Background: Although Candida albicans and Candida dubliniensis are most closely related, both species behave significantly different with respect to morphogenesis and virulence. In order to gain further insight into the divergent routes for morphogenetic adaptation in both species, we investigated qualitative along with quantitative differences in the transcriptomes of both organisms by cDNA deep sequencing.
Results: Following genome-associated assembly of sequence reads we were able to generate experimentally verified databases containing 6016 and 5972 genes for C. albicans and C. dubliniensis, respectively. About 95% of the transcriptionally active regions (TARs) contain open reading frames while the remaining TARs most likely represent non-coding RNAs. Comparison of our annotations with publically available gene models for C. albicans and C. dubliniensis confirmed approximately 95% of already predicted genes, but also revealed so far unknown novel TARs in both species. Qualitative cross-species analysis of these databases revealed in addition to 5802 orthologs also 399 and 49 species-specific protein coding genes for C. albicans and C. dubliniensis, respectively. Furthermore, quantitative transcriptional profiling using RNA-Seq revealed significant differences in the expression of orthologs across both species. We defined a core subset of 84 hyphal-specific genes required for both species, as well as a set of 42 genes that seem to be specifically induced during hyphal morphogenesis in C. albicans.
Conclusions: Species-specific adaptation in C. albicans and C. dubliniensis is governed by individual genetic repertoires but also by altered regulation of conserved orthologs on the transcriptional level.
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http://dx.doi.org/10.1186/1471-2164-14-212 | DOI Listing |
Infect Drug Resist
December 2024
Departamento de Biología, División de Ciencias Naturales y Exactas, Universidad de Guanajuato, Guanajuato, Gto, Mexico.
Fungal infections have become a growing public health concern, aggravated by the emergence of new pathogenic species and increasing resistance to antifungal drugs. The most common candidiasis is caused by ; however, has become an emerging opportunistic pathogen, and although less prevalent, it can cause superficial and systemic infections, especially in immunocompromised individuals. This yeast can colonize the oral cavity, skin, and other tissues, and has been associated with oral infections in patients with human immunodeficiency virus (HIV) and acquired immunodeficiency syndrome (AIDS), making it difficult to treat.
View Article and Find Full Text PDFMicrob Pathog
December 2024
Beijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing, China; Beijing Institute of Chinese Medicine, Beijing, China; Beijing Key Laboratory of Basic Research with Traditional Chinese Medicine on Infectious Diseases, Beijing, China. Electronic address:
A striking characteristic of the human fungal pathogen Candida albicans is its ability to switch between budding yeast morphology and the filamentous form, facilitating its adaptation to changing host environments. The filamentous growth of C. albicans is mediated by various environmental factors, such as carbon dioxide (CO), N-acetylglucosamine (GlcNAc), serum, and high temperature.
View Article and Find Full Text PDFJ Oral Microbiol
December 2024
Innovation Research Centre, John Paul II University in Biała Podlaska, Biala Podlaska, Poland.
Arch Microbiol
November 2024
Department of Biotechnology, National Institute of Technology, Raipur, Chhattisgarh, 492010, India.
Systemic mycoses, particularly those caused by Candida albicans, represent a serious global health concern due to rising multidrug resistance and limited treatment options. This study explores the antifungal potential of sodium lignosulfonate (LIG), a natural phenolic compound, as a multitarget therapeutic agent against various virulence proteins of C. albicans and other pathogenic Candida species.
View Article and Find Full Text PDFTrop Med Health
November 2024
Department of Medical Microbiology, School of Biomedical Sciences, College of Health Sciences, Makerere University, P.O. Box 7072, Kampala, Uganda.
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