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ARS Home » Pacific West Area » Pullman, Washington » Grain Legume Genetics Physiology Research » Research » Publications at this Location » Publication #298658
Title: Investigating the role of solanapyrone toxins in Ascochyta blight using toxin-deficient mutants of Asochyta rabiei

Author
item KIM, WONYONG - Washington State University
item AKAMATSU, H - Washington State University
item PEEVER, TOBIN - Washington State University
item Vandemark, George
item Chen, Weidong

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 3/15/2013
Publication Date: 5/1/2013
Citation: Kim, W., Akamatsu, H.O., Peever, T., Vandemark, G.J., Chen, W. 2013. Investigating the role of solanapyrone toxins in Ascochyta blight using toxin-deficient mutants of Asochyta rabiei. First Legume Society Conference Abstract Book. May 9-11, 2013, Novi Sad, Serbia. 203.

Interpretive Summary: Abstract Only

Technical Abstract: Ascochyta rabiei, the causal agent of Ascochyta blight of chickpea, produces solanapyrone toxins (solanapyrone A, B and C). However, very little is known about the genetics of toxin production and the role of the toxins in pathogenesis. Generating mutants deficient in the toxin biosynthesis would provide information on the role of the toxins during infection processes. Partial genomic sequences of the solanapyrone biosynthesis gene cluster in A. rabiei were identified, based on the homologous sol gene cluster (sol1 - sol6) in Alternaria solani, which also produces the same toxins. The sol5 and sol4 genes which encode solanapyrone synthase and a fungal specific transcription factor, respectively, were targeted to generate toxin-deficient mutants. Deletion of either the sol4 or the sol5 gene abolished production of solanopayrone toxins. The sol5-deletion mutants produced no solanapyrone toxxins and accumulated the precursor prosolanapyrone II, whereas the sol4-deletion mutants did not produce either solanapyrone toxins or the prosolanapyrone II. Solanopyrone toxins, but not the prosolanopyrone II precursor, showed toxicity to chickpea. Both the mutants showed normal growth patterns and conidiation in culture. Virulence of the toxin-deficient mutants was examined in pathogenicity assay using two-week old chickpea seedlings. Both sol4 and sol5 mutants showed no reduction in virulence, producing disease similar to the disease levels produced by wild-type strain. These findings indicate that sol4 gene is a positive regulator for solanapyrone biosynthesis, and that solanapyrone is not essential for the chickpea seedling infection.