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Overexpression of the cytokinesis regulator PRC1 activates the p53 pathway due to cytoplasmic microtubule-bundling resulting in senescence of A549 lung cancer cells

ABSTRACT: Overexpression of the cytokinesis regulator PRC1 activates the p53 pathway due to cytoplasmic microtubule-bundling resulting in senescence of A549 lung cancer cells

PROVIDER: PRJNA573912 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10174280.fastq.gz	Fastqsanger.gz
	SRR10174281.fastq.gz	Fastqsanger.gz
	SRR10174282.fastq.gz	Fastqsanger.gz
	SRR10174283.fastq.gz	Fastqsanger.gz
	SRR10174284.fastq.gz	Fastqsanger.gz

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Overexpression of the cytokinesis regulator PRC1 activates the p53 pathway due to cytoplasmic microtubule-bundling resulting in senescence of A549 lung cancer cells

Project description:Protein regulator of cytokinesis 1 (PRC1) is a microtubule-bundling protein with essential roles in mitosis and cytokinesis. In this study we investigated the potential nuclear functions of PRC1 and the consequences of overexpression of PRC1 by using lung cancer cell lines stably expressing inducible expression constructs for PRC1. Ectopically expressed PRC1 resulted in proliferation defects, multi-nucleation and enlargement of cells which were directly linked to microtubule-bundling within the cytoplasm. Genome wide expression profiling by RNA sequencing revealed that the p53 pathway is activated upon overexpression of PRC1 resulting in cellular senescence. A mutant of PRC1 unable to enter into the nucleus induced the same gene sets as wildtype PRC1, suggesting that PRC1 has no nuclear-specific functions in lung cancer cells. The depletion of p53 switched the response to PRC1 overexpression or depletion from senescence to apoptosis. In addition, treatment with cisplatin, a commonly used chemotherapeutic drug, enhanced the proliferation defects due to deregulated PRC1, implicating PRC1 as a possible therapeutic target for cancer. Taken together, PRC1 needs to be tightly regulated to allow unperturbed proliferation of lung cancer cells.

2021-09-01 | GSE137940 | GEO

RNA helicase MOV10 suppresses fear memory and dendritic arborization and regulates microtubule dynamics in hippocampal neurons [eCLIP-seq]

Project description:RNA helicase MOV10 is highly expressed in postnatal brain and associates with FMRP and AGO2, suggesting a role in translation regulation in learning and memory. We generated a brain-specific knockout mouse (Mov10 Deletion) with greatly reduced MOV10 expression in cortex and hippocampus. Behavior testing revealed enhanced fear memory, similar to that observed in a mouse with reduced brain microRNA production, supporting MOV10’s reported role as an AGO2 cofactor. Cultured hippocampal neurons have elongated distal dendrites, a reported feature of augmin/HAUS over-expression in Drosophila da sensory neurons. In mitotic spindle formation, HAUS is antagonized by the microtubule bundling protein NUMA1. Numa1 mRNA is a MOV10 CLIP target and is among the genes significantly decreased in Mov10 Deletion hippocampus. Restoration of NUMA1 expression and knockdown of HAUS rescued microtubule comet formation in dendritic growth cones. This is the first evidence of translation regulation of NUMA1 as a control point in dendritogenesis.

2024-10-04 | GSE278282 | GEO

RNA helicase MOV10 suppresses fear memory and dendritic arborization and regulates microtubule dynamics in hippocampal neurons [RNA-seq]

2024-10-04 | GSE232771 | GEO

PRC1 phosphorylation by CDK1 and PLK1

Project description:This work study the effects of PRC1 phosphorylation by CDK1 and PLK1.

2024-11-01 | PXD055933 | Pride

PCGF1-PRC1 links chromatin repression with DNA replication during hematopoietic cell lineage commitment

Project description:Polycomb repressive complexes 1 and 2 (PRC1 and 2) repress lineage inappropriate genes during development to maintain proper cellular identities. To reveal the function of a variant PRC1 containing PCGF1 (PCGF1-PRC1), we prepared PCGF1 interacting proteins by immunoprecipitation and characterized them by LC-MS/MS.

2022-11-30 | PXD036330 | Pride

The midbody component Prc1-like is required for microtubule reorganization during cytokinesis and dorsal determinant segregation in the early zebrafish embryo.

Project description:We show that the zebrafish maternal-effect mutation too much information (tmi) corresponds to zebrafish prc1-like (prc1l), which encodes a member of the MAP65/Ase1/PRC1 family of microtubule-associated proteins. Embryos from tmi homozygous mutant mothers display cytokinesis defects in meiotic and mitotic divisions in the early embryo, indicating that Prc1l has a role in midbody formation during cell division at the egg-to-embryo transition. Unexpectedly, maternal Prc1l function is also essential for the reorganization of vegetal pole microtubules required for the segregation of dorsal determinants. Whereas Prc1 is widely regarded to crosslink microtubules in an antiparallel conformation, our studies provide evidence for an additional function of Prc1l in the bundling of parallel microtubules in the vegetal cortex of the early embryo during cortical rotation and prior to mitotic cycling. These findings highlight common yet distinct aspects of microtubule reorganization that occur during the egg-to-embryo transition, driven by maternal product for the midbody component Prc1l and required for embryonic cell division and pattern formation.

| S-EPMC10112900 | biostudies-literature

Kdm2b regulates somatic reprogramming through variant PRC1 complex dependent function [RNA-seq]

Project description:Polycomb repressive complex 1 (PRC1) plays essential roles in cell fate determination. Recent studies have found that the composition of mammalian PRC1 is particularly varied and complicated, whereas the function of such variant PRC1 complexes on cell fate determination remains unknown. Here we show that Kdm2b, which recruits a variant PRC1 complex (PRC1.1) to CpG islands (CGIs), elevates Oct4 induced somatic reprogramming. Interaction with PRC1 is critical for Kdm2b’s promotion on the process of induced pluripotency. Furthermore, we find that bone morphogenetic proteins (BMPs) repress Oct4/Kdm2b induced somatic reprogramming selectively. Mechanistically, BMP-Smad pathway attenuates PRC1.1 occupation and H2AK119 ubiquitination on development genes, resulting in the release of meso-endoderm factors such as Sox17 and suppression of somatic reprogramming. These observations reveal that PRC1.1 participates in the establishment of pluripotency as well as cellular differentiation and identify BMP signal as a modulator of PRC1.1 function.

2017-11-19 | GSE93974 | GEO

Microtubule acetylation is required for mechanosensation in Drosophila

Project description:At the cellular level, α-tubulin acetylation alters the structure of microtubules to render them mechanically resistant to compressive forces. How this biochemical property of microtubule acetylation relates to mechanosensation remains unknown, though prior studies have shown that microtubule acetylation influences touch perception. Here, we identify the major Drosophila α-tubulin acetylase (dTAT) and show that it plays key roles in several forms of mechanosensation. dTAT is highly expressed in the larval peripheral nervous system (PNS), but is largely dispensable for neuronal morphogenesis. Mutation of the acetylase gene or the K40 acetylation site in α-tubulin impairs mechanical sensitivity in sensory neurons and behavioral responses to gentle touch, harsh touch, gravity, and vibration stimuli, but not noxious thermal stimulus. Finally, we show that dTAT is required for mechanically-induced activation of NOMPC, a microtubule-associated transient receptor potential channel, and functions to maintain integrity of the microtubule cytoskeleton in response to mechanical stimulation.

2018-09-22 | GSE120305 | GEO

Kdm2b regulates somatic reprogramming through variant PRC1 complex dependent function [ChIP-seq, MeDIP-seq]

2017-11-19 | GSE93972 | GEO

AUTS2 confers transcriptional activation to PRC1 in the CNS (RNA-Seq)

Project description:Naturally occurring variations of Polycomb Repressive Complex 1 (PRC1) comprise a core assembly of Polycomb group proteins and additional factors that include, surprisingly, Autism Susceptibility Candidate 2 (AUTS2). While AUTS2 is often disrupted in patients with neuronal disorders, the underlying mechanism is unclear. We investigated the role of AUTS2 as part of a previously identified PRC1 complex (PRC1-AUTS2), and in the context of neurodevelopment. In contrast to the canonical role of PRC1 in gene repression, PRC1-AUTS2 activates transcription. Biochemical studies demonstrate that the CK2 component of PRC1-AUTS2 thwarts PRC1 repressive activity and AUTS2-mediated recruitment of P300 leads to gene activation. ChIP-seq of AUTS2 shows that it regulates neuronal gene expression through promoter association. Conditional CNS targeting of Auts2 in a mouse model leads to various developmental defects. These findings reveal a natural means of subverting PRC1 activity, linking key epigenetic modulators with neuronal functions and diseases. mRNA profiles of P1 brain from wild type mice were generated by deep sequencing

2014-12-18 | E-GEOD-60410 | biostudies-arrayexpress

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