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Identification of pathogenicity-related genes and the role of a subtilisin-related peptidase S8 (PePRT) in authophagy and virulence of Penicillium expansum on apples

AuthorsLevin, E.; Kishore, A.; Ballester Frutos, Ana Rosa ; Raphael, G.; Feigenberg, O.; Liu, Y.; Norelli, J.; González-Candelas, Luis ; Wisniewski, M.; Droby, Samir
KeywordsPenicillium expansum
Host-pathogen interaction
Issue Date15-Dec-2018
CitationPostharvest Biology and Technology 14: 209-220 (2019)
AbstractBlue mold caused by Penicillium expansum is a major postharvest disease of pome fruit. Several mechanisms possibly involved in P. expansum pathogenicity and virulence. However, factors that mediate pathogenicity and virulence are largely not yet characterized. In this work we analyzed P. expansum predicted secretome to reveal potential genes that have a role in host-pathogen interaction. A prediction pipeline was designed using an approach that combines common effector features, transcriptomic data and homology to proteins reported to be involved in pathogenicity of other pytopathogenic fungi. Among 297 genes predicted in P. expansum secretome, 103 genes (35%) were found to code for hydrolytic enzymes. The majority of the secreted enzymes are carbohydrate-degrading enzymes among which five coding for pectin-degrading enzymes are highly induced during the infection and decay of apple fruit by P. expansum, indicating that they may represent an important aspect of pathogenicity and virulence. Applying the pipeline we have predicted 17 candidate genes coding for proteins that are most likely involved in pathogenicity and virulence. One of the top candidates is a subtilisin-related peptidase, S8 (PePRT), proteolytic enzyme highly expressed in planta, and potentially involved in authophagy process. Deletion of PePRT-coding gene resulted in reduced virulence of P. expansum on apples. Moreover, ΔPeprt exhibited decreased sporulation as well as affected mycelial morphology and internal mycelial cell structure.
Publisher version (URL)https://doi.org/10.1016/j.postharvbio.2018.10.011
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