Genetic evidence for vitamin B3 acquisition from rice cells.

Following penetration, the devastating rice blast fungus , like some other important eukaryotic phytopathogens, grows in intimate contact with living plant cells before causing disease. Cell-to-cell growth during this biotrophic growth stage must involve nutrient acquisition, but experimental evidence for the internalization and metabolism of host-derived compounds is exceedingly sparse. This striking gap in our knowledge of the infection process undermines accurate conceptualization of the plant-fungal interaction. Here, through our general interest in metabolism and with a specific focus on the signalling and redox cofactor nicotinamide adenine dinucleotide (NAD), we deleted the gene encoding quinolinate phosphoribosyltransferase, catalyst of the last step in NAD biosynthesis from tryptophan. We show how is essential for axenic growth on minimal media lacking nicotinic acid (NA, an importable NAD precursor). However, Δ mutant strains were fully pathogenic, indicating NAD biosynthesis is dispensable for lesion expansion following invasive hyphal growth in leaf tissue. Because overcoming the loss of NAD biosynthesis can only occur if importable NAD precursors (which solely comprise the NA, nicotinamide and nicotinamide riboside forms of vitamin B3) are accessible, we unexpectedly but unequivocally demonstrate that vitamin B3 can be acquired from the host and assimilated into metabolism during growth in rice cells. Our results furnish a rare, experimentally determined example of host nutrient acquisition by a fungal plant pathogen and are significant in expanding our knowledge of events at the plant-fungus metabolic interface.