The Elongator complex is conserved in a wide range of species and plays crucial roles in diverse cellular processes. We have previously shown that the Elongator protein PoElp3 was involved in the asexual development, pathogenicity, and autophagy of the rice blast fungus. In this study, we further revealed that PoElp3 functions via tRNA-mediated protein integrity. Phenotypic analyses revealed that overexpression of two of the tRNAs, tK(UUU) and tQ(UUG) could rescue the defects in ΔPoelp3 strain. TMT-based proteomic and transcriptional analyses demonstrated that 386 proteins were down-regulated in ΔPoelp3 strain compared with wild type strain Guy11, in a transcription-independent manner. Codon usage assays revealed an enrichment of Glutamine CAA-biased mRNA in the 386 proteins compared with the 70-15 genome. In addition to those reported previously, we also found that PoErp9, a sphingolipid C9-methyltransferase, was down-regulated in the ΔPoelp3 strain. Through an ILV2-specific integration of PoERP9-GFP into the wild type and ΔPoelp3 strain, we were able to show that PoErp9 was positively regulated by PoElp3 translationally but not transcriptionally. Functional analyses revealed that PoErp9 was involved in the fungal growth, conidial development, pathogenicity, and TOR-related autophagy homeostasis in Pyricularia oryzae. Taken together, our results suggested that PoElp3 acts through the tRNA-mediated translational efficiency to regulate asexual development, pathogenicity, sphingolipid metabolism, and autophagy in the rice blast fungus.

Rice blast caused by Magnaporthe oryzae is the most destructive disease affecting the rice production (Oryza sativa), with an average global loss of 10–30% per annum. Recent reports have indicated that the fungus also inflicts blast disease on wheat (Triticum aestivum) posing a serious threat to the wheat production. Due to its easily detected infectious process and manoeuvrable genetic manipulation, M. oryzae is considered a model organism for exploring the molecular mechanism underlying fungal pathogenicity during the pathogen–host interaction. M. oryzae utilises an infectious structure called appressorium to breach the host surface by generating high turgor pressure. The appressorium development is induced by physical and chemical cues which are coordinated by the highly conserved cAMP/PKA, MAPK and calcium signalling cascades. Genes involved in the appressorium development have been identified and well studied in M. oryzae, a summary of the working gene network linking stimuli sensing and physiological transformation of appressorium is needed. This review provides a comprehensive discussion regarding the regulatory networks underlying appressorium development with particular emphasis on sensing of appressorium inducing stimuli, signal transduction, transcriptional regulation and the corresponding developmental and physiological responses. We also discussed the crosstalk and interaction of various pathways during the appressorium development.