Nance-Horan-syndrome-like 1b controls mesodermal cell migration by regulating protrusion and actin dynamics during zebrafish gastrulation

Abstract Cell migrations are crucial for embryonic development, wound healing, the immune response, as well as for cancer progression. During mesenchymal cell migration, the Rac1-WAVE-Arp2/3 signalling pathway induces branched actin polymerisation, which protrudes the membrane and allows migration....

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Main Authors: Sophie Escot, Yara Hassanein, Amélie Elouin, Jorge Torres-Paz, Lucille Mellottee, Amandine Ignace, Nicolas B. David
Format: Article
Language:English
Published: Nature Portfolio 2025-02-01
Series:Communications Biology
Online Access:https://doi.org/10.1038/s42003-025-07689-6
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author Sophie Escot
Yara Hassanein
Amélie Elouin
Jorge Torres-Paz
Lucille Mellottee
Amandine Ignace
Nicolas B. David
author_facet Sophie Escot
Yara Hassanein
Amélie Elouin
Jorge Torres-Paz
Lucille Mellottee
Amandine Ignace
Nicolas B. David
author_sort Sophie Escot
collection DOAJ
description Abstract Cell migrations are crucial for embryonic development, wound healing, the immune response, as well as for cancer progression. During mesenchymal cell migration, the Rac1-WAVE-Arp2/3 signalling pathway induces branched actin polymerisation, which protrudes the membrane and allows migration. Fine-tuning the activity of the Rac1-WAVE-Arp2/3 pathway modulates protrusion lifetime and migration persistence. Recently, NHSL1, a novel interactor of the Scar/WAVE complex has been identified as a negative regulator of cell migration in vitro. We here analysed its function in vivo, during zebrafish gastrulation, when nhsl1b is expressed in migrating mesodermal cells. Loss and gain of function experiments revealed that nhsl1b is required for the proper migration of the mesoderm, controlling cell speed and migration persistence. Nhsl1b localises to the tip of actin-rich protrusions where it controls protrusion dynamics, its loss of function reducing the length and lifetime of protrusions, whereas overexpression has the opposite effect. Within the protrusion, Nhsl1b knockdown increases F-actin assembly rate and retrograde flow. These results identify Nhsl1b as a cell type specific regulator of cell migration and highlight the importance of analysing the function of regulators of actin dynamics in physiological contexts.
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spelling doaj-art-7105d7ec546f4ec6ad685a7fce458e5e2025-08-20T02:01:39ZengNature PortfolioCommunications Biology2399-36422025-02-018111410.1038/s42003-025-07689-6Nance-Horan-syndrome-like 1b controls mesodermal cell migration by regulating protrusion and actin dynamics during zebrafish gastrulationSophie Escot0Yara Hassanein1Amélie Elouin2Jorge Torres-Paz3Lucille Mellottee4Amandine Ignace5Nicolas B. David6Laboratoire d’Optique et Biosciences (LOB), CNRS, INSERM, Ecole Polytechnique, Institut Polytechnique de ParisLaboratoire d’Optique et Biosciences (LOB), CNRS, INSERM, Ecole Polytechnique, Institut Polytechnique de ParisLaboratoire d’Optique et Biosciences (LOB), CNRS, INSERM, Ecole Polytechnique, Institut Polytechnique de ParisParis-Saclay Institute of Neuroscience, CNRS and University Paris-SaclayLaboratoire d’Optique et Biosciences (LOB), CNRS, INSERM, Ecole Polytechnique, Institut Polytechnique de ParisLaboratoire d’Optique et Biosciences (LOB), CNRS, INSERM, Ecole Polytechnique, Institut Polytechnique de ParisLaboratoire d’Optique et Biosciences (LOB), CNRS, INSERM, Ecole Polytechnique, Institut Polytechnique de ParisAbstract Cell migrations are crucial for embryonic development, wound healing, the immune response, as well as for cancer progression. During mesenchymal cell migration, the Rac1-WAVE-Arp2/3 signalling pathway induces branched actin polymerisation, which protrudes the membrane and allows migration. Fine-tuning the activity of the Rac1-WAVE-Arp2/3 pathway modulates protrusion lifetime and migration persistence. Recently, NHSL1, a novel interactor of the Scar/WAVE complex has been identified as a negative regulator of cell migration in vitro. We here analysed its function in vivo, during zebrafish gastrulation, when nhsl1b is expressed in migrating mesodermal cells. Loss and gain of function experiments revealed that nhsl1b is required for the proper migration of the mesoderm, controlling cell speed and migration persistence. Nhsl1b localises to the tip of actin-rich protrusions where it controls protrusion dynamics, its loss of function reducing the length and lifetime of protrusions, whereas overexpression has the opposite effect. Within the protrusion, Nhsl1b knockdown increases F-actin assembly rate and retrograde flow. These results identify Nhsl1b as a cell type specific regulator of cell migration and highlight the importance of analysing the function of regulators of actin dynamics in physiological contexts.https://doi.org/10.1038/s42003-025-07689-6
spellingShingle Sophie Escot
Yara Hassanein
Amélie Elouin
Jorge Torres-Paz
Lucille Mellottee
Amandine Ignace
Nicolas B. David
Nance-Horan-syndrome-like 1b controls mesodermal cell migration by regulating protrusion and actin dynamics during zebrafish gastrulation
Communications Biology
title Nance-Horan-syndrome-like 1b controls mesodermal cell migration by regulating protrusion and actin dynamics during zebrafish gastrulation
title_full Nance-Horan-syndrome-like 1b controls mesodermal cell migration by regulating protrusion and actin dynamics during zebrafish gastrulation
title_fullStr Nance-Horan-syndrome-like 1b controls mesodermal cell migration by regulating protrusion and actin dynamics during zebrafish gastrulation
title_full_unstemmed Nance-Horan-syndrome-like 1b controls mesodermal cell migration by regulating protrusion and actin dynamics during zebrafish gastrulation
title_short Nance-Horan-syndrome-like 1b controls mesodermal cell migration by regulating protrusion and actin dynamics during zebrafish gastrulation
title_sort nance horan syndrome like 1b controls mesodermal cell migration by regulating protrusion and actin dynamics during zebrafish gastrulation
url https://doi.org/10.1038/s42003-025-07689-6
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