Iron deprivation enhances transcriptional responses to growth arrest of Mycobacterium tuberculosis
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ABSTRACT:
PROVIDER: PRJNA883243 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21675918_1.fastq.gz | Fastqsanger.gz | |||
| SRR21675918_2.fastq.gz | Fastqsanger.gz | |||
| SRR21675919_1.fastq.gz | Fastqsanger.gz | |||
| SRR21675919_2.fastq.gz | Fastqsanger.gz | |||
| SRR21675920_1.fastq.gz | Fastqsanger.gz |
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Project description:The establishment of Mycobacterium tuberculosis (Mtb) long-term infection in vivo depends on several factors, one of which is bacterial availability of key nutrients such as iron. The relation between Fe deprivation inside the granuloma and the capacity of Mtb to accumulate lipids and persist in the absence of growth is not well understood. In this context, current knowledge of how Mtb modifies its lipid composition in response to iron starvation is scarce.
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Project description:Triplicate experiments from T98G cells under asynchronously growing, and growth arrest by serum deprivation and contact inhibition. Keywords: other
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Project description:To ensure their high proliferation rate, tumor cells display an iron metabolic disorder with increased iron needs, making them more susceptible to iron deprivation. This vulnerability could be a therapeutic target. In breast cancers, the development of new therapeutic approaches is urgently needed for patients with triple negative tumors which frequently relapse after chemotherapy and suffer from a lack of targeted therapies. Anticancer activity of iron chelator deferasirox (DFX) assessed in monotherapy do not appear to be effective enough to treat breast cancer progression. In this work, we demonstrated that DFX synergizes with standard chemotherapeutic agents such as with doxorubicin, cisplatin and carboplatin to inhibit cell proliferation and induce apoptosis and autophagy in TNBC cell lines. Moreover, the combination of DFX with doxorubicin and cyclophosphamide allowed to delay or avoid recurrences in breast cancer patient-derived xenografts without increasing the side-effects of chemotherapies alone or altering global iron storage of mice. Antitumor synergy of DFX and doxorubicin involves down-regulation of PI3K and NF-κB pathways. Furthermore, as TNBC patients with low iron tumor dynamic in their tumor present a good prognosis, we thought that iron deprivation mediated by iron chelators may all the more increase the effectiveness of conventional chemotherapies for TNBC treatments.
2020-11-06 | GSE106618 | GEO
Project description:Glutamine deprivation enhances directed differentiation of renal organoids
| PRJNA529412 | ENA
Project description:Due to its aquatic saprophytic lifestyle, the fungus Blastocladiella emersonii seems to be adapted to low aerated environments and thus can be an interesting model of study of the hypoxic stress response. Iron deprivation, a hypoxia-mimicking stimulus due to HIF-1 stabilization, and geldanamycin, that causes HIF-1 depletion by HSP90 inhibition, are helpful parameters to find an evidence of an oxygen-dependent regulatory mechanism in B. emersonii similar to the metazoan HIF-1 pathway. Direct transcript comparison between cells grown under normoxic conditions (70%sat. O2 in air) and cells submitted to oxygen deprivation (direct and gradual) and iron (II) deprivation. It was also compared transcripts of cells submitted to direct 1-hour hypoxia (1%sat. O2) with cells treated with geldanamycin for 1 hour, followed to 1-hour hypoxia (1%sat. O2). There are at least 3 biological replicates (independent harvest) and 2 technical replicates of each array (L - left and R - right).
2010-06-24 | E-GEOD-17524 | biostudies-arrayexpress
Project description:The establishment of Mycobacterium tuberculosis (Mtb) long-term infection in vivo depends on several factors, one of which is the availability of key nutrients such as iron (Fe). The relation between Fe deprivation inside and outside the granuloma, and the capacity of Mtb to accumulate lipids and persist in the absence of growth is not well understood. In this context, current knowledge of how Mtb modifies its lipid composition in response to growth arrest, depending on iron availability, is scarce. To shed light on these matters, in this work we compare genome-wide transcriptomic and lipidomic profiles of Mtb at exponential and stationary growth phases using cultures with glycerol as a carbon source, in the presence or absence of iron. As a result, we found that transcriptomic responses to growth arrest, considered as the transition from exponential to stationary phase, are iron dependent for as many as 714 genes (iron-growth interaction contrast, FDR <0.05), and that, in a majority of these genes, iron deprivation enhances the magnitude of the transcriptional responses to growth arrest in either direction. On the one hand, genes whose upregulation upon growth arrest is enhanced by iron deprivation were enriched in functional terms related to homeostasis of ion metals, and responses to several stressful cues considered cardinal features of the intracellular environment. On the other hand, genes showing negative responses to growth arrest that are stronger in iron-poor medium were enriched in energy production processes (TCA cycle, NADH dehydrogenation and cellular respiration), and key controllers of ribosomal activity shut-down, such as the T/A system mazE6/F6. Despite of these findings, a main component of the cell envelope, lipid phthiocerol dimycocerosate (PDIM), was not detected in the stationary phase regardless of iron availability, suggesting that lipid changes during Mtb adaptation to non-dividing phenotypes appear to be iron-independent. Taken together, our results indicate that environmental iron levels act as a key modulator of the intensity of the transcriptional adaptations that take place in the bacterium upon its transition between dividing and dormant-like phenotypes in vitro.
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Project description:Iron restriction is a growth limiting condition encountered by M. tuberculosis in the host. In this study we examined the survival and physiology of iron depleted M. tuberculosis. We found that iron depleted M. tuberculosis survive for long time with little or no replication and is able to resume normal growth when iron becomes available. To understand the mechanism used by M. tuberculosis to survive under iron starvation we examine the transcriptional profile of iron-starving in comparison to that of iron-sufficient M. tuberculosis.
2017-09-15 | GSE84554 | GEO
Project description:The budding yeast S. cerevisiae responds to depletion of iron in the environment by activating Aft1p, the major iron-dependent transcription factor, and by transcribing systems involved in the uptake of iron. Here we have studied the transcriptional response to iron deprivation, and have identified new Aft1p target genes. We find that other metabolic pathways are regulated by iron: biotin uptake and biosynthesis, nitrogen assimilation, and purine biosynthesis. Two enzymes active in these pathways, biotin synthase and glutamate synthase, require an iron-sulfur cluster for activity. Iron deprivation activates transcription of the biotin importer and simultaneously represses transcription of the entire biotin biosynthetic pathway. Multiple genes involved in nitrogen assimilation and amino acid metabolism are induced by iron deprivation, while glutamate synthase, a key enzyme in nitrogen assimilation, is repressed. A CGG palindrome within the promoter of glutamate synthase confers iron-regulated expression, suggesting control by a transcription factor of the binuclear zinc cluster family. We provide evidence that yeast subjected to iron deprivation undergo a transcriptional remodeling, resulting in a shift from iron-dependent to parallel, but iron-independent, metabolic pathways. A dose response design type examines the relationship between the size of the administered dose and the extent of the response of the organism(s). Keywords: dose_response_design
2006-02-08 | GSE4196 | GEO
Project description:The budding yeast S. cerevisiae responds to depletion of iron in the environment by activating Aft1p, the major iron-dependent transcription factor, and by transcribing systems involved in the uptake of iron. Here we have studied the transcriptional response to iron deprivation, and have identified new Aft1p target genes. We find that other metabolic pathways are regulated by iron: biotin uptake and biosynthesis, nitrogen assimilation, and purine biosynthesis. Two enzymes active in these pathways, biotin synthase and glutamate synthase, require an iron-sulfur cluster for activity. Iron deprivation activates transcription of the biotin importer and simultaneously represses transcription of the entire biotin biosynthetic pathway. Multiple genes involved in nitrogen assimilation and amino acid metabolism are induced by iron deprivation, while glutamate synthase, a key enzyme in nitrogen assimilation, is repressed. A CGG palindrome within the promoter of glutamate synthase confers iron-regulated expression, suggesting control by a transcription factor of the binuclear zinc cluster family. We provide evidence that yeast subjected to iron deprivation undergo a transcriptional remodeling, resulting in a shift from iron-dependent to parallel, but iron-independent, metabolic pathways. A dose response design type examines the relationship between the size of the administered dose and the extent of the response of the organism(s). Using regression correlation
2006-02-07 | E-GEOD-4196 | biostudies-arrayexpress