was associated with enhanced host responses involving energy metabolism, transport, signalling, defence and oxidative stress as well as a decrease in photosynthesis. The fungus expresses distinct classes of stage-specific genes encoding potential effectors, probably first suppressing plant defence responses/facilitating the symptomless growth and later triggering life style transition and inducing host necrosis/facilitating the necrotrophic growth. Transport, signalling, anti-oxidative stress mechanisms and apoplastic nutrient acquisition play important roles in the entire infection process of S. tritici. Our findings uncover systematic S. tritici -induced expression profiles of wheat related to specific fungal infection strategies and provide a transcriptome resource for studying both hosts and pathogens in plant-Dothideomycete interactions.

OriginalsprogEngelsk
Artikelnummere81606
TidsskriftP L o S One
Vol/bind8
Udgave nummer11
Antal sider15
ISSN1932-6203
DOI
StatusUdgivet - 26 nov. 2013

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