Abstract
BackgroundSome species of fungi can cause serious human diseases, particularly to immuno-compromised individuals. Opportunistic fungal infections are a leading cause of mortality, and present an emerging challenge that requires development of new and effective therapeutics. Aminoacyl-tRNA synthetases (aaRSs) are indispensable components of cellular protein translation machinery and can be targeted for discovery of novel anti-fungal agents.ResultsValidation of aaRSs as potential drug targets in pathogenic microbes prompted us to investigate the genomic distribution of aaRSs within three fungi that infect humans – A. niger, C. albicans and C. neoformans. Hidden Markov Models were built for aaRSs and related proteins to search for homologues in these fungal genomes. Here, we provide a detailed and comprehensive annotation for 3 fungal genome aaRSs and their associated proteins. We delineate predicted localizations, subdomain architectures and prevalence of unusual motifs within these aaRSs. Several fungal aaRSs have unique domain appendages of unknown function e.g. A. niger AsxRS and C. neoformans TyrRS have additional domains that are absent from human homologs.ConclusionsDetailed comparisons of fungal aaRSs with human homologs suggest key differences that could be exploited for specific drug targeting. Our cataloging and structural analyses provide a comprehensive foundation for experimentally dissecting fungal aaRSs that may enable development of new anti-fungal agents.Electronic supplementary materialThe online version of this article (doi:10.1186/1471-2164-15-1069) contains supplementary material, which is available to authorized users.
Highlights
Some species of fungi can cause serious human diseases, to immuno-compromised individuals
Our results show that there are a total of 29 Aminoacyl-tRNA synthetases (aaRSs) in A. niger, 28 in C. albicans and 26 in C. neoformans (Tables 1, 2 and 3)
Our results show that there are 8 A. niger aaRSs that are present in two versions (AspRS, GluRS, GlyRS, IleRS, LeuRS, PheRS, TrpRS and AsxRS), 7 C. albicans aaRSs that are present in two versions (GluRS, IleRS, LeuRS, PheRS, TrpRS, TyrRS and AsxRS), and 5 C. neoformans aaRSs that are present in two versions (AsnRS, GluRS, IleRS, PheRS and TyrRS, Figure 1A)
Summary
Some species of fungi can cause serious human diseases, to immuno-compromised individuals. Data suggest that diseases caused by opportunistic fungi result in scores of human deaths worldwide, and containment of human fungal infections is a pressing challenge [1,2,3,4,5]. The pathogenesis of such opportunistic fungi is a complex phenomenon since these organisms more often than not lack dedicated ‘virulence’ factors [1,2,3,4,5]. In addition to genome sequencing, transcriptomics analyses for these three fungi are available [13,14,15]
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