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Phosphopantetheinyl transferase (Ppt)-mediated biosynthesis of lysine, but not siderophores or DHN melanin, is required for virulence of Zymoseptoria tritici on wheat

Authors :
Derbyshire, Mark C.
Gohari, Amir Mirzadi
Mehrabi, Rahim
Kilaru, Sreedhar
Steinberg, Gero
Ali, Solaf
Bailey, Andy
Hammond-Kosack, Kim
Kema, Gert H.J.
Rudd, Jason J.
Derbyshire, Mark C.
Gohari, Amir Mirzadi
Mehrabi, Rahim
Kilaru, Sreedhar
Steinberg, Gero
Ali, Solaf
Bailey, Andy
Hammond-Kosack, Kim
Kema, Gert H.J.
Rudd, Jason J.
Source :
ISSN: 2045-2322
Publication Year :
2018

Abstract

Zymoseptoria tritici is the causal agent of Septoria tritici blotch (STB) disease of wheat. Z. tritici is an apoplastic fungal pathogen, which does not penetrate plant cells at any stage of infection, and has a long initial period of symptomless leaf colonisation. During this phase it is unclear to what extent the fungus can access host plant nutrients or communicate with plant cells. Several important primary and secondary metabolite pathways in fungi are regulated by the post-translational activator phosphopantetheinyl transferase (Ppt) which provides an essential co-factor for lysine biosynthesis and the activities of non-ribosomal peptide synthases (NRPS) and polyketide synthases (PKS). To investigate the relative importance of lysine biosynthesis, NRPS-based siderophore production and PKS-based DHN melanin biosynthesis, we generated deletion mutants of ZtPpt. The ∆ZtPpt strains were auxotrophic for lysine and iron, non-melanised and non-pathogenic on wheat. Deletion of the three target genes likely affected by ZtPpt loss of function (Aar- lysine; Nrps1-siderophore and Pks1- melanin), highlighted that lysine auxotrophy was the main contributing factor for loss of virulence, with no reduction caused by loss of siderophore production or melanisation. This reveals Ppt, and the lysine biosynthesis pathway, as potential targets for fungicides effective against Z. tritici.

Details

Database :
OAIster
Journal :
ISSN: 2045-2322
Notes :
application/pdf, Scientific Reports 8 (2018) 1, ISSN: 2045-2322, ISSN: 2045-2322, English
Publication Type :
Electronic Resource
Accession number :
edsoai.on1200322394
Document Type :
Electronic Resource