Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

An alternative transcriptome shapes cell fate transitions in yeast (TSS-seq)

ABSTRACT: An alternative transcriptome shapes cell fate transitions in yeast (TSS-seq)

PROVIDER: PRJNA566359 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR10144900.fastq.gz	Fastqsanger.gz
	SRR10144901.fastq.gz	Fastqsanger.gz
	SRR10144902.fastq.gz	Fastqsanger.gz
	SRR10144903.fastq.gz	Fastqsanger.gz
	SRR10144904.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 82

Similar Datasets

An alternative transcriptome shapes cell fate transitions in yeast (TSS-seq)

Project description:Alternative mRNA isoforms and long noncoding RNAs (lncRNA) make up a large fraction of the transcriptome and play key functions in cell-fate programming. These transcripts often initiate upstream of coding gene promoters from alternative transcription start sites (TSS) where they can regulate gene expression in cis through transcription-coupled chromatin alterations. How, when and where transcription of alternative cis-acting RNAs regulates local gene expression remains poorly understood. Here, we use a high-resolution quantitative approach to study alternative TSS and transcript end site (TES) usage during three different cell fate transitions in yeast: entry into gametogenesis, commitment to meiotic divisions and return to vegetative growth. We propose that an alternative transcriptome of mRNA isoforms and lncRNAs shapes local gene expression during cell fate transitions. Hence, changes in the types and proportions of different RNAs transcribed at a locus are important inputs for gene expression at distinct stages of development.

2020-12-15 | GSE137707 | GEO

An alternative transcriptome shapes cell fate transitions in yeast (MNase-seq)

2020-12-15 | GSE137709 | GEO

An alternative transcriptome shapes cell fate transitions in yeast (TIF-seq)

2020-12-15 | GSE141269 | GEO

An alternative transcriptome shapes cell fate transitions in yeast (TES-seq)

2020-12-15 | GSE137708 | GEO

An alternative transcriptome shapes cell fate transitions in yeast (mRNA-seq)

2020-12-15 | GSE137706 | GEO

An alternative transcriptome shapes cell fate transitions in yeast (mRNA-seq)

Project description:An alternative transcriptome shapes cell fate transitions in yeast (mRNA-seq)

| PRJNA566360 | ENA

An alternative transcriptome shapes cell fate transitions in yeast (TES-seq)

Project description:An alternative transcriptome shapes cell fate transitions in yeast (TES-seq)

| PRJNA566361 | ENA

An alternative transcriptome shapes cell fate transitions in yeast (MNase-seq)

Project description:An alternative transcriptome shapes cell fate transitions in yeast (MNase-seq)

| PRJNA566362 | ENA

An alternative transcriptome shapes cell fate transitions in yeast (TIF-seq)

Project description:An alternative transcriptome shapes cell fate transitions in yeast (TIF-seq)

| PRJNA592981 | ENA

Mechano-osmotic signals control chromatin state and fate transitions in pluripotent stem cells

Project description:Acquisition of specific cell shapes and morphologies is a central component of cell fate transitions. Although the signaling circuits and gene regulatory networks regulating pluripotent stem cell differentiation have been intensely studied, how these networks are integrated in space and time with morphological transitions and mechanical deformations that occur during state transitions remains a fundamental open question. Here, we discover that stem cell fate transitions are gated by two critical signals - nuclear envelope fluctuations and osmotic stress - that emanate from growth factor signaling-controlled changes in nuclear volume and nucleoplasm viscosity/density to subsequently trigger changes in nuclear architecture and transcription. We observe that fate transitions in the early human embryo and in an in vitro model of exit from pluripotency are associated with rapid changes in nuclear volume and nuclear envelope mechanics. These changes alter nuclear mechanosensitivity and trigger changes in nucleoplasmic viscosity and nuclear condensates to prime chromatin for a cell fate transition. However, while this mechanical priming accelerates fate transitions, sustained biochemical signals are required for efficient induction of differentiation. Our findings establish a critical mechanochemical feedback mechanism that integrates nuclear mechanics, shape and volume with biochemical signaling and chromatin state to control cell fate transition dynamics.

2025-08-11 | PXD052588 | Pride

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