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Human cytomegalovirus infection coopts chromatin organization to modulate TEAD1 transcription factor activity

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE254741 | GEO | 2024/12/06

REPOSITORIES: GEO

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Human cytomegalovirus infection coopts chromatin organization to modulate TEAD1 transcription factor activity [HiChIP]

Project description:Human cytomegalovirus (HCMV) infects up to 80% of the world’s population and is linked to serious morbidity in immunocompromised individuals and newborns. Here, using multiple genome-scale assays and computational approaches, we show that HCMV infection leads to widespread changes in chromatin accessibility and chromatin looping, with hundreds of thousands of human genomic regions affected 48 hours after infection. Integrative analyses reveal that HCMV infection perturbs the Hippo signaling pathway by drastically diminishing TEA domain transcription factor 1 (TEAD1) activity. Chromatin immunoprecipitation experiments confirm extensive concordant loss of TEAD1 binding and H3K27ac active histone marks upon infection. TEAD transcription factors are direct effectors of the Hippo signaling pathway, and our data support a position for TEAD1 at the top of a hierarchy involving key developmental pathways with differential expression subsequent to HMCV infection. Known gene targets of TEAD1, including Cellular Communication Network Factor 1 (CCN1) and Thrombospondin 1 (THBS1), are significantly downregulated with HCMV infection, reflecting diminished TEAD1-mediated activity. HCMV infection reduces TEAD1 binding through four distinct mechanisms: closing of TEAD1-bound chromatin, reduction of Yes1 associated transcriptional regulator (YAP1) and phosphorylated YAP (pYAP1) levels, reduction of TEAD1 transcript and protein levels, and alteration of TEAD1 exon-6 usage. Collectively, these comprehensive genome-scale analyses reveal novel mechanisms induced by HCMV infection.

2024-12-06 | GSE254737 | GEO

Human cytomegalovirus infection coopts chromatin organization to modulate TEAD1 transcription factor activity [ChIP-seq]

2024-12-06 | GSE254736 | GEO

Human cytomegalovirus infection coopts chromatin organization to modulate TEAD1 transcription factor activity [RNA-Seq]

2024-12-06 | GSE254735 | GEO

Human cytomegalovirus infection coopts chromatin organization to modulate TEAD1 transcription factor activity [ATAC-seq]

2024-12-06 | GSE254734 | GEO

Human cytomegalovirus infection coopts chromatin organization to modulate TEAD1 transcription factor activity

Project description:Human cytomegalovirus infection coopts chromatin organization to modulate TEAD1 transcription factor activity

| PRJNA1071598 | ENA

Human cytomegalovirus infection coopts chromatin organization to modulate TEAD1 transcription factor activity [HiChIP]

Project description:Human cytomegalovirus infection coopts chromatin organization to modulate TEAD1 transcription factor activity [HiChIP]

| PRJNA1071597 | ENA

Human cytomegalovirus infection coopts chromatin organization to modulate TEAD1 transcription factor activity [ATAC-seq]

Project description:Human cytomegalovirus infection coopts chromatin organization to modulate TEAD1 transcription factor activity [ATAC-seq]

| PRJNA1071590 | ENA

Human cytomegalovirus infection coopts chromatin organization to modulate TEAD1 transcription factor activity [ChIP-seq]

Project description:Human cytomegalovirus infection coopts chromatin organization to modulate TEAD1 transcription factor activity [ChIP-seq]

| PRJNA1071593 | ENA

Human cytomegalovirus infection coopts chromatin organization to modulate TEAD1 transcription factor activity [RNA-Seq]

Project description:Human cytomegalovirus infection coopts chromatin organization to modulate TEAD1 transcription factor activity [RNA-Seq]

| PRJNA1071594 | ENA

Variable Glutamine-Rich Repeats Modulate Transcription Factor Activity.

Project description:Excessive expansions of glutamine (Q)-rich repeats in various human proteins are known to result in severe neurodegenerative disorders such as Huntington's disease and several ataxias. However, the physiological role of these repeats and the consequences of more moderate repeat variation remain unknown. Here, we demonstrate that Q-rich domains are highly enriched in eukaryotic transcription factors where they act as functional modulators. Incremental changes in the number of repeats in the yeast transcriptional regulator Ssn6 (Cyc8) result in systematic, repeat-length-dependent variation in expression of target genes that result in direct phenotypic changes. The function of Ssn6 increases with its repeat number until a certain threshold where further expansion leads to aggregation. Quantitative proteomic analysis reveals that the Ssn6 repeats affect its solubility and interactions with Tup1 and other regulators. Thus, Q-rich repeats are dynamic functional domains that modulate a regulator's innate function, with the inherent risk of pathogenic repeat expansions.

| S-EPMC4543046 | biostudies-literature

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