|Kistler, H - Corby|
Submitted to: Eukaryotic Cell
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/17/2009
Publication Date: 4/17/2009
Citation: Ding, S., Mehrabi, R., Hou, Z., Seong, K., Kistler, H.C., Xu, J. 2009. The Transducin Beta Like Gene FTL1 is Essential for Pathogenesis in Fusarium graminearum. Eukaryotic Cell. 8:867-876. Interpretive Summary: Fungi are the most common organisms causing infectious disease in plants and may also contaminate harvested crops with harmful mycotoxins. The fungus Fusarium graminearum causes extensive losses on wheat and barley crops world-wide and contaminates harvested grain with a compound known as vomitoxin, whose levels in the food supply are strictly regulated. This study describes a new fungal gene which controls the ability of the fungus to cause disease on wheat and to reproduce by sporulation. Reduction of disease symptoms on the plant does not occur through reduction in vomitoxin content or other known mechanisms controlling disease. Thus this report points out a new potential target for designing control strategies aimed at ameliorating the effects of this plant disease on production of grain.
Technical Abstract: Fusarium head blight (FHB) or scab caused by Fusarium graminearum is an important disease of wheat and barley. In addition to yield losses, infected grains are reduced in grain quality and contaminated with mycotoxins. In a previous study, we identified several mutants with reduced virulence by random insertional mutagenesis. In one of these mutants, the transforming vector was inserted in a transducin beta-like gene named FTL1. FTL1 is homologous to the mouse TBLR1 gene encoding a putative nuclear receptor corepressor and yeast SIF2, which is a component of the Set3 complex involved in ascospore formation. The FTL1 protein contains several WD40 repeats and an N-terminal LisH domain. Deletion analysis indicated that the LisH domain is essential for the FTL1 function. The FTL1 gene replacement mutant was significantly reduced in conidiation and failed to cause typical head blight symptoms on flowering wheat heads. It was defective in causing necrosis on the rachis of inoculated wheat heads and failed to colonize the vascular tissues of rachis. The FTL1 mutant also was defective in spreading from inoculated anthers to ovaries and more sensitive to defensins MsDef1 and osmotin. However, the activation of Mgv1 and Gpmk1 MAP kinases, the production of deoxynivalenol, and the expression of several known virulence genes were not affected. The defects of the ftl1 mutant in plant infection must be unrelated with those known virulence factors and likely involved some novel mechanisms. Many member of the yeast Set3 complex are conserved in F. graminearum, including SNT1, a gene directly interacting with SIF2. Mutants deleted of FgSNT1 had similar defects with the ftl1 mutant in conidiation and plant infection. FTL1 appears to be a component of this well conserved protein complex and plays a critical role in response to plant defense compounds and causing head blight on wheat.