Characterization of the transcriptional response of Candida parapsilosis to the antifungal peptide MAF-1A

PeerJ. 2020 Sep 7:8:e9767. doi: 10.7717/peerj.9767. eCollection 2020.

Abstract

Candida parapsilosis is a major fungal pathogen that leads to sepsis. New and more effective antifungal agents are required due to the emergence of resistant fungal strains. MAF-1A is a cationic antifungal peptide isolated from Musca domestica that is effective against a variety of Candida species. However, the mechanism(s) of its antifungal activity remains undefined. Here, we used RNA-seq to identify differentially expressed genes (DEGs) in Candida parapsilosis following MAF-1A exposure. The early (6 h) response included 1,122 upregulated and 1,065 downregulated genes. Late (18 h) responses were associated with the increased expression of 101 genes and the decreased expression of 151 genes. Upon MAF-1A treatment for 18 h, 42 genes were upregulated and 25 genes were downregulated. KEGG enrichment showed that the DEGs in response to MAF-1A were mainly involved in amino acid synthesis and metabolism, oxidative phosphorylation, sterol synthesis, and apoptosis. These results indicate that MAF-1A exerts antifungal activity through interference with Candida parapsilosis cell membrane integrity and organelle function. This provides new insight into the interaction between Candida parapsilosis and this antimicrobial peptide and serves as a reference for future Candida parapsilosis therapies.

Keywords: Antifungal; Antimicrobial peptide; Candida parapsilosis; MAF-1A; RNA-seq; Transcriptional response.

Grants and funding

This work was supported by the Science and Technology Department of Gui Zhou Province ((2019)2827, (2015)4015, (2018)5706); Doctoral Foundation of Guizhou Provincial People’s Hospital (GZSYBS(2015)12); Non-profit Central Research Institute Fund of Chinese Academy of Medical Sciences (2019PT320003). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.