Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genomic repeats coordinate macroscopic gene function and expression

ABSTRACT: Genomic repeats coordinate macroscopic gene function and expression

PROVIDER: PRJNA517472 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR8496526_1.fastq.gz	Fastqsanger.gz
	SRR8496526_2.fastq.gz	Fastqsanger.gz
	SRR8496527_1.fastq.gz	Fastqsanger.gz
	SRR8496527_2.fastq.gz	Fastqsanger.gz
	SRR8496528_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

Genomic repeats coordinate macroscopic gene function and expression

Project description:Despite abundant distribution of repetitive elements, the roles they have been coopted in mammalian genomes are insufficiently characterized. Here we reveal a pervasive role for genic repeat in shaping macroscopic gene function and expression in both human and mouse. Specifically, genes enriched in SINE, L1 and simple repeat produce proteins with functions in distinct categories. To maintain/regulate the homeostatic expression of gene with diversified functions, SINE and L1 are targeted by different classes of transcriptional regulators and also show a nonrandom genomic and nuclear distribution, with B1 in the nuclear interior and L1 in the nuclear and nucleolar peripheries. Abnormal expression of L1-enriched gene compromise proliferation of embryonic stem cells. Moreover, L1 transcripts tend to bind L1-enriched genes, transacting L1 DNA information and mainly function as transcriptional repressors. These results demonstrate that genomic repeats have subtly shaped the function of host-gene they embedded in, and provide a paradigm shift in understanding function of genomic “parasites” in their host-genome.

2020-03-10 | GSE125766 | GEO

Variable glutamine-rich repeats modulate the function of the transcriptional regulator SSN6

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 repeats 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 Ssn6p (Cyc8p) result in systematic, repeat-length dependent variation in expression of target genes that result in direct phenotypic changes. The function of Ssn6p increases with its repeat number, until a certain threshold where further expansion leads to aggregation. Quantitative proteomic analysis reveals that the Ssn6p 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. Transcriptome profiles of two biological replicates of each SSN6 tandem repeat number variant and the WT grown in a glucose-rich medium (4% glucose - glu4) or in a glucose-starved medium (0 % glucose - glu0)

2015-07-01 | E-GEOD-70209 | biostudies-arrayexpress

Variable glutamine-rich repeats modulate the function of the transcriptional regulator SSN6

2015-07-01 | GSE70209 | GEO

Genomic context sensitivity of insulator function

Project description:Genomic context sensitivity of insulator function

| PRJNA743932 | ENA

Small RNA-mediated genetic switches coordinate ALG-3/4 small RNA pathway function

Project description:Small RNA-mediated genetic switches coordinate ALG-3/4 small RNA pathway function

| PRJNA941966 | ENA

A mechanism of gene evolution generating mucin function

Project description:How novel gene functions evolve is a fundamental question in biology. Mucin proteins, a functionally but not evolutionarily defined group of proteins, allow to study convergent evolution of gene function. By analyzing the genomic variation of mucins across a wide range of mammalian genomes, we propose that exonic repeats and their copy number variation contribute substantially to the de novo evolution of new gene functions. By integrating bioinformatic, phylogenetic, proteomic, and immunohistochemical approaches, we identified 15 undescribed instances of evolutionary convergence, where novel mucins originated by gaining densely O-glycosylated exonic repeat domains. Our results suggest that secreted proteins rich in proline are natural precursors for acquiring mucin function. Our findings have broad implications for understanding the role of exonic repeats in the parallel evolution of new gene functions, especially those involving protein glycosylation.

2022-10-15 | PXD033197 | Pride

Expression data from early and macroscopic HCC lesions isolated from the Rb family Triple Knock Out model (scRNA-Seq)

Project description:we report the mRNA expression of single cells at two different time points of HCC development upon inactivation of Rb family. The first time point corresponds to lesions appearing in the portal triad area 9 weeks after Rb family inactivation. The second time point corresponds to macroscopic tumors, typically visible at the 20-25 weeks time point.

2024-05-05 | GSE173951 | GEO

Coordinate genomic association of transcription factors controlled by an imported quorum sensing peptide in Cryptococcus neoformans

Project description:Coordinate genomic association of transcription factors controlled by an imported quorum sensing peptide in Cryptococcus neoformans

| PRJNA614461 | ENA

The cis-regulatory function of long mononucleotide A-T repeats in maintaining high transcription activity in cancer

Project description:The cis-regulatory function of long mononucleotide A-T repeats in maintaining high transcription activity in cancer

| PRJNA477540 | ENA

MeCP2 is a microsatellite binding protein that protects CA repeats from nucleosome invasion

Project description:The Rett syndrome protein MeCP2 was described as a methyl-CpG-binding protein, but its exact function remains unknown. Here we show that MeCP2 is a microsatellite binding protein that specifically recognizes hydroxymethylated CA repeats. Depletion of MeCP2 alters chromatin organization of CA repeats and lamina-associated domains and results in nucleosome accumulation on CA repeats and genome-wide transcriptional dysregulation. The structure of MeCP2 in complex with a hydroxymethylated CA repeat reveals a characteristic DNA shape, with significantly modified geometry at the 5-hydroxymethylcytosine, which is recognized specifically by Arg133, a key residue whose mutation causes Rett syndrome. Our work identifies MeCP2 as a microsatellite DNA binding protein that targets the 5hmC-modified CA-rich strand and maintains genome regions nucleosome-free, suggesting a role for MeCP2 dysfunction in Rett syndrome.

2021-06-25 | GSE124238 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data