GPCR-induced calcium transients trigger nuclear actin assembly for chromatin dynamics

Ying Wang (), Alice Sherrard, Bing Zhao, Michael Melak, Jonathan Trautwein, Eva-Maria Kleinschnitz, Nikolaos Tsopoulidis, Oliver T. Fackler, Carsten Schwan and Robert Grosse ()
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Ying Wang: University of Marburg
Alice Sherrard: University of Bristol, University Walk
Bing Zhao: University of Freiburg
Michael Melak: University of Marburg
Jonathan Trautwein: University of Marburg
Eva-Maria Kleinschnitz: University of Marburg
Nikolaos Tsopoulidis: Heidelberg University Hospital
Oliver T. Fackler: Heidelberg University Hospital
Carsten Schwan: University of Freiburg
Robert Grosse: University of Freiburg

Nature Communications, 2019, vol. 10, issue 1, 1-9

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 Gαq 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.

Date: 2019
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DOI: 10.1038/s41467-019-13322-y

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