In yeast, both lipid metabolism and peroxisomal proliferation are under the regulation of SNF1 pathway. As opposed to the wealthy information in yeast, the function of SNF1 in these critical processes has not yet been studied in filamentous fungi. In this study, the M. oryzae SNF1 pathway was systematically characterized by targeted deletions of the three SNF1 complex subunits and two putative upstream Snf1-activating kinases. Through investigation of GFP-PTS1 signals, we found SNF1 pathway is indispensable for peroxisomal maintenance, which might account for its essential role in lipid metabolism. Furthermore, the interruption of SNF1 pathway resulted in enlarged size of appressorial wall pore and decreased turgor pressure, ultimately the loss of pathogenicity. Our results highlight the importance of SNF1 complex integrity, the upstream kinases, and their contributions to energy homeostasis. When dipped in glycerol solution, Leupeptin hemisulfate plasmolysis was frequently observed in the appressoria of the mutants. Thus we speculated the SNF1 pathway might also play a key role in appressorial cell wall integrity. Furthermore, the plasmolysis was more severe in mutants than WT as shown in Figure 7C. These data suggest the SNF1 function is essential for maintaining proper porosity of the appressorial wall. Transmission electron microscopy was also performed to observe the appressorial structures in detail. As a result, electron-dense melanin layer, with identical thickness, was distinctly observed in both wild type and the mutants, suggesting the appressorial wall defects of the SNF1 pathway mutants are not associated with melanin layer biosynthesis. Lipid degradation not only liberates glycerol but also feeds the acetyl-CoA pool produced by beta-oxidation of fatty acids. The end product acetyl-CoA can be shuttled to the glyoxylate cycle and gluconeogenesis which enable it to synthesize components of cell wall such as glucans and chitin. Hence, we inferred why the SNF1 pathway mutants failed to maintain sufficient turgor pressure was caused by the reduced accumulation of intracellular osmolites and increased appressorial cell wall porosity, both of which were the results of lipid metabolism GNE-7915 inability.