Abstract
Candida albicans is a diploid fungus and a predominant opportunistic human pathogen. Notably, C. albicans employs reversible chromosomal aneuploidies as a means of survival in adverse environments. We previously characterized transcription on the monosomic chromosome 5 (Ch5) that arises with adaptation to growth on the toxic sugar sorbose in the mutant Sor125(55). We now extend this analysis to the trisomic hybrid Ch4/7 within Sor125(55) and a diverse group of three mutants harboring a single Ch5. We find a similar pattern of transcriptional changes on either type of aneuploid chromosome within these mutants wherein expression of many genes follows chromosome ploidy, consistent with a direct mechanism to regulate genes important for adaptation to growth. In contrast, a significant number of genes are expressed at the disomic level, implying distinct mechanisms compensating for gene dose on monosomic or trisomic chromosomes consistent with maintaining cell homeostasis. Finally, we find evidence for an additional mechanism that elevates expression of genes on normal disomic Ch4 and Ch7 in mutants to levels commensurate with that found on the trisomic Ch4/7b in Sor125(55). Several of these genes are similarly differentially regulated among mutants, suggesting they play key functions in either maintaining aneuploidy or adaptation to growth conditions.
Highlights
Candida albicans is a diploid fungus and a predominant opportunistic human pathogen
In order to determine if these observations are a general feature of related aneuploidy in C. albicans, we analyzed two additional mutants carrying a single chromosome 5 (Ch5): JMC200-3-4 and SMC60-2-5, which were selected for laboratory resistance to caspofungin, and a third mutant, Sor1210(60), a.k.a
Approximately 30% of genes across this chromosome were upregulated to the disomic level suggesting a dosage compensation mechanism is operative in this strain that is required for continued growth[2]
Summary
Candida albicans is a diploid fungus and a predominant opportunistic human pathogen. Notably, C. albicans employs reversible chromosomal aneuploidies as a means of survival in adverse environments. We previously characterized transcription on the monosomic chromosome 5 (Ch5) that arises with adaptation to growth on the toxic sugar sorbose in the mutant Sor125(55). We find evidence for an additional mechanism that elevates expression of genes on normal disomic Ch4 and Ch7 in mutants to levels commensurate with that found on the trisomic Ch4/7b in Sor125(55) Several of these genes are differentially regulated among mutants, suggesting they play key functions in either maintaining aneuploidy or adaptation to growth conditions. We have previously addressed the intriguing question of how aneuploidy affects transcription in C. albicans For this purpose, we analyzed the transcriptional profile of the monosomic Ch5 in the mutant Sor125(55), a.k.a. Sor[55], which has lost one Ch5 as an adaptation to growth on sorbose as a sole source of carbon. Does monosomic Ch5 in other, independently derived mutants exhibit dosage compensation, and if so, in a similar pattern? Does transcription from a trisomic chromosome, which we identified in Sor125(55), involve dosage compensation?
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
