Abstract
The important human pathogen Candida albicans possesses an unusual form of gene regulation, in which the copy number of an entire specific chromosome or a large portion of a specific chromosome changes in response to a specific adverse environment, thus, insuring survival. In the absence of the adverse environment, the altered portion of the genome can be restored to its normal condition. One major question is how C. albicans copes with gene imbalance arising by transitory aneuploid states. Here, we compared transcriptomes from cells with either two copies or one copy of chromosome 5 (Ch5) in, respectively, a diploid strain 3153A and its representative derivative Sor55. Statistical analyses revealed that at least 40% of transcripts from the monosomic Ch5 are fully compensated to a disomic level, thus, indicating the existence of a genome-wide mechanism maintaining cellular homeostasis. Only approximately 15% of transcripts were diminished twofold in accordance with what would be expected for Ch5 monosomy. Another minor portion of approximately 6% of transcripts, unexpectedly, increased up to twofold and higher than the disomic level, demonstrating indirect control by monosomy. Array comparative genome hybridization revealed that only few out of approximately 500 genes on the monosomic Ch5b were duplicated, thus, not causing a global up regulation. Dosage compensation was confirmed with several representative genes from another monosomic Ch5a in the mutant Sor60. We suggest that C. albicans's unusual regulation of gene expression by the loss and gain of entire chromosomes is coupled with widespread compensation of gene dosage at the transcriptional level.
Highlights
Candida albicans is a unicellular fungus that is a benign inhabitant of the mucosal surfaces of gastrointestinal tract in approximately two thirds of the healthy human population
Sor55 derived from the laboratory strain 3153A by exposure to toxic sorbose, which caused the loss of chromosome 5a (Ch5a)
In order to assure that we are analyzing the transcriptom from cells with monosomic, but not with spontaneously duplicated chromosome 5b (Ch5b) [7], we confirmed the electro-karyotype of Sor55
Summary
Candida albicans is a unicellular fungus that is a benign inhabitant of the mucosal surfaces of gastrointestinal tract in approximately two thirds of the healthy human population. C. albicans is an obligate diploid organism with 8 pairs of chromosomes, whose unusual instability has been systematically investigated by us and others [1]. Throughout years, we have accumulated evidence that C. albicans generates aneuploidies as a response to environmental stresses [1,2,3], despite aneuploidy having detrimental effects on cell division and growth similar to other organisms [4,5]. We have demonstrated that reversible loss or gain of specific chromosomes, or large portions of specific chromosomes, each occurring in a specific adverse environment, constitute unusual gene regulatory systems that allow C. albicans survival [1,2]. In the best-studied case, adaptation to the toxic sugar sorbose, the major mechanism conferring survival is the loss of an entire chromosome 5a (Ch5a) or an entire chromosome 5b (Ch5b)
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