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• W2989650452 abstract "Abstract Although the properties of the actin cytoskeleton in the cytoplasm are well characterized, the regulation and function of nuclear actin filaments are only recently emerging. We previously demonstrated serum-induced, transient assembly of filamentous actin within somatic cell nuclei. However, the extracellular cues, cell surface receptors as well as underlying signaling mechanisms have been unclear. Here we demonstrate that physiological ligands for G protein-coupled receptors (GPCRs) promote nuclear F-actin assembly via heterotrimeric Gα q proteins. Signal-induced nuclear actin responses require calcium release from the endoplasmic reticulum (ER) targeting the ER-associated formin INF2 at the inner nuclear membrane (INM). Notably, calcium signaling promotes the polymerization of linear actin filaments emanating from the INM towards the nuclear interior. We show that GPCR and calcium elevations trigger nuclear actin-dependent alterations in chromatin organization, uncovering a general cellular mechanism by which physiological ligands and calcium promote nuclear F-actin assembly for rapid responses towards chromatin dynamics." @default.
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• W2989650452 date "2019-11-21" @default.
• W2989650452 modified "2023-10-13" @default.
• W2989650452 title "GPCR-induced calcium transients trigger nuclear actin assembly for chromatin dynamics" @default.
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• W2989650452 doi "https://doi.org/10.1038/s41467-019-13322-y" @default.
• W2989650452 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6872576" @default.
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