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RAB11A and RAB11B redundantly regulate mitotic spindle function in dividing tissue progenitor cells

ABSTRACT: RAB11A and RAB11B redundantly regulate mitotic spindle function in dividing tissue progenitor cells

PROVIDER: PRJNA972314 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24545615.fastq.gz	Fastqsanger.gz
	SRR24545616.fastq.gz	Fastqsanger.gz
	SRR24545617.fastq.gz	Fastqsanger.gz
	SRR24545618.fastq.gz	Fastqsanger.gz
	SRR24545619.fastq.gz	Fastqsanger.gz

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RAB11A and RAB11B redundantly regulate mitotic spindle function in dividing tissue progenitor cells

Project description:To investigate the role of Rab11 isoforms in intestinal epithelial cells and its downstream effects on intestinal homeostasis.

2023-06-09 | GSE232493 | GEO

Canonical Hedgehog Signaling Controls Astral Microtubules and Mitotic Spindle Orientation in Neural Progenitors and iPSCs

Project description:Mitotic spindle orientation is crucial for cell fate determination and tissue organization. Although the intracellular machinery governing spindle orientation is well characterized, whether and how secreted factors, such as morphogens, regulate this process remains poorly understood. This study investigated the role of Hedgehog (HH) signaling in modulating mitotic spindle orientation in neural progenitor cells and in induced pluripotent stem cells (iPSCs). Time-lapse microscopy of cerebral organoids and iPSCs revealed that HH signaling increases the angle of the mitotic spindle relative to the apical surface, prolongs mitosis, and enhances spindle rotation. Mechanistically, HH signaling reduces both the number and the length of astral microtubules, key regulators of spindle orientation. This reduction correlates with increased spindle angle in iPSCs. Furthermore, we show that canonical HH signaling, involving GLI-dependent transcriptional regulation, contributes to these effects. RNA sequencing and gene set enrichment analysis (GSEA) revealed that HH signaling upregulates genes associated with microtubule depolymerization, suggesting a transcriptional mechanism by which HH signaling influences astral microtubule dynamics and, consequently, mitotic spindle orientation. These findings highlight a novel link between a morphogen, transcriptional regulation, and the control of mitotic spindle orientation, with implications for development and tissue homeostasis.

2025-06-25 | GSE296672 | GEO

Centrosomal ALIX regulates mitotic spindle orientation by modulating astral microtubule dynamics

Project description:The orientation of the mitotic spindle (MS) is tightly regulated, but the molecular mechanisms are incompletely understood. Here we report a novel role for the multifunctional adaptor protein ALG-2-interacting protein X (ALIX) in regulating MS orientation in addition to its well-established role in cytokinesis. We show that ALIX is recruited to the pericentriolar material (PCM) of the centrosomes and promotes correct orientation of the MS in asymmetrically dividing Drosophila stem cells and epithelial cells, and symmetrically dividing Drosophila and human epithelial cells. ALIX-deprived cells display defective formation of astral microtubules (MTs), which results in abnormal MS orientation. Specifically, ALIX is recruited to the PCM via Drosophila Spindle defective 2 (DSpd-2)/Cep192, where ALIX promotes accumulation of g-tubulin and thus facilitates efficient nucleation of astral MTs. In addition, ALIX promotes MT stability by recruiting Microtubule Associated Protein 1S (MAP1S), which stabilizes newly formed MTs. Altogether, our results demonstrate a novel evolutionarily conserved role of ALIX in providing robustness to the orientation of the MS by promoting astral MT formation during asymmetric and symmetric cell division.

2018-06-04 | PXD009747 | Pride

FAM83D directs protein kinase CK1α to the mitotic spindle for proper spindle positioning

Project description:The concerted action of many protein kinases helps orchestrate the error-free progression through mitosis of mammalian cells. The roles and regulation of some prominent mitotic kinases, such as cyclin-dependent kinases, are well-established. However, these and other known mitotic kinases alone cannot account for the extent of protein phosphorylation that has been reported during mammalian mitosis. Here we demonstrate that CK1α, of the casein kinase 1 family of protein kinases, localises to the spindle and is required for proper spindle-positioning and timely cell division. CK1α is recruited to the spindle by FAM83D, and cells devoid of FAM83D, or those harbouring CK1α-binding-deficient FAM83DF283A/F283A knockin mutation, display pronounced spindle-positioning defects, and a prolonged mitosis. Restoring FAM83D at the endogenous locus in FAM83D-/- cells, or artificially delivering CK1α to the spindle in FAM83DF283A/F283A cells, rescues these defects. These findings implicate CK1α as new mitotic kinase that orchestrates the kinetics and orientation of cell division.

2019-07-15 | PXD013808 | Pride

Signaling pathways altered at the mitotic spindle in clathrin depleted cells

Project description:We present a snapshot of the regulation of mitotic-spindle proteins and their phosphorylation status in the absence of clathrin during metaphase. A reference list of proteins and phosphosites identified from a mitotic spindle preparation was generated using a label-free and a parallel chemical dimethyl isotopic peptide labelling approach. We further designed experiments to analyse proteins and phosphosites at the mitotic spindle whose abundance was affected by the knock-down of clathrin. We used dimethylation labelling of peptides in combination with fractionation strategies to identify and quantify phosphopeptides enriched by TiO2 beads and the flow-through non-phoshopeptides by ESI-LC-MS/MS for a broad coverage of the mitotic spindle proteome in the absence of clathrin.

2016-05-17 | PXD001603 | Pride

Spindle-localized mRNA translation mediated by CPEB1 and CPEB4 controls mitotic progression

Project description:Sequencial functions of CPEB1 and CPEB4 in the localization of repressed mRNAs to the mitotic spindle and their subsequent phase-specific activation to promote cell phase transitions and correct chromosome segregation

2018-02-15 | GSE100764 | GEO

Spindle-localized mRNA translation mediated by CPEB1 and CPEB4 controls mitotic progression

Project description:Here we show sequential functions of CPEB1 and CPEB4 in the localization of repressed mRNAs to the mitotic spindle and their subsequent phase -specific activation to promote cell phase transitions and correct chromosome segregation.

2021-06-29 | GSE99810 | GEO

Knockout of Staufen1 impairs the localization of specific subsets of mRNAs on the mitotic spindle of colorectal cancer cells

Project description:Staufen1 (STAU1) is an RNA-binding protein involved in maturation, localization, translation and decay of mRNAs. STAU1 expression is modulated during the cell cycle and decreases during mitosis. In prometaphase, STAU155 binds specific classes of mRNAs that code for proteins implicated in transcription and cell cycle regulation. In this paper, we report that STAU155 co-localizes with microtubules on the mitotic spindle in human colorectal cancer cell line HCT116, and map the molecular determinant required for this association within the N-terminal 88 amino acids (aa 25-37). Interestingly, STAU1 co-purifies with ribosomal proteins and co-localizes with active sites of translation on the mitotic spindle. To characterize STAU1-dependent mRNA transport and localization on the spindle, we used RNAseq analysis to identify spindle-associated mRNAs on purified spindles of wild-type and STAU1-KO CRISPR cell lines. Our datasets identify 161 protein-coding transcripts that are less abundant on the mitotic spindle of STAU1-KO cells compared to WT, and 660 that are more abundant. Altogether, these data demonstrate that STAU1 controls the transport and the localization of specific sub-populations of mRNAs to the mitotic spindle of cancer cells and suggest that at least some spindle-localized mRNAs undergo local translation during mitosis.

2019-10-05 | GSE138441 | GEO

MYC Dysregulates Mitotic Spindle Function Creating a Dependency on TPX2

Project description:MYC Dysregulates Mitotic Spindle Function Creating a Dependency on TPX2

| PRJNA541944 | ENA

Matrin3 regulates mitotic spindle dynamics by controlling alternative splicing of CDC14B [Iso-Seq]

Project description:Purpose: Matrin3 (MATR3) is a DNA and RNA-binding protein and one of the major components of the nuclear matrix. Matrin3 is upregulated in colorectal cancer (CRC) compared to normal tissues, indicating potential oncogenic function in CRC. We found that depletion of Matrin3 results in decreased proliferation and colony formation in two CRC cell lines. To understand the molecular mechanism(s) by which Matrin3 mediates these effects, we aimed to find Matrin3 direct RNA targets and the effects of Matrin3 on them. Methods: We performed PAR-CLIP for endogenous Matrin3 and RNA-seq after Matrin3 silencing in HCT116 cells, a colorectal cancer cell line. Results: We uncovered Matrin3-mediated regulation of spindle dynamics in colorectal cancer (CRC) cells. We identified bound and regulated Matrin3 target RNAs transcriptome-wide in CRC cells, and found that Matrin3 broadly regulates alternative splicing. Among the top Matrin3 targets, we focused on CDC14B and found that Matrin3 loss resulted in misprocessing of the CDC14B transcript that has a premature termination codon and simultaneous down-regulation of the standard CDC14B transcript in our model. Selective knockdown of the CDC14B standard variant phenocopied the loss of Matrin3 and resulted in reduced CRC cell proliferation, stabilized microtubules, and defects in mitotic spindle formation with tumbled mitotic spindles, suggesting that CDC14B is a key downstream effector of Matrin3. Conclusions: Our data show that by regulating the abundance of CDC14B standard variant, Matrin3 contributes to maintenance of microtubules dynamics, spindle morphology and proper mitotic spindle orientation and suggest that defects in this pathway may contribute to the reduced proliferation of cells after depletion of Matrin3.

2023-03-17 | GSE205565 | GEO

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