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Atypical function of a centrosomal module in WNT signalling drives contextual cancer cell motility

ABSTRACT: Atypical function of a centrosomal module in WNT signalling drives contextual cancer cell motility

PROVIDER: PRJNA534108 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8942940_1.fastq.gz	Fastqsanger.gz
	SRR8942940_2.fastq.gz	Fastqsanger.gz
	SRR8942950_1.fastq.gz	Fastqsanger.gz
	SRR8942950_2.fastq.gz	Fastqsanger.gz
	SRR8942960_1.fastq.gz	Fastqsanger.gz

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Atypical function of a centrosomal module in WNT signalling drives contextual cancer cell motility

Project description:Centrosomes control cell motility, polarity and migration that are thought to be mediated by their microtubule-organizing capacity. In this study we demonstrate that WNT signalling drives a distinct form of non-directional cell motility that requires a key centrosome module, but not microtubules or centrosomes. Upon exosome mobilization of Planar Cell Polarity proteins, we show that DVL2 orchestrates recruitment of a CEP192-PLK4/AURKB complex to the cell cortex where PLK4/AURKB act redundantly to drive protrusive activity and cell motility. This is mediated by coordination of formin-dependent actin remodelling through displacement of cortically localized DAAM1 for DAAM2. Furthermore, abnormal expression of PLK4, AURKB and DAAM1 is associated with poor outcomes in breast and bladder cancers. Thus, a centrosomal module plays an atypical function in WNT signalling and actin nucleation that is critical for cancer cell motility and is associated with more aggressive cancers. These studies have broad implications in how contextual signalling controls distinct modes of cell migration.

2019-04-26 | GSE129871 | GEO

Atypical function of a centrosomal module in WNT signalling drives contextual cancer cell motility.

Project description:Centrosomes control cell motility, polarity and migration that is thought to be mediated by their microtubule-organizing capacity. Here we demonstrate that WNT signalling drives a distinct form of non-directional cell motility that requires a key centrosome module, but not microtubules or centrosomes. Upon exosome mobilization of PCP-proteins, we show that DVL2 orchestrates recruitment of a CEP192-PLK4/AURKB complex to the cell cortex where PLK4/AURKB act redundantly to drive protrusive activity and cell motility. This is mediated by coordination of formin-dependent actin remodelling through displacement of cortically localized DAAM1 for DAAM2. Furthermore, abnormal expression of PLK4, AURKB and DAAM1 is associated with poor outcomes in breast and bladder cancers. Thus, a centrosomal module plays an atypical function in WNT signalling and actin nucleation that is critical for cancer cell motility and is associated with more aggressive cancers. These studies have broad implications in how contextual signalling controls distinct modes of cell migration.

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Analysis of centrosomal protein

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Project description:This dataset constitutes the first RNA-seq study of gene expression following contextual fear conditioning in the mouse hippocampus.

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Project description:This dataset constitutes the first Sono-Seq study of chromatin accessibility following contextual fear conditioning in the mouse hippocampus.

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Project description:The intestinal epithelium is a single-cell layer comprising a constellation of specialized cell types that functionally interconnect host physiological systems with extrinsic microbial communities, metabolites, and dietary factors1. Active renewal of the intestinal epithelium relies on stem cells that reside in invaginations of the epithelium known as crypts. Inflammatory Bowel Disease (IBD) disrupts normal functions and/or proportions of cells in the intestinal epithelium, including stem cell programming during epithelial restitution. Genome-wide association studies have provided a powerful means to identify loci and genes contributing to IBD risk and functional annotation of candidate genes have unveiled cellular programs and molecular mechanisms involved in IBD etiology. Here we find that risk for a major form of IBD, Crohn’s disease (CD), is linked to a variant of the Fibroblast Growth Factor Receptor 1 Oncogene Partner (FGFR1OP) locus, which encodes a protein of the centrosome, the microtubule organizing center that generates microtubule structures involved in cell division, polarity, and motility. Deletion of Fgfr1op in mouse intestinal epithelium impaired stem cell division and intestinal crypt architecture causing crypt loss, inflammation and death. Transcriptional, biochemical and morphological analyses demonstrated that Fgfr1op coordinates the centrosome with the actin cytoskeleton and with specialized cell junctions known as desmosomes. We conclude that a genetically inherited centrosomal defect predisposes to CD by affecting renewal of the intestinal epithelium.

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