Location: Toxicology and Mycotoxin Research
Title: Detoxification of nitric oxide by flavohemoglobin and the denitrification pathway in the maize pathogen Fusarium verticillioides Authors
Submitted to: Fungal Genetics Reports
Publication Type: Abstract Only
Publication Acceptance Date: December 12, 2012
Publication Date: March 12, 2013
Citation: Baldwin, T.T., Glenn, A.E. 2013. Detoxification of nitric oxide by flavohemoglobin and the denitrification pathway in the maize pathogen Fusarium verticillioides [abstract]. Fungal Genetics Reports. 60(Suppl):538. Interpretive Summary: Abstract - no summary required.
Technical Abstract: The ephemeral nitric oxide (NO) is a free radical, highly reactive, environmentally rare, and a potent signaling molecule in organisms across kingdoms of life. This gaseous small molecule can freely transverse membranes and has been implicated in aspects of pathogenicity both in animal and plant hosts. Fusarium verticillioides is a mycotoxigenic pathogen of maize, notable for its ability to persist as an asymptomatic endophyte. One potential determinant of this lifestyle conversion between overt pathogen and symptomless endophyte may be the regulation of NO. Detoxification of NO is a known pathogenicity factor for the fungal human pathogen Candida albicans and the bacterial plant pathogen Erwinia chrysanthemi. Both mediate detoxification by a flavohemoglobin protein (CaYHB1 and HmpX, respectively). BLASTP search of the F. verticillioides genome revealed two putative flavohemoglobin homologs, denoted FHB1 and FHB2. Microarray analysis revealed a significant induction of FHB2 (13-fold) when the fungus was exposed to exogenous NO. FHB1 had a 2-fold increase. Also noteworthy from the microarray data is the distinct induction of genes within the denitrification pathway, including dissimilatory nitrate reductase (dNaR, 16-fold increase), dissimilatory nitrite reductase (dNiR, 226-fold), and P450 nitric oxide reductase (P450nor, 27-fold). Flavohemoglobin has been noted as a component of the denitrification pathway, having a role in converting NO to nitrate. Thus, FHB2 is postulated to be the paralog involved in the F. verticillioides denitrification pathway. Deletion mutants are being created in dNiR, P450nor, FHB1, and FHB2 to further evaluate functions of these genes in F. verticillioides. Mutants will be assayed for their endogenous production and regulation of NO, response to exogenous NO, virulence against maize, and mycotoxin production. Elucidating the function of these genes will give insight into the role of NO in F. verticillioides development, maize-fungal interactions, and denitrification, which has previously only been assessed in relation to anaerobic growth.