MoLrp1-mediated signaling induces nuclear accumulation of MoMsn2 to facilitate fatty acid oxidation for infectious growth of the rice blast fungus.

Fatty acid β-oxidation is critical for fatty acid degradation and cellular development. In the rice blast fungus Magnaporthe oryzae, fatty acid β-oxidation is reported to be important mainly for turgor generation in the appressorium. However, the role of fatty acid β-oxidation during invasive hyphal growth is rarely documented. We demonstrated that blocking peroxisomal fatty acid β-oxidation impaired lipid droplet (LD) degradation and infectious growth of M. oryzae. We found that the key regulator of pathogenesis, MoMsn2, which we identified previously, is involved in fatty acid β-oxidation by targeting MoDCI1 (encoding dienoyl-coenzyme A [CoA] isomerase), which is also important for LD degradation and infectious growth. Cytological observations revealed that MoMsn2 accumulated from the cytosol to the nucleus during early infection or upon treatment with oleate. We determined that the low-density lipoprotein receptor-related protein MoLrp1, which is also involved in fatty acid β-oxidation and infectious growth, plays a critical role in the accumulation of MoMsn2 from the cytosol to the nucleus by activating the cyclic AMP signaling pathway. Our results provide new insights into the importance of fatty acid oxidation during invasive hyphal growth, which is modulated by MoMsn2 and its related signaling pathways in M. oryzae.