V erticillium transcription activator of adhesion V ta2 suppresses microsclerotia formation and is required for systemic infection of plant roots

• Published in: The New phytologist 2014-04, Vol.202 (2), p.565-581
• Main Authors: Tran, Van‐Tuan, Braus‐Stromeyer, Susanna A., Kusch, Harald, Reusche, Michael, Kaever, Alexander, Kühn, Anika, Valerius, Oliver, Landesfeind, Manuel, Aßhauer, Kathrin, Tech, Maike, Hoff, Katharina, Pena‐Centeno, Tonatiuh, Stanke, Mario, Lipka, Volker, Braus, Gerhard H.
• Format: Article
• Language: English
• ISSN: 0028-646X; 1469-8137
• DOI: 10.1111/nph.12671

Six transcription regulatory genes of the V erticillium plant pathogen, which reprogrammed nonadherent budding yeasts for adhesion, were isolated by a genetic screen to identify control elements for early plant infection. V erticillium transcription activator of adhesion V ta2 is highly conserved in filamentous fungi but not present in yeasts. The M agnaporthe grisea ortholog conidiation regulator C on7 controls the formation of appressoria which are absent in V erticillium species. V ta2 was analyzed by using genetics, cell biology, transcriptomics, secretome proteomics and plant pathogenicity assays. Nuclear V ta2 activates the expression of the adhesin‐encoding yeast flocculin genes FLO 1 and FLO 11 . V ta2 is required for fungal growth of V erticillium where it is a positive regulator of conidiation. V ta2 is mandatory for accurate timing and suppression of microsclerotia as resting structures. V ta2 controls expression of 270 transcripts, including 10 putative genes for adhesins and 57 for secreted proteins. V ta2 controls the level of 125 secreted proteins, including putative adhesins or effector molecules and a secreted catalase‐peroxidase. V ta2 is a major regulator of fungal pathogenesis, and controls host‐plant root infection and H 2 O 2 detoxification. V erticillium impaired in V ta2 is unable to colonize plants and induce disease symptoms. V ta2 represents an interesting target for controlling the growth and development of these vascular pathogens.