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

Author

Listed:
  • 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
    University of Freiburg)

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.

Suggested Citation

  • Ying Wang & Alice Sherrard & Bing Zhao & Michael Melak & Jonathan Trautwein & Eva-Maria Kleinschnitz & Nikolaos Tsopoulidis & Oliver T. Fackler & Carsten Schwan & Robert Grosse, 2019. "GPCR-induced calcium transients trigger nuclear actin assembly for chromatin dynamics," Nature Communications, Nature, vol. 10(1), pages 1-9, December.
    • Handle: RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-13322-y
    DOI: 10.1038/s41467-019-13322-y
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    Cited by:

    1. Maria Dilia Palumbieri & Chiara Merigliano & Daniel González-Acosta & Danina Kuster & Jana Krietsch & Henriette Stoy & Thomas Känel & Svenja Ulferts & Bettina Welter & Joël Frey & Cyril Doerdelmann & , 2023. "Nuclear actin polymerization rapidly mediates replication fork remodeling upon stress by limiting PrimPol activity," Nature Communications, Nature, vol. 14(1), pages 1-15, December.
    2. Buer Sen & Zhihui Xie & Michelle D. Thomas & Samantha G. Pattenden & Sean Howard & Cody McGrath & Maya Styner & Gunes Uzer & Terrence S. Furey & Janet Rubin, 2024. "Nuclear actin structure regulates chromatin accessibility," Nature Communications, Nature, vol. 15(1), pages 1-15, December.

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