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TGF-β-induced DACT1 biomolecular condensates repress Wnt signalling to promote bone metastasis
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TGF-β-induced DACT1 biomolecular condensates repress Wnt signalling to promote bone metastasis
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Journal Article
TGF-β-induced DACT1 biomolecular condensates repress Wnt signalling to promote bone metastasis
2021
Overview
The complexity of intracellular signalling requires both a diversity of molecular players and the sequestration of activity to unique compartments within the cell. Recent findings on the role of liquid–liquid phase separation provide a distinct mechanism for the spatial segregation of proteins to regulate signalling pathway crosstalk. Here, we discover that DACT1 is induced by TGFβ and forms protein condensates in the cytoplasm to repress Wnt signalling. These condensates do not localize to any known organelles but, rather, exist as phase-separated proteinaceous cytoplasmic bodies. The deletion of intrinsically disordered domains within the DACT1 protein eliminates its ability to both form protein condensates and suppress Wnt signalling. Isolation and mass spectrometry analysis of these particles revealed a complex of protein machinery that sequesters casein kinase 2—a Wnt pathway activator. We further demonstrate that DACT1 condensates are maintained in vivo and that DACT1 is critical to breast and prostate cancer bone metastasis.
Esposito et al. show that TGF-β-induced DACT1 forms biomolecular condensates that sequester CK2 to repress Wnt signalling and modulate bone metastasis in cancer.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ 13/109
/ 13/31
/ 13/51
/ 13/89
/ 13/95
/ 14/19
/ 14/35
/ 14/5
/ 14/63
/ 631/80
/ Adaptor Proteins, Signal Transducing - genetics
/ Adaptor Proteins, Signal Transducing - metabolism
/ Animals
/ Biomedical and Life Sciences
/ Breast Neoplasms - metabolism
/ Breast Neoplasms - pathology
/ Casein
/ Casein Kinase II - metabolism
/ Cell Movement - drug effects
/ Cell Proliferation - drug effects
/ Female
/ Gene Expression Regulation, Neoplastic
/ Humans
/ Kinases
/ Male
/ Mice
/ Nuclear Proteins - metabolism
/ Prostatic Neoplasms - genetics
/ Prostatic Neoplasms - metabolism
/ Prostatic Neoplasms - pathology
/ Proteins
/ Transforming Growth Factor beta - pharmacology
