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, Robert Grosse

Research output: Contribution to journalArticle (Academic Journal)peer-review

43 Citations (Scopus)
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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.

Original languageEnglish
Article number5271 (2019)
Number of pages9
JournalNature Communications
Publication statusPublished - 21 Nov 2019


  • actin
  • calcium signalling


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