Nitric oxide (NO) homeostasis plays a versatile role in pathogen-host interactions. To maintain NO homeostasis in favor of pathogens, microbes have evolved NO degradation systems besides NO synthesis pathway, in which the flavohemoglobin and S-nitrosoglutathione (GSNO) reductase are two key enzymes. We previously proved that MoSFA1, a GSNO reductase, is required for the growth and pathogenicity in Magnaporthe oryzae. In the present work, MoFHB1, a flavohemoglobin-encoding gene in M. oryzae was functionally characterized. Although the expression of the MoFHB1 gene was developmentally regulated during conidial germination and appressorium development, disruption of MoFHB1 did not change vegetative growth, conidiation and virulence. However, compared with the Δmosfa1 mutant, the Δmofhb1 mutant was significantly more sensitive to NO stress, and the expression of MoSFA1 gene in the Δmofhb1 mutant was significantly upregulated. Double deletion of MoSFA1 and MoFHB1 led to greater sensitivity of the fungus to NO stress than either of the single gene mutant, but no further reduction in pathogenicity was found compared with that of Δmosfa1 mutant. Taken together, MoFHB1 played an important role in NO detoxification but was dispensable for virulence of M. oryzae.
Keywords: Magnaporthe oryzae; NO degradation; flavohemoglobin.
© The Author(s) 2022. Published by Oxford University Press on behalf of FEMS.