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Book of Abstracts <strong>First</strong> <strong>Legume</strong> <strong>Society</strong> <strong>Conference</strong> 2013: A <strong>Legume</strong> Odyssey Novi Sad, Serbia, 9-11 May 2013<br />

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Investigating the role of solanapyrone toxins in Ascochyta blight using toxin-deficient<br />

mutants of Ascochyta rabiei<br />

W Kim 1 , HO Akamatsu 1 , TL Peever 1 , GJ Vandemark 1,2 , W Chen 1,2<br />

1 Department of Plant Pathology, Washington State University, Pullman, USA<br />

2 USDA-ARS, Grain <strong>Legume</strong> Genetic and Physiology Research Unit, Washington State University, Pullman,<br />

USA<br />

Ascochyta rabiei, the causal agent of Ascochyta blight of chickpea, produces solanapyrone toxins<br />

(solanapyrone A, B and C). However, very little is known about the genetics of toxin production<br />

and the role of the toxins in pathogenesis. Generating mutants deficient in the toxin biosynthesis<br />

would provide information on the role of the toxins during infection processes. Partial genomic<br />

sequences of the solanapyrone biosynthesis gene cluster in A.rabiei were identified, based on the<br />

homologous sol gene cluster (sol1 - sol6) in Alternaria solani, which also produces the same toxins.<br />

The sol5 and sol4 genes which encode solanapyrone synthase and a fungal specific transcription<br />

factor, respectively, were targeted to generate toxin-deficient mutants. Deletion of either the sol4<br />

or the sol5 gene abolished production of solanopayrone toxins. The sol5-deletion mutants<br />

produced no solanapyrone toxxins and accumulated the precursor prosolanapyrone II, w<strong>here</strong>as<br />

thesol4-deletion mutants did not produce either solanapyrone toxins or the prosolanapyrone II.<br />

Solanopyrone toxins, but not the prosolanopyrone II precursor, showed toxicity to chickpea.<br />

Both the mutants showed normal growth patterns and conidiation in culture. Virulence of the<br />

toxin-deficient mutants was examined in pathogenicity assay using two-week old chickpea<br />

seedlings. Both sol4 and sol5 mutants showed no reduction in virulence, producing disease similar<br />

to the disease levels produced by wild-type strain. These findings indicate that sol4 gene is a<br />

positive regulator for solanapyrone biosynthesis, and that solanapyrone is not essential for the<br />

chickpea seedling infection.<br />

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