Ontology highlight
ABSTRACT:
PROVIDER: PRJNA338896 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR4031065_1.fastq.gz | Fastqsanger.gz | |||
| SRR4031065_2.fastq.gz | Fastqsanger.gz |
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Project description:In this paper, we examine orthologs of a transcriptional regulator in three fungal species, Saccharomyces cerevisiae, Candida albicans, and Histoplasma capsulatum. We show that, despite an estimated 600 million years since those species diverged from a common ancestor, Wor1 in C. albicans, Ryp1 in H. capsulatum, and Mit1 in S. cerevisiae recognize the same DNA motif. Previous work established that Wor1 regulates white-opaque switching in C. albicans and that its ortholog Ryp1 regulates the yeast to mycelial transition in H. capsulatum. Here we show that the ortholog Mit1 in S. cerevisiae also regulates a morphological transition, in this case pseudohyphal growth. Full genome chromatin immunoprecipitation experiments show that Mit1 binds to the control regions of approximately 94 genes including the previously known regulators of pseudohyphal growth. Through a comparison of full genome chromatin immunoprecipitation experiments for Mit1 in S. cerevisiae, Wor1 in C. albicans, and Wor1 ectopically expressed in S. cerevisiae, we conclude that genes controlled by the orthologous regulators overlap only slightly between these two species. We suggest that the ancestral Wor1/Mit1/Ryp1 protein controlled aspects of cell morphology and that evolutionary movement of genes in and out of the Wor1/Mit1/Ryp1 regulon is responsible, in part, for the differences of morphological forms among these species. Consistent with this idea, ectopic expression of C. albicans Wor1 or H. capsulatum Ryp1 can drive the pseudohyphal growth program in S. cerevisiae.
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Project description:Histoplasma capsulatum is a fungal pathogen that infects both healthy and immunocompromised hosts. In endemic regions, H. capsulatum grows in the soil and causes respiratory and systemic disease when inhaled by humans. An interesting aspect of H. capsulatum biology is that it adopts specialized developmental programs in response to its environment. In the soil, it grows as filamentous chains of cells (mycelia) that produce asexual spores (conidia). When the soil is disrupted, conidia aerosolize and are inhaled by mammalian hosts. Inside a host, conidia germinate into yeast-form cells that colonize immune cells and cause disease. Despite the ability of conidia to initiate infection and disease, they have not been explored on a molecular level. Here we develop methods to purify H. capsulatum conidia and show that these cells germinate into either filaments at room temperature or into yeast-form cells at 37C. Conidia internalized by macrophages germinate into the yeast form and proliferate within the macrophages, ultimately lysing the host cells. Similarly, infection of mice with purified conidia is sufficient to establish infection and yield viable yeast-form cells in vivo. To characterize conidia on a molecular level, we perform whole-genome expression profiling of conidia, yeast, and mycelia from two highly diverged H. capsulatum strains. In parallel, we use homology and protein domain analysis to manually annotate the predicted genes of both strains. Analyses of the resultant data define sets of transcripts that reflect the unique molecular states of H. capsulatum conidia, yeast and mycelia. This series gives the results for the G186AR strain.
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Project description:Histoplasma capsulatum is a fungal pathogen that infects both healthy and immunocompromised hosts. In endemic regions, H. capsulatum grows in the soil and causes respiratory and systemic disease when inhaled by humans. An interesting aspect of H. capsulatum biology is that it adopts specialized developmental programs in response to its environment. In the soil, it grows as filamentous chains of cells (mycelia) that produce asexual spores (conidia). When the soil is disrupted, conidia aerosolize and are inhaled by mammalian hosts. Inside a host, conidia germinate into yeast-form cells that colonize immune cells and cause disease. Despite the ability of conidia to initiate infection and disease, they have not been explored on a molecular level. Here we develop methods to purify H. capsulatum conidia and show that these cells germinate into either filaments at room temperature or into yeast-form cells at 37C. Conidia internalized by macrophages germinate into the yeast form and proliferate within the macrophages, ultimately lysing the host cells. Similarly, infection of mice with purified conidia is sufficient to establish infection and yield viable yeast-form cells in vivo. To characterize conidia on a molecular level, we perform whole-genome expression profiling of conidia, yeast, and mycelia from two highly diverged H. capsulatum strains. In parallel, we use homology and protein domain analysis to manually annotate the predicted genes of both strains. Analyses of the resultant data define sets of transcripts that reflect the unique molecular states of H. capsulatum conidia, yeast and mycelia. This series gives the results for the G217B strain.
2013-04-10 | GSE45415 | GEO
Project description:Analyzed 84 genes from macrophages infected with Histoplasma capsulatum for changes in expression over 24 hours Macrophages infected with Histoplasma capsulatum were analyzed for alterations in apoptosis genes, 5 biological replicate (rep1-5)
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