Format

Send to

Choose Destination
See comment in PubMed Commons below
Eukaryot Cell. 2009 Jun;8(6):867-76. doi: 10.1128/EC.00048-09. Epub 2009 Apr 17.

Transducin beta-like gene FTL1 is essential for pathogenesis in Fusarium graminearum.

Author information

  • 1Department of Botany and Plant Pathology, 915 West State Street, Lilly Hall, Purdue University, West Lafayette, IN 47907, USA.

Abstract

Fusarium head blight caused by Fusarium graminearum is an important disease of wheat and barley. In a previous study, we identified several mutants with reduced virulence by insertional mutagenesis. A transducin beta-like gene named FTL1 was disrupted in one of these nonpathogenic mutants. FTL1 is homologous to Saccharomyces cerevisiae SIF2, which is a component of the Set3 complex involved in late stages of ascospore formation. The Delta ftl1 mutant was significantly reduced in conidiation and failed to cause typical disease symptoms. It failed to colonize the vascular tissues of rachis or cause necrosis on the rachis of inoculated wheat heads. The Delta ftl1 mutant also was defective in spreading from infected anthers to ovaries and more sensitive than the wild type to plant defensins MsDef1 and osmotin. However, the activation of two mitogen-activated protein kinases, Mgv1 and Gpmk1, production of deoxynivalenol, and expression of genes known to be important for plant infection in F. graminearum were not affected, indicating that the defect of the Delta ftl1 mutant in plant infection is unrelated to known virulence factors in this pathogen and may involve novel mechanisms. The Delta ftl1 deletion mutant was significantly reduced in histone deacetylation, and many members of the yeast Set3 complex are conserved in F. graminearum. FTL1 appears to be a component of this well-conserved protein complex that plays a critical role in the penetration and colonization of wheat tissues.

PMID:
19377037
PMCID:
PMC2698311
DOI:
10.1128/EC.00048-09
[PubMed - indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for HighWire Icon for PubMed Central
    Loading ...
    Support Center