Location: Toxicology & Mycotoxin ResearchTitle: RNA-Seq analysis of stuA mutants in Fusarium verticillioides indicates dramatic genomic wide transcriptional reprogramming
|RATH, MANISHA - University Of Georgia|
Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 3/15/2016
Publication Date: 3/15/2016
Citation: Rath, M., Crenshaw, N.J., Gold, S.E. 2016. RNA-Seq analysis of stuA mutants in Fusarium verticillioides indicates dramatic genomic wide transcriptional reprogramming. International Symposium of Molecular Biology and Biotechnology, Irapuato, Mexico, May 12-14, 2015
Technical Abstract: StuA, first discovered in Aspergillus nidulans and a member of the APSES class of transcription factors, regulates several essential developmental stages in fungi such as virulence, sporulation and toxin production in phytopathogenic fungi. Fusarium verticillioides (Fv), a maize phytopathogen, produces fumonisin mycotoxins in maize. Fumonisin-contaminated corn causes fatal toxicity in livestock, is associated with neural tube birth defects and growth stunting in children and is also a potential carcinogen to humans. Our objective is to explore the impact of the stuA homolog on morphogenesis and toxin production in Fv. 'stuA mutants were generated via Agrobacterium-mediated transformation of Fv with an OSCAR deletion construct. Characterization of the mutants indicate slower vegetative growth on solid media, reduced sporulation and macroconidiation. A cracked corn assay on maize kernels and virulence assay on maize seedlings revealed reduced fumonisin accumulation and reduced virulence respectively in stuA mutant infected maize as compared to the wild-type pathogen infection. To characterize the mutants transcriptomally, RNA-sequencing of three of the mutants and the wild-type Fv strain M3125 was done via Illumina NextSeq and the Tuxedo pipeline is being utilized for differential expression analysis. Preliminary RNA-seq analysis indicates major alteration of numerous transcription factors, transporters and signaling in the stuA mutants.