Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Acetylated microtubules refine cytomegalovirus interactions with and remodeling of host chromatin [TT-seq]

ABSTRACT: Human cytomegalovirus extensively alters nuclear organization and the cellular transcriptome, yet our understanding of these events remains relatively limited. Here, chromatin conformation capture reveals that cytomegalovirus dramatically alters chromosome organization at both large-scale and local compartment levels. Nascent transcriptomics further reveals the extent to which transcriptional changes correlate with compartment changes, while also uncovering infection-induced read-in and read-through events that result in the expression of normally repressed neuronal genes in infected fibroblasts. Moreover, we find that viral genomes preferentially localize to the most abundant and euchromatic compartments of the host, further dysregulating transcription of subsets of host genes. Finally, we show that microtubule-derived forces on the nucleus regulate viral interactions with host chromatin as well as local compartment interactions, which in turn influences infection-induced transcriptional reprogramming. Combined, our findings reveal the extent to which HCMV alters chromatin organization and transcriptional activity, along with the contribution of microtubules to these processes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE284780 | GEO | 2025/07/23

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Acetylated microtubules refine cytomegalovirus interactions with and remodeling of host chromatin [CUT&Run]

Project description:Human cytomegalovirus extensively alters nuclear organization and the cellular transcriptome, yet our understanding of these events remains relatively limited. Here, chromatin conformation capture reveals that cytomegalovirus dramatically alters chromosome organization at both large-scale and local compartment levels. Nascent transcriptomics further reveals the extent to which transcriptional changes correlate with compartment changes, while also uncovering infection-induced read-in and read-through events that result in the expression of normally repressed neuronal genes in infected fibroblasts. Moreover, we find that viral genomes preferentially localize to the most abundant and euchromatic compartments of the host, further dysregulating transcription of subsets of host genes. Finally, we show that microtubule-derived forces on the nucleus regulate viral interactions with host chromatin as well as local compartment interactions, which in turn influences infection-induced transcriptional reprogramming. Combined, our findings reveal the extent to which HCMV alters chromatin organization and transcriptional activity, along with the contribution of microtubules to these processes.

2025-07-23 | GSE284782 | GEO

Acetylated microtubules refine cytomegalovirus interactions with and remodeling of host chromatin [RNA-seq]

2025-07-23 | GSE284781 | GEO

Acetylated microtubules refine cytomegalovirus interactions with and remodeling of host chromatin [Hi-C]

2025-07-23 | GSE284783 | GEO

Multiomics profiling of HIV-infected cells

Project description:The restructuring of chromatin architecture following lentiviral integration is not well elucidated. We jointly interrogate (HIV-distal & -local) chromatin organization (via Hi-C & ATAC-seq) and the RNA landscape around defined sites of proviral integration using HIV-inducible cellular models. We report chromatin interaction networks and nuclear ultrastructure around integrated HIV-1 are predominantly preserved, suggesting HIV integration does not induce large scale remodeling of cellular chromatin. Instead, we find that induction of proviral transcription leads to stark local changes in nucleosome organization with chromatin accessibility increasing at the intergenic junction between the HIV-1 3’ LTR and flanking cellular genome. This result suggests subtle changes in chromatin structure may be mediating proviral activation. Using long-read Nanopore RNA-seq, we interrogate the local host & HIV transcriptomes, observing a small fraction of HIV-1 transcripts are chimeric read-through products, where transcription initiates at the HIV-1 5’ LTR promoter and continues extensively into the flanking cellular genome. Despite provirus-driven read-through, HIV-1 appears to have only a modest effect on the local transcriptional environment. The changes in chromatin accessibility and read-through at activated proviruses closely resembles lytic Herpes simplex virus type 1 (HSV-1) induced cellular chromatin reprogramming. We propose chromatin “opening” at the 3’ LTR HIV-host junction is important for sustained proviral activity, and overall, HIV proviruses do not significantly alter local host transcription and chromatin structure. Our studies provide the first in-depth integrative investigation of 3D chromatin organization, nucleosome density, and HIV-host transcriptomes at HIV-host genic boundaries.

2021-10-26 | GSE184345 | GEO

Multiomic Profiling Reveals Unexpected Increased Chromatin Accessibility Downstream from the 3’ LTR OF Active HIV-1 Proviruses (Hi-C)

Project description:The three-dimensional structure of the genome is a regulator of transcription and cell function; HIV-1 infection can influence host cell function, but the degree to which this is mediated through changes to host chromatin architecture is unclear. We interrogated genome-wide chromatin organization and the structure of chromatin around latently infected HIV-1 integration sites using Hi-C and ATAC-seq and combined these data with RNA transcriptional analysis of the provirus and neighboring genes in HIV-inducible cellular models. We found chromatin interaction networks around integrated HIV-1 are predominantly preserved with respect to uninfected cells, proving the lack of an obligate association between latent integration and major chromatin remodeling. Instead, we find that induction of proviral transcription may lead to local changes in chromatin accessibility downstream from the 3’ LTR, demonstrating that HIV-1 can alter local cellular chromatin structure post-integration. Using long-read Nanopore RNA-seq, we interrogated the local host and HIV-1 transcriptomes and observed that 1-5% of HIV-1 transcripts initiated at the 5’ LTR promoter extended into the flanking cellular genome, generating chimeric virus-host RNAs. Thus, integration leading to latency (and provirus activation) may not lead to obligate global chromatin rearrangements; we also observed, previously unreported, novel changes in chromatin accessibility during HIV-1 transcription.

2022-08-26 | GSE189178 | GEO

Vaccinia virus infection induces concurrent alterations in host chromatin architecture, accessibility, and gene expression [ATAC-seq]

Project description:Genomic DNA folds into complex configurations that produce particular local and globalstructures thought to profoundly impact genome function. To understand the dynamic nature ofthis relationship, we investigated the extent of host chromatin structural and functional changesin response to a viral agent. We performed comprehensive assessments of host architecture (Hi-C), accessibility (ATAC-seq), and gene expression (RNA-seq) in a paired manner in response toattenuated vaccinia (smallpox) virus. Over time, infection significantly increased long-rangeintra-chromosomal interactions and decreased chromatin accessibility. Fine-scale accessibilitychanges were independent of broad-scale chromatin compartment exchange, which increased (upto 12% of the genome) over time, underscoring potential independent mechanisms for global andlocal chromatin reorganization. The majority of differentially expressed genes, including thosedownregulated in immune responses, had concurrent alterations in local accessibility and loopdomain restructuring. Increased B compartmentalization, intra-chromosomal interactions, anddecreased inter-chromosomal interactions and chromatin accessibility together indicate thatinfection converts the host genome into a more condensed state with nearly equal bidirectionaldifferential gene expression. These changes in host chromatin features may have implications fordeveloping efficacious anti-viral countermeasures. Overall, our empirical data provides evidenceof orchestrated concurrent alterations in chromatin architecture, accessibility, and geneexpression in response to infection, further reinforcing the notion of coordinated structurefunctiondynamics of the genome.

2024-05-07 | GSE248048 | GEO

Vaccinia virus infection induces concurrent alterations in host chromatin architecture, accessibility, and gene expression [RNA-seq]

2024-05-11 | GSE248050 | GEO

Vaccinia virus infection induces concurrent alterations in host chromatin architecture, accessibility, and gene expression [Hi-C]

2024-05-11 | GSE248049 | GEO

The white adipose tissue is a hub for memory T cells and promotes memory responses

Project description:The white adipose tissue represents 15% of healthy mammalian hosts and bridges body organs. In addition to serving as a scaffold for the lymphatic and blood vasculature, this compartment plays a fundamental role in the control of host metabolism. To which extent the adipose tissue also contributes to immune surveillance and long-term protective defense remains largely unknown. Here, we show that under steady state conditions, the white adipose tissue is home to abundant and diverse memory lymphocyte populations. Following infection, the adipose tissue accumulates large numbers of pathogen-specific memory T cells, including tissue-resident (TRM) cells. Memory T cells found in the adipose tissue express a distinct metabolic profile and are characterized by heightened proliferative and effector capacity. As such, adipose tissue from previously infected mice is sufficient to protect from lethal challenge. Local reactivation of adipose tissue memory T cells leads to rapid responses with local impacts on both immune and metabolic pathways, including direct responses by adipocytes. Notably, induction of recall responses within the adipose tissue is associated with the collapse of lipid metabolism in favor of antimicrobial responses. Thus, our results propose that the white adipose tissue, a compartment that interfaces with all body organs, may represent a unique immune compartment, able to provide early warning and potent effector memory responses. Together, these results uncover the adipose tissue as a dominant reservoir of memory T cells endowed with long-term protective functions, positioning this compartment as a potential major contributor of immunological memory.

2017-11-21 | GSE104955 | GEO

primate metagenome

Project description:Cytomegalovirus alters gut microbiota-immune system relationships

| PRJNA430083 | ENA