KIF20A/MKLP2 regulates the division modes of neural progenitor cells during cortical development
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA427903 | ENA |
REPOSITORIES: ENA
Dataset's files
| 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 |
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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
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.
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Project description:Balanced proliferation and differentiation of neural progenitor cells (NPCs) are critical for brain development, but how the process is regulated and what components of the cell division machinery is involved are not well understood. Here we report that SEPT7, a cell division regulator originally identified in Saccharomyces cerevisiae, interacts with KIF20A in the intercellular bridge of dividing NPCs and plays an essential role in maintaining the proliferative state of NPCs during cortical development. Knockdown of SEPT7 in NPCs results in displacement of KIF20A from the midbody and early neuronal differentiation. NPC-specific inducible knockout of Sept7 causes early cell cycle exit, precocious neuronal differentiation, and ventriculomegaly in the cortex, but surprisingly does not lead to noticeable cytokinesis defect. Our data uncover an interaction of SEPT7 and KIF20A during NPC divisions and demonstrate a crucial role of SEPT7 in cell fate determination. In addition, this study presents a functional approach for identifying additional cell fate regulators of the mammalian brain.
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Project description:Understanding how transcriptional programs help to coordinate cell growth and division is an important unresolved problem. Here we report that the nutrient- and stress-regulated transcription factor Sfp1 is rate-limiting for expression of a large suite of genes involved in yeast cell growth, including ribosomal protein, ribosome biogenesis, and snoRNA genes. Remarkably, the spectrum of Sfp1 transcription effects is concordant with a combination of chromatin immunoprecipitation and chromatin endogenous cleavage binding analyses, which together provide evidence for two distinct modes of Sfp1 promoter binding, one requiring a co-factor and the other a specific DNA-recognition motif. In addition to growth-related genes, Sfp1 binds to and regulates the promoters of key G1/S regulon genes and that of MRS6, whose product regulates Sfp1 nuclear localization. Our findings suggest that Sfp1 acts as a master regulator of cell growth and cell size by coordinating the expression of genes implicated in mass accumulation and cell division.
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Project description:Breast cancer stem cells (BCSCs), known to fuel TNBC malignancy, are now being exploited as the vulnerability for TNBC treatment. In this study, we dissected the transcriptome of BCSCs and identified Kinesin Family Member 20A (KIF20A) as an essential gene for BCSC survival and TNBC tumorigenesis. To understand the potential mechanism, we infected MDA-MB-231 cells with either control or V5-tagged KIF20A followed by V5 antibody pull down and mass spectrometry to identify KIF20A interaction proteins that may mediate its effect on gene regulation and TNBC cancer stem cell phenotype.
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