Phosphatidylcholine (PC) plays crucial biological roles in eukaryotic cells. InSaccharomyces cerevisiae, apart from phosphatidylethanolamine (PE) methylation pathway, PC is also synthesized via CDP–choline pathway. Phosphocholine cytidylyltransferase Pct1 is the rate-limiting enzyme to catalyze the conversion from phosphocholine to CDP–choline in this pathway. Here, we report the identification and functional characterization of an ortholog of the budding yeastPCT1inMagnaporthe oryzae, namedMoPCT1. Targeted gene deletion mutants ofMoPCT1were impaired in vegetative growth, conidiation, appressorium turgor accumulation and cell wall integrity. Also, the mutants were severely compromised in appressorium-mediated penetration, infectious growth and pathogenicity. Western blot analysis revealed that cell autophagy was activated by the deletion ofMoPCT1under nutrient-rich conditions. Moreover, we found several key genes in PE methylation pathway, such asMoCHO2,MoOPI3, andMoPSD2, were significantly up-regulated in theΔMopct1mutants, indicating that a pronounced compensation effect exists between the two PC biosynthesis pathways inM. oryzae. Interestingly, in theΔMopct1mutants, histone H3 was hypermethylated and expression levels of several methionine cycling-related genes were significantly up-regulated, suggesting thatMoPCT1is involved in histone H3 methylation and methionine metabolism. Taken together, we conclude that the phosphocholine cytidylyltransferase coding geneMoPCT1plays important roles in vegetative growth, conidiation and appressorium-mediated plant infection byM. oryzae.