Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

KIF20A/MKLP2 regulates the division modes of neural progenitor cells during cortical development

ABSTRACT: KIF20A/MKLP2 regulates the division modes of neural progenitor cells during cortical development

PROVIDER: PRJNA427903 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR6429810.fastq.gz	Fastqsanger.gz
	SRR6429811.fastq.gz	Fastqsanger.gz
	SRR6429806.fastq.gz	Fastqsanger.gz
	SRR6429807.fastq.gz	Fastqsanger.gz
	SRR6429808.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 11

Similar Datasets

KIF20A/MKLP2 regulates the division modes of neural progenitor cells during cortical development

Project description:Balanced symmetric and asymmetric divisions of neural progenitor cells (NPCs) are crucial for orderly progression of brain development, but the underlying mechanisms are not fully understood. Here, we report that mitotic kinesin KIF20A/MKLP2 interacts with RGS3 and plays a crucial role in controlling the division modes of NPCs during the mouse cortical neurogenesis. KIF20A is selectively expressed by daughter progenitors in NPC divisions. Knockdown of KIF20A causes dislocation of RGS3 from the intercellular bridge (ICB) of dividing NPCs, impairs the function of EphrinB-RGS cell fate signaling complex, and leads to a transition in NPCs from proliferative to differentiative divisions. Germ-line and inducible knockout of KIF20A causes a loss of progenitor cells and neurons and results in thinner cortex and ventriculomegaly. Interestingly, loss-of-function of KIF20A induces early cell cycle exit and precocious neuronal differentiation without causing substantial multinucleation or apoptosis in mutant NPCs. Our results thus uncover a novel RGS-KIF20A axis in regulation of cell division mode and suggest a potential link of cytokinesis control within the ICB to regulation of cell fate determination.

2018-05-14 | GSE108624 | GEO

Transcriptome analysis of mouse cerebral cortical neural progenitor cells

Project description:Transcriptome analysis of neural progenitor/stem cells is limited by the lack of a reliable method for cell isolation. We have designed a genetic dual reporter strategy that can allow prospective isolation of cortical neural progenitor cells and their neuronal progeny form the same animals. These cells should be a good cell source for comparative global analysis. Cortical neural progenitor cells and their neuronal progeny were purified using a dual reporter strategy. The purified cells were used for comparative expression profiling.

2011-09-19 | E-GEOD-22946 | biostudies-arrayexpress

Transcriptome analysis of mouse cerebral cortical neural progenitor cells

2011-09-20 | GSE22946 | GEO

KIF20A/MKLP2 regulates the division modes of neural progenitor cells during cortical development.

Project description:Balanced symmetric and asymmetric divisions of neural progenitor cells (NPCs) are crucial for brain development, but the underlying mechanisms are not fully understood. Here we report that mitotic kinesin KIF20A/MKLP2 interacts with RGS3 and plays a crucial role in controlling the division modes of NPCs during cortical neurogenesis. Knockdown of KIF20A in NPCs causes dislocation of RGS3 from the intercellular bridge (ICB), impairs the function of Ephrin-B-RGS cell fate signaling complex, and leads to a transition from proliferative to differentiative divisions. Germline and inducible knockout of KIF20A causes a loss of progenitor cells and neurons and results in thinner cortex and ventriculomegaly. Interestingly, loss of function of KIF20A induces early cell cycle exit and precocious neuronal differentiation without causing substantial cytokinesis defect or apoptosis. Our results identify a RGS-KIF20A axis in the regulation of cell division and suggest a potential link of the ICB to regulation of cell fate determination.

| S-EPMC6045631 | biostudies-literature

Symmetric neural progenitor divisions require chromatin-mediated homologous recombination DNA repair by Ino80 [RNA-seq]

Project description:Chromatin regulates spatiotemporal gene expression during neurodevelopment, but it also mediates DNA damage repair crucial to proliferating neural progenitor cells (NPCs). Here, we uncover molecularly dissociable roles for nucleosome remodeler INO80 in chromatin-mediated transcriptome and genome maintenance in corticogenesis. We find that conditional Ino80 deletion from cortical NPCs impairs DNA double-strand break repair, triggering p53 activation, robust apoptosis, and microcephaly, whereas co-deletion of Trp53 with Ino80 leads to remarkable reversal of these phenotypes. Using an in vivo DNA repair assay, we find that Ino80 is selectively required for homologous recombination (HR) DNA repair, which is mechanistically distinct from INO80 function in YY1-associated transcription. Unexpectedly, sensitivity to loss of INO80-mediated HR is dependent on the mode of NPC division: Ino80 deletion causes extensive DNA damage and apoptosis in symmetric NPC-NPC divisions, but not in asymmetric neurogenic divisions. Thus, distinct modes of NPC division have divergent requirements for Ino80-dependent HR DNA repair.

2020-06-25 | GSE133799 | GEO

Symmetric neural progenitor divisions require chromatin-mediated homologous recombination DNA repair by Ino80 [ATAC-seq]

2020-06-23 | GSE153061 | GEO

E12.5 Murine lateral cortical progenitor cells: Pax6sey/sey vs. Pax6+/+

Project description:The mechanisms by which the early spatiotemporal expression patterns of transcription factors such as Pax6 regulate the region-specific proliferation rates of neural progenitors are poorly understood. Pax6 is expressed in a gradient across the developing cortex and is essential for normal corticogenesis. We found that constitutive or conditional loss of Pax6 increases cortical progenitor proliferation by amounts that vary regionally with normal Pax6 levels. We compared the gene expression profiles of equivalent Pax6-expressing progenitors isolated from Pax6+/+ and Pax6-/- cortices and identified many negatively-regulated cell cycle genes including those encoding Cyclins and Cdks. Biochemical assays indicated that Pax6 directly represses Cdk6 expression. Cyclin/Cdk repression inhibits retinoblastoma protein (pRb) phosphorylation, thereby limiting the transcription of genes directly promoting mitosis, and we showed that Pax6 inhibits pRb phosphorylation and represses several genes involved in DNA replication. Our results indicate that Pax6M-bM-^@M-^Ys modulation of the cell cycles of cortical progenitors is regional and direct. Two condition experiment, Pax6sey/sey vs Pax6+/+ cortical progenitor cells from lateral cortex. 3 biological replicates. Each replicate contains RNA from cells pooled from 4 individual E12.5 embryos

2013-01-31 | E-GEOD-38703 | biostudies-arrayexpress

Unveiling the Neuroprotective Potential of Nobiletin in human Neural Progenitor Cells (hNPCs)

Project description:The data belongs to the proteomic analysis of human neural progenitor cells exposed to sodium arsinate and treated with Nobielin.

2023-12-02 | MSV000093554 | MassIVE

A Comparison of the Sexually Dimorphic Pravastatin Transcriptome in Mouse Cerebral Cortical Embryonic Neural Stem Cells

Project description:We used RNA-Seq analysis to identify the sexually dimorphic pravastatin regulated gene expression profile in primary cultures of mouse embryonic cerebral cortical neural progenitor/stem cells.

2018-04-25 | GSE111945 | GEO

A Comparison of the Sexually Dimorphic Dexamethasone Transcriptome in Mouse Cerebral Cortical and Hypothalamic Embryonic Neural Stem Cells

Project description:We used RNA-Seq analysis to identify the sexually dimorphic dexamethasone regulated gene expression profile in primary mouse embryonic cerebral cortical and hypothalamic neural progenitor/stem cells.

2017-05-26 | GSE95363 | 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