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Research Project: DEVELOPING RESISTANCE TO AFLATOXIN THROUGH SEED-BASED TECHNOLOGIES

Location: Food and Feed Safety Research

Title: The veA gene of the pine needle pathogen Dothistroma septosporum regulates sporulation and secondary metabolism

Authors
item Chettri, Pranav -
item Calvo, Ana -
item Cary, Jeffrey
item Dhingra, Sourabh -
item Guo, Yanan -
item Mcdougal, Rebecca -
item Bradshaw, Rosie -

Submitted to: Fungal Genetics and Biology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: November 22, 2011
Publication Date: January 31, 2012
Citation: Chettri, P., Calvo, A.M., Cary, J.W., Dhingra, S., Guo, Y., McDougal, R.L., Bradshaw, R.E. 2012. The veA gene of the pine needle pathogen Dothistroma septosporum regulates sporulation and secondary metabolism. Fungal Genetics and Biology. 49:141-151.

Interpretive Summary: Dothistroma septosporum, is a fungus that infects pine needles eventually leading to tree death. During growth it produces dothistromin, a polyketide toxin very closely related to aflatoxin (AF) and sterigmatocystin (ST) synthesized by Aspergillus spp. This work describes experiments that have been conducted in an effort to better understand the genetic mechanisms that control dothistomin production and growth and development in D. septosporum. We have succeeded identifying a gene, designated veA, from D. septosporum that when inactivated greatly reduces the amount of dothistromin and reproductive spores produced that help the fungus to survive in nature. In addition, this study showed that veA also controls the production of a number of other secondary metabolites in D. septosporum, some of which may also help the fungus to survive and infect pine trees. Results of this study indicate that the veA gene may be a good target for inactivation as one strategy to eliminate outbreaks of D. septosporum pine needle infection.

Technical Abstract: Fungi possess genetic systems to regulate the expression of genes involved in complex processes such as development and secondary metabolite biosynthesis. The product of the velvet gene veA, first identified and characterized in Aspergillus nidulans, is a key player in the regulation of both of these processes. Since its discovery and characterization in many Aspergillus species, VeA has been found to have similar functions in other fungi, including the Dothideomycete Mycosphaerella graminicola. Another Dothideomycete, Dothistroma septosporum, is a pine needle pathogen that produces dothistromin, a polyketide toxin very closely related to aflatoxin (AF) and sterigmatocystin (ST) synthesized by Aspergillus spp.. Dothistromin is unusual in that, unlike most other secondary metabolites, it is produced mainly during the early exponential growth phase in culture. It was therefore of interest to determine whether the regulation of dothistromin production in D. septosporum differs from the regulation of AF/ST in Aspergillus spp.. To begin to address this question, a veA ortholog was identified and its function analyzed in D. septosporum. Inactivation of the veA gene resulted in reduced dothistromin production and a corresponding decrease in expression of dothistromin biosynthetic genes. Expression of other putative secondary metabolite genes in D. septosporum such as polyketide synthases and non-ribosomal peptide synthases showed a range of different responses to loss of Ds-veA. Asexual sporulation was also significantly reduced in the mutants, accompanied by a reduction in the expression of a putative stuA regulatory gene. The mutants were, however, able to infect Pinus radiata seedlings and complete their life cycle under laboratory conditions. Overall this work suggests that D. septosporum has a functional veA ortholog that is involved in the control of both developmental and secondary metabolite biosynthetic pathways.

   

 
Project Team
Cary, Jeffrey
Brown, Robert
Rajasekaran, Kanniah - Rajah
Bhatnagar, Deepak
Yu, Jiujiang
 
Publications
   Publications
 
Related National Programs
  Food Safety, (animal and plant products) (108)
 
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Last Modified: 05/18/2013
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