Transcriptional profiling of the Candida albicans response to the DNA damage stressing agent methyl methanesulfonate
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ABSTRACT:
PROVIDER: PRJNA804021 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17908612_1.fastq.gz | Fastqsanger.gz | |||
| SRR17908612_2.fastq.gz | Fastqsanger.gz | |||
| SRR17908613_1.fastq.gz | Fastqsanger.gz | |||
| SRR17908613_2.fastq.gz | Fastqsanger.gz | |||
| SRR17908614_1.fastq.gz | Fastqsanger.gz |
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Project description:We explored the global transcription profile in response to MMS in C. albicans through RNAseq assay. Here, we identified 407 genes (log2 fold cut off 1.0, P<0.05) whose levels of transcription were significantly affected under the MMS treatment condition; 207 genes were upregulated, and 200 genes were down-regulated. GO term analysis revealed that a small portion of changed genes showed direct roles in DNA repair progress, but a large number of induced genes are involved in antioxidant responses, and some down-regulated genes are involved in nucleosome packing and nitrogen utilization. In addition, the changed transcription of some DNA repair genes, as well as antioxidants genes, are blocked by deleting RAD53. Taken together, treatment of the DNA damage agent MMS induces a global transcriptional change in C. albicans, but not only DNA damage response genes.
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Project description:The human gut acts as the main reservoir of microbes and a relevant source of life-threatening infections, especially in immunocompromised patients. There, the opportunistic fungal pathogen Candida albicans adapts to the host environment and additionally interacts with residing bacteria. We investigated fungal-bacterial interactions by coinfecting enterocytes with the yeast Candida albicans and the Gram-negative bacterium Proteus mirabilis resulting in enhanced host cell damage. This synergistic effect was conserved across different P. mirabilis isolates and occurred also with non-albicans Candida species and C. albicans mutants defective in filamentation or candidalysin production. Using bacterial deletion mutants, we identified the P. mirabilis hemolysin HpmA to be the key effector for host cell destruction. Spatially separated coinfections demonstrated that synergism between Candida and Proteus is induced by contact, but also by soluble factors. Specifically, we identified Candida-mediated glucose consumption and farnesol production as potential triggers for Proteus virulence. In summary, our study demonstrates that coinfection of enterocytes with C. albicans and P. mirabilis can result in increased host cell damage which is mediated by bacterial virulence factors as a result of fungal niche modification via nutrient consumption and production of soluble factors. This supports the notion that certain fungal-bacterial combinations have the potential to result in enhanced virulence in niches such as the gut and might therefore promote translocation and dissemination.
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Project description:Methyl methanesulfonate (MMS) is a DNA damage agent that induces the DNA damage response (DDR). Recent findings in the literature suggest a role for phosphatidylinositol signaling in regulating the DDR. In budding yeast, inositol biosynthesis is fine-tuned by the transcriptional repressor Opi1. We conducted RNA-seq of OPI1 knockout and wild-type yeast cells in conditions with or without treatment with 0.1% MMS for 1 hour to investigate the role of Opi1 in the response to genotoxic stress.
2023-07-05 | E-MTAB-13057 | biostudies-arrayexpress
Project description:We explored transcriptional responses of the fission yeast Schizosaccharomyces pombe to DNA damage. RNA-seq was used to characterize changes in expression profiles of all known lncRNAs and mRNAs in response to four DNA damage agents: Camptothecin, Hydroxyurea, Methyl methanesulfonate, Phleomycin.
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Project description:We explored transcriptional responses of the fission yeast to DNA damage. RNA-seq was used to characterize changes in expression profiles of all known lncRNAs and mRNAs in wild type cells and cells treated by four DNA damage agents: Camptothecin, Hydroxyurea, Methyl methanesulfonate and Phleomycin.
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Project description:Candida albicans and Candida dubliniensis are closely related species displaying differences in virulence and genome content, therefore providing potential opportunities to identify novel C. albicans virulence genes. C. albicans gene arrays were used for comparative analysis of global gene expression in the two species in reconstituted human oral epithelium (RHE). C. albicans (SC5314) showed upregulation of hypha-specific and virulence genes within 30 min postinoculation, coinciding with rapid induction of filamentation and increased RHE damage. C. dubliniensis (CD36) showed no detectable upregulation of hypha-specific genes, grew as yeast, and caused limited RHE damage. Several genes absent or highly divergent in C. dubliniensis were upregulated in C. albicans. One such gene, SFL2 (orf19.3969), encoding a putative heat shock factor, was deleted in C. albicans. ÎÎsfl2 cells failed to filament under a range of hypha-inducing conditions and exhibited greatly reduced RHE damage, reversed by reintroduction of SFL2 into the ÎÎsfl2 strain. Moreover, SFL2 overexpression in C. albicans triggered hyphal morphogenesis. Although SFL2 deletion had no apparent effect on host survival in the murine model of systemic infection, ÎÎsfl2 strain-infected kidney tissues contained only yeast cells. These results suggest a role for SFL2 in morphogenesis and an indirect role in C. albicans pathogenesis in epithelial tissues. Global gene expression in Candida albicans SC5314 or Candida dubliniensis CD36 on reconstituted human oral epithelium (RHE) 90 min postinoculation. Gene expression on RHE was compared to gene expression on polycarbonate filter (PCF; used as RHE support matrix) 90 min postinoculation. Performed in two biological replicates with reciprocal dye swaps for each biological replicate. Gene expression of Candida cells on RHE was normalized to gene expression in reference control (PCF); log2 ratios were calculated by dividing spot intensity of experimental by that of the reference control.
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Project description:Candida albicans and Candida dubliniensis are closely related species displaying differences in virulence and genome content, therefore providing potential opportunities to identify novel C. albicans virulence genes. C. albicans gene arrays were used for comparative analysis of global gene expression in the two species in reconstituted human oral epithelium (RHE). C. albicans (SC5314) showed upregulation of hypha-specific and virulence genes within 30 min postinoculation, coinciding with rapid induction of filamentation and increased RHE damage. C. dubliniensis (CD36) showed no detectable upregulation of hypha-specific genes, grew as yeast, and caused limited RHE damage. Several genes absent or highly divergent in C. dubliniensis were upregulated in C. albicans. One such gene, SFL2 (orf19.3969), encoding a putative heat shock factor, was deleted in C. albicans. ÎÎsfl2 cells failed to filament under a range of hypha-inducing conditions and exhibited greatly reduced RHE damage, reversed by reintroduction of SFL2 into the ÎÎsfl2 strain. Moreover, SFL2 overexpression in C. albicans triggered hyphal morphogenesis. Although SFL2 deletion had no apparent effect on host survival in the murine model of systemic infection, ÎÎsfl2 strain-infected kidney tissues contained only yeast cells. These results suggest a role for SFL2 in morphogenesis and an indirect role in C. albicans pathogenesis in epithelial tissues. Global gene expression in Candida albicans SC5314 or Candida dubliniensis CD36 on reconstituted human oral epithelium (RHE) 30 min postinoculation. Gene expression on RHE was compared to gene expression in cells used as inoculum (0 min). Performed in three biological replicates with dye swaps across the biological replicates. Gene expression of Candida cells on RHE was normalized to gene expression in reference control (0 min); log2 ratios were calculated by dividing spot intensity of experimental by that of the reference control.
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