Transcriptome Analysis and Functional Characterization Reveal That Peclg Gene Contributes to the Virulence of Penicillium expansum on Apple Fruits

Abstract

Penicillium expansum is the causal agent of blue mold decay on apple fruits and is also known to be the major producer of patulin, a mycotoxin that represents serious hazard to human health. Several mechanisms have been suggested to explain the pathogenesis of P. expansum in host plants. Secreted effector proteins are vital for the pathogenicity of many fungal pathogens through manipulating their hosts for efficient colonization. In this study, we performed a RNA-Seq analysis followed by computational prediction of effector proteins from P. expansum during infection of the host apple fruits, and a total of 212 and 268 candidate effector protein genes were identified at 6 and 9 h after inoculation (hai), respectively. One of the candidate effector protein genes was identified as a concanavalin A-like lectin/glucanase (Peclg), which was dramatically induced during the pathogen–host interaction. Targeted knockout of Peclg resulted in significant reduction in conidial production and germination relative to the wild type. Further studies showed that in addition to salt stress, the mutant was much more sensitive to SDS and Congo red, suggesting a defect in cell wall integrity. Pathogenicity assays revealed that the ΔPeclg mutant showed significant decrease in virulence and infectious growth on apple fruits. All these results suggest that Peclg is required for fungal growth, stress response, and the virulence of P. expansum.

Endoglucanase H from Aspergillus westerdijkiae Plays an Important Role in the Virulence on Pear Fruits

“…Recent work in P. expansum, a concanavalin A-like lectin/glucanase (PeCLG) lacking a mutant strain, showed several abnormalities concerning vegetative growth or development, including reduced conidia production and germination. 32 These data demonstrated the involvement of AwEGH in fungal growth and development. However, the roles of AwEGH and its homologues might regulate the fungal growth and development in a species-dependent manner, and further experiments are required to reveal the potential intrinsic mechanisms associated with this regulation.…”

“…Recent work in P. expansum, a concanavalin A-like lectin/glucanase ( PeCLG ) lacking a mutant strain, showed several abnormalities concerning vegetative growth or development, including reduced conidia production and germination . These data demonstrated the involvement of AwEGH in fungal growth and development.…”

Wide transcriptional outlook to uncover Penicillium expansum genes underlying fungal incompatible infection

“…Interestingly, among the effectors there is a large proportion that correspond to genes for enzymes that degrade the cell wall, which include lectins/glucanases similar to concanavalin A, pectin lyase and pectinesterase. A new effector gene, Peclg, has been identified and showed that it is relevant in conidiation, germination and environmental stress response [ 37 ]. Interestedly, in this study this group is also represented by an endoglucanase (PEX1_094750) and by another Glycoside hydrolase of family 12 that could have similarity with Concanavalin A-like lectins/glucanases (PEX1_081540).…”

The Identification and Comparative Analysis of Non-Coding RNAs in Spores and Mycelia of Penicillium expansum

“…Zhao et al (2022) found that nine transcription factors were closely related to pears being infected with P. expansum [15]. A large number of genes, such as PeRacA, PeRmtC, PeSCP, PeSntB, PeNIP, PeNox, PeSet1, PeLae, PeVeA, PeCreA, PeLysMs, PeNLPs, and PePRT, were also proven to be critical to the virulence of P. expansum [16][17][18][19][20][21][22][23]. In addition, the biosynthesis pathway of patulin, which is the most important secondary metabolite of P. expansum and poses severe genotoxicity and cytotoxicity to animals and humans, has been systematically dissected at the molecular and biochemical level [1,24,25].…”