Nutrient Acquisition Strategies Employed by the Rice Blast Fungus Magnaporthe Oryzae During Infection

Magnaporthe oryzae is the causal agent of rice blast, one of the most devastating rice diseases worldwide. Understanding the metabolic strategies by which plant pathogenic fungi adapt to the changing nutrient landscapes within their hosts, would be a major step towards identifying potential targets to generate durable resistant rice cultivars. Using genetic, physiological, and biochemical approaches, here we describe novel insights into the metabolic mechanisms and strategies that underpin appressorium development and biotrophic growth in M. oryzae. On the leaf surface, Asd4-dependent glutaminolysis drives appressorium formation by suppressing the conserved target of rapamycin (TOR) inhibition of cAMP/PKA signaling pathways. This is the first report indicating that TOR is a negative-acting regulator of appressoria formation in M. oryzae, thus adding to our knowledge about how these specialized infection cells develop. Moreover, we demonstrate that appressorial differentiation is controlled by a novel glucose-ABL1-TOR signalling axis, which modulates cell cycle progression in response to glucose. Inside the rice cell, M. oryzae must manipulate plant innate immunity in order to grow undetected by the plant during its biotrophic phase. We show NMO2 (nitronate monooxygense) is essential for mitigating nitrooxidative cellular damage and, in rice cells, maintain redox balance to avoid triggering rice innate immunity. This provide insight on a previously unknown aspect of molecular plant-microbe interactions and, more broadly, identify a new requisite for nitrate and nitrite metabolism in fungi. Finally, we show what host-derived nutrients might facilitate rice cell invasion. Transcript and genetic analysis demonstrate ammonium is acquired from the plant under nitrogen starvation conditions via the ammonium transporters MEP1 and MEP2 during early biotrophy, while at least some amino acids are synthesized de novo through TCA cycle intermediates. Amino acid uptake via the general amino acid permease GAP1 occurs later in biotrophy in a Nut1-dependent manner