Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18067116.fastq.gz | Fastqsanger.gz | |||
| SRR18067117.fastq.gz | Fastqsanger.gz | |||
| SRR18067118.fastq.gz | Fastqsanger.gz | |||
| SRR18067119.fastq.gz | Fastqsanger.gz | |||
| SRR18067120.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Latent tuberculosis infection (LTBI) relies on a homeostasis of macrophages and Mycobacterium tuberculosis (Mtb). The small heat shock protein, Mtb Hsp16.3 (also known as latency-associated antigen), plays an important role in Mtb persistence within macrophages. However, the mechanism of LTBI remains elusive. The aim of this study was to delineate LTBI-related miRNA expression in U937 macrophages expressing Mtb Hsp16.3 protein. This study intends to explore the potential function of miRNAs in the interaction of macrophages with Mtb Hsp16.3 and provide insights for investigating the role of macrophage homeostasis in LTBI.
2014-03-17 | GSE54630 | GEO
Project description:Unlike many pathogens that are overtly toxic to their hosts, the primary virulence determinant of Mycobacterium tuberculosis appears to be its ability to persist for years or decades within humans in a clinically latent state. Since early in the 20th century latency has been linked to hypoxic conditions within the host, but the response of M. tuberculosis to a hypoxic signal remains poorly characterized. The M. tuberculosis alpha-crystallin (acr) gene is powerfully and rapidly induced at reduced oxygen tensions, providing us with a means to identify regulators of the hypoxic response. Using a whole genome microarray, we identified >100 genes whose expression is rapidly altered by defined hypoxic conditions. Numerous genes involved in biosynthesis and aerobic metabolism are repressed, whereas a high proportion of the induced genes have no known function. Among the induced genes is an apparent operon that includes the putative two-component response regulator pair Rv3133cy Rv3132c. When we interrupted expression of this operon by targeted disruption of the upstream gene Rv3134c, the hypoxic regulation of acr was eliminated. These results suggest a possible role for Rv3132cy3133cy3134c in mycobacterial latency.
2007-09-12 | E-TABM-312 | biostudies-arrayexpress
Project description:Unlike many pathogens that are overtly toxic to their hosts, the primary virulence determinant of Mycobacterium tuberculosis appears to be its ability to persist for years or decades within humans in a clinically latent state. Since early in the 20th century latency has been linked to hypoxic conditions within the host, but the response of M. tuberculosis to a hypoxic signal remains poorly characterized. The M. tuberculosis alpha-crystallin (acr) gene is powerfully and rapidly induced at reduced oxygen tensions, providing us with a means to identify regulators of the hypoxic response. Using a whole genome microarray, we identified >100 genes whose expression is rapidly altered by defined hypoxic conditions. Numerous genes involved in biosynthesis and aerobic metabolism are repressed, whereas a high proportion of the induced genes have no known function. Among the induced genes is an apparent operon that includes the putative two-component response regulator pair Rv3133cy Rv3132c. When we interrupted expression of this operon by targeted disruption of the upstream gene Rv3134c, the hypoxic regulation of acr was eliminated. These results suggest a possible role for Rv3132cy3133cy3134c in mycobacterial latency. Keywords: comparative genome hybridization design and stimulus or stress design Six samples were analyzed. The quality controls were biological replicate and technical replicate
2010-06-05 | E-GEOD-8639 | biostudies-arrayexpress
Project description:The ability of Mycobacterium tuberculosis (Mtb) to establish latency directly impacts disease and response to treatment but the host’s influence on this switch remains elusive. Using a novel Mtb reporter strain to separate macrophages infected with replicating or latent Mtb, we performed transcriptomics and genome-wide CRISPR screens. After validating the recovery of known susceptibility loci from TB GWAS as modifiers of active replication, we identified multiple pathways and novel modulators of latency. We validated multiple controllers of latency and mechanistically characterized the transporter MMGT1. MMGT1-deficient macrophages upregulated lipid metabolism genes and accumulated lipid droplets during infection. Critically, targeting triacylglycerol synthesis reduced both droplet formation and Mtb latency. We identified GPR156, an orphan GPCR as a key inducer of droplet accumulation in ΔMMGT1 cells. Altogether, our work uncovers the role of MMGT1-GPR156-lipid droplets in the induction of Mtb latency, suggesting that host-directed therapies could be used to modulate Mtb phenotypes during infection.
2023-06-01 | GSE210690 | GEO
Project description:The ability of Mycobacterium tuberculosis (Mtb) to establish latency directly impacts disease and response to treatment but the host’s influence on this switch remains elusive. Using a novel Mtb reporter strain to separate macrophages infected with replicating or latent Mtb, we performed transcriptomics and genome-wide CRISPR screens. After validating the recovery of known susceptibility loci from TB GWAS as modifiers of active replication, we identified multiple pathways and novel modulators of latency. We validated multiple controllers of latency and mechanistically characterized the transporter MMGT1. MMGT1-deficient macrophages upregulated lipid metabolism genes and accumulated lipid droplets during infection. Critically, targeting triacylglycerol synthesis reduced both droplet formation and Mtb latency. We identified GPR156, an orphan GPCR as a key inducer of droplet accumulation in ΔMMGT1 cells. Altogether, our work uncovers the role of MMGT1-GPR156-lipid droplets in the induction of Mtb latency, suggesting that host-directed therapies could be used to modulate Mtb phenotypes during infection.
2023-06-01 | GSE210689 | GEO
Project description:The ability of Mycobacterium tuberculosis (Mtb) to establish latency directly impacts disease and response to treatment but the host’s influence on this switch remains elusive. Using a novel Mtb reporter strain to separate macrophages infected with replicating or latent Mtb, we performed transcriptomics and genome-wide CRISPR screens. After validating the recovery of known susceptibility loci from TB GWAS as modifiers of active replication, we identified multiple pathways and novel modulators of latency. We validated multiple controllers of latency and mechanistically characterized the transporter MMGT1. MMGT1-deficient macrophages upregulated lipid metabolism genes and accumulated lipid droplets during infection. Critically, targeting triacylglycerol synthesis reduced both droplet formation and Mtb latency. We identified GPR156, an orphan GPCR as a key inducer of droplet accumulation in ΔMMGT1 cells. Altogether, our work uncovers the role of MMGT1-GPR156-lipid droplets in the induction of Mtb latency, suggesting that host-directed therapies could be used to modulate Mtb phenotypes during infection.
2023-06-01 | GSE210687 | GEO
Project description:Unlike many pathogens that are overtly toxic to their hosts, the primary virulence determinant of Mycobacterium tuberculosis appears to be its ability to persist for years or decades within humans in a clinically latent state. Since early in the 20th century latency has been linked to hypoxic conditions within the host, but the response of M. tuberculosis to a hypoxic signal remains poorly characterized. The M. tuberculosis alpha-crystallin (acr) gene is powerfully and rapidly induced at reduced oxygen tensions, providing us with a means to identify regulators of the hypoxic response. Using a whole genome microarray, we identified >100 genes whose expression is rapidly altered by defined hypoxic conditions. Numerous genes involved in biosynthesis and aerobic metabolism are repressed, whereas a high proportion of the induced genes have no known function. Among the induced genes is an apparent operon that includes the putative two-component response regulator pair Rv3133cy Rv3132c. When we interrupted expression of this operon by targeted disruption of the upstream gene Rv3134c, the hypoxic regulation of acr was eliminated. These results suggest a possible role for Rv3132cy3133cy3134c in mycobacterial latency. Keywords: comparative genome hybridization design and stimulus or stress design
2007-08-01 | GSE8639 | GEO
Project description:Spontaneous Latency in a Rabbit Model of Pulmonary Tuberculosis
| PRJNA170243 | ENA
Project description:The epigenetic mechanisms established by histone modifications may affect the transcriptional silencing of HIV-1 and viral latency. A systematic epigenome profiling could be applicable to develop new epigenetic diagnostic markers for detecting HIV-1 latency. In this study, histone modification profiles of HIV-1 latency cell lines were compared with those of uninfected CD4+ T cell line. The HIV-1 latency gave rise to differential histone modification regions. The differential enrichment patterns helped us to define potential effector genes leading to the viral latency. The histone H3K4me3 and H3K9ac profiles were obtained from the HIV-1 latency cell lines (NCHA1, NCHA2, and ACH2) and control CD4+ T cell line (A3.01)
2014-06-06 | E-GEOD-58247 | biostudies-arrayexpress
Project description:Mycobacterium tuberculosis is an example of a bacterial pathogen with a specialized SecA2-dependent protein export system that contributes to its virulence. Our understanding of the mechanistic basis of SecA2-dependent export and the role(s) of the SecA2 pathway in M. tuberculosis pathogenesis has been hindered by our limited knowledge of the proteins exported by the pathway. Here, we set out to identify M. tuberculosis proteins that use the SecA2 pathway for their export from the bacterial cytoplasm to the cell wall. Using label-free quantitative (LFQ) proteomics involving spectral counting, we compared the cell wall and cytoplasmic proteomes of wild type M. tuberculosis to that of a ΔsecA2 mutant. This work revealed a role for the M. tuberculosis SecA2 pathway in the cell wall localization of solute binding proteins (SBPs) that work with ABC transporters to import solutes. Another discovery was a profound effect of SecA2 on the cell wall localization of the Mce1 and Mce4 lipid transporters, which contribute to M. tuberculosis virulence. In addition to the effects on SBP and Mce transporter export, our LFQ analysis revealed an unexpected relationship between SecA2 and the hypoxia-induced DosR regulon, which is associated with M. tuberculosis latency. Nearly half of the transcriptionally controlled DosR regulon of cytoplasmic proteins were detected at higher levels in the ΔsecA2 mutant versus wild type M. tuberculosis. By increasing the list of M. tuberculosis proteins known to be affected by the SecA2 pathway, this study expands our appreciation of the types of proteins exported by this pathway and guides our understanding of the mechanism of SecA2-dependent protein export in mycobacteria. At the same time, the newly identified SecA2-dependent proteins are helpful for understanding the significance of this pathway to M. tuberculosis virulence and physiology
2018-10-24 | PXD002144 | Pride