A microsporidia possesses robust transcriptional response to heat shock impacting diverse cellular processes despite lack of HSF
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA527270 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8734360_1.fastq.gz | Fastqsanger.gz | |||
| SRR8734360_2.fastq.gz | Fastqsanger.gz | |||
| SRR8734361_1.fastq.gz | Fastqsanger.gz | |||
| SRR8734361_2.fastq.gz | Fastqsanger.gz | |||
| SRR8734356_1.fastq.gz | Fastqsanger.gz |
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Project description:The majority of fungal species prefer the 12°–30° C range and relatively few species tolerate temperatures higher than 35° C . Our understanding of the mechanisms underpinning the ability of some species to grow at higher temperatures is incomplete. Nosema ceranae is an obligate intracellular fungal parasite that infects honey bees and can cause individual mortality and contribute to colony collapse. Despite a reduced genome, this species is strikingly thermotolerant, growing optimally at the colony temperature of 35° C. In characterizing the HSR in N. ceranae, we found that this and other microsporidian species have lost the transcriptional regulator HSF and possess a reduced set of putative core HSF1-dependent HSR target genes. Despite these losses, N. ceranae demonstrates robust upregulation of the remaining HSR target genes after heat shock. In addition, thermal stress leads to alterations in genes involved in various metabolic pathways, ribosome biogenesis and translation, and DNA repair. These results provide important insight into the stress responses of microsporidia. Such new understanding will allow new comparisons with other pathogenic fungi and potentially enable discovery of novel treatment strategies for microsporidia infections affecting food production and human health.
2019-04-30 | GSE128364 | GEO
Project description:Microsporidia are intracellular eukaryotic pathogens that pose a substantial threat to immunocompromised hosts. The way these pathogens manipulate host cells during infection remains poorly understood. Using a proximity biotinylation strategy we established that microsporidian EnP1 is a nucleus-targeted effector that modifies the host cell environment. EnP1's translocation to the host nucleus is meditated by nuclear localization signals (NLSs). In the nucleus, EnP1 interacts with host histone H2B. This interaction disrupts H2B monoubiquitination (H2Bub), subsequently impacting p53 expression. Crucially, this inhibition of p53 weakens its control over the downstream target gene SLC7A11, enhancing the host cell's resilience against ferroptosis during microsporidian infection. This favorable condition promotes the proliferation of microsporidia within the host cell. These findings shed light on the molecular mechanisms by which microsporidia modify their host cells to facilitate their survival.
2023-11-21 | GSE247835 | GEO
Project description:The majority of fungal species prefer the 12° to 30°C range, and relatively few species tolerate temperatures higher than 35°C. Our understanding of the mechanisms underpinning the ability of some species to grow at higher temperatures is incomplete. Nosema ceranae is an obligate intracellular fungal parasite that infects honey bees and can cause individual mortality and contribute to colony collapse. Despite a reduced genome, this species is strikingly thermotolerant, growing optimally at the colony temperature of 35°C. In characterizing the heat shock response (HSR) in N. ceranae, we found that this and other microsporidian species have lost the transcriptional regulator HSF and possess a reduced set of putative core HSF1-dependent HSR target genes. Despite these losses, N. ceranae demonstrates robust upregulation of the remaining HSR target genes after heat shock. In addition, thermal stress leads to alterations in genes involved in various metabolic pathways, ribosome biogenesis and translation, and DNA repair. These results provide important insight into the stress responses of microsporidia. Such a new understanding will allow new comparisons with other pathogenic fungi and potentially enable the discovery of novel treatment strategies for microsporidian infections affecting food production and human health.IMPORTANCE We do not fully understand why some fungal species are able to grow at temperatures approaching mammalian body temperature. Nosema ceranae, a microsporidium, is a type of fungal parasite that infects honey bees and grows optimally at the colony temperature of 35°C despite possessing cellular machinery for responding to heat stress that is notably simpler than that of other fungi. We find that N. ceranae demonstrates a robust and broad response to heat shock. These results provide important insight into the stress responses of this type of fungus, allow new comparisons with other pathogenic fungi, and potentially enable the discovery of novel treatment strategies for this type of fungus.
| S-EPMC6531884 | biostudies-literature
Project description:Comparative genomic analysis of nematode-infecting microsporidia
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Project description:uncultured Microsporidia Transcriptome or Gene expression
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Project description:Impaired protein homeostasis promotes age-associated tissue dysregulation, presenting a need for therapeutic approaches that can restore proteome integrity. The heat shock factor HSF-1 is the master transcriptional regulator of proteostasis and regulates the expression of heat shock proteins (HSPs), which facilitate proper protein folding, localisation, and degradation. Increased HSF-1 activity can suppress proteotoxicity and enhance longevity across species. Studies into the mechanisms behind these beneficial effects have mostly focused on HSPs; however, the precise mechanisms by which increased HSF-1 activity extends lifespan are not known. To address this, we conducted an RNAi screen for genes that promote longevity, in C. elegans over expressing HSF-1 (hsf-1 OE). We found that ubiquilin-1 (ubql-1), a multifaceted shuttle protein that functions in protein degradation pathways is necessary for full lifespan extension in hsf-1OE worms. Surprisingly, we find that lack of ubql-1 does not impact proteostasis capacity, but does alter mitochondrial dynamics, in hsf-1 OE worms. These effects are independent of mitophagy or the mitochondrial unfolded protein response (mitoUPR) suggesting enhanced turnover of mitochondrial outer membrane proteins may be important for increased longevity via the HSF-1-ubiquilin-1 axis. Additionally, we reveal a role for ubql-1, a protein quality control regulator in regulating lipid homeostasis in hsf-1 OE animals. Lack of ubql-1 in hsf-1 OE animals supresses the expression of a key mitochondrial β-oxidation and lipid mobilization gene regulated by NHR-49 - acyl-CoA synthetase-2, ACS-2 amongst other genes. We propose that ubql-1 is required for mito-fusion and metabolic modulations that promote longevity in hsf-1 OE by interacting with NHR-49.
2024-10-17 | PXD044595 | Pride
Project description:Sequence-specific transcription factors (TFs) are critical for specifying patterns and levels of gene expression, but the DNA elements to which they can bind are not always sufficient to specify their binding in vivo. In eukaryotes, the binding of a TF is in competition with a constellation of other proteins, including histones which package DNA into nucleosomes. Here, we examine using the ChIP-seq assay, the genome-wide distribution of Drosophila Heat Shock Factor (HSF), a TF whose binding activity is mediated by heat shock-induced trimerization. We detect HSF binding to 464 sites, the vast majority of which contain HSF Sequence-binding Elements (HSEs) in Drosophila S2 cells, but these HSF-bound sites represent only a small fraction of HSEs present in the genome. We find a strong correlation of bound HSEs to active chromatin marks present prior to HSF binding, indicating an HSEM-bM-^@M-^Ys residence in open chromatin is a primary determinant of whether HSF can bind following heat shock. A single mock immunoprecipitation (IP) using the pre-innoculated animal serum was used as a background dataset for this study. For each condition (NHS and 20minute HS), we performed two independent HSF-ChIP-seq experiments. In addition, we performed two independent HSF-ChIP-seq experiments for each condition (NHS and 20minute HS) in cells that were highly depleted of HSF by RNAi.
2010-09-02 | E-GEOD-19025 | biostudies-arrayexpress
Project description:In order to recover nuclei with two active X chromosomes (class I), we developed a reprogramming strategy by supplementing hESC media with the small molecules sodium butyrate, and 3-deazaneplanocin A (DZNep). In order to determine how B+D affects global gene expression, we performed microarray analysis in triplicate in the HSF-6 (8) C and HSF-6 (8) B+D treated cultures. We also evaluated HSF-6 (S9) B+D in triplicate and identified no statistically significant changes in gene expression in HSF-6 (S9) B+D compared to HSF-6 (8) B+D treated cultures. This suggests that global transcriptional differences are more strongly modulated by presence or absence of B+D and not the percentage of class I, II or III nuclei. We performed gene expression profiling on hESC HSF-6 (8, S9) in absent (control) and presence of butyrate and DZNep. All cell were collected after 11 passages in absent and presence of butyrate and DZNep.
2011-11-22 | E-GEOD-33864 | biostudies-arrayexpress