Atypical cofilin signaling drives dendritic cell migration through the extracellular matrix via nuclear deformation

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Standard

Atypical cofilin signaling drives dendritic cell migration through the extracellular matrix via nuclear deformation. / Warner, Harry; Franciosa, Giulia; van der Borg, Guus; Coenen, Britt; Faas, Felix; Koenig, Claire; de Boer, Rinse; Classens, René; Maassen, Sjors; Baranov, Maksim V.; Mahajan, Shweta; Dabral, Deepti; Bianchi, Frans; van Hilten, Niek; Risselada, Herre Jelger; Roos, Wouter H.; Olsen, Jesper Velgaard; Cano, Laia Querol; van den Bogaart, Geert.

I: Cell Reports, Bind 43, Nr. 3, 113866, 2024.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Warner, H, Franciosa, G, van der Borg, G, Coenen, B, Faas, F, Koenig, C, de Boer, R, Classens, R, Maassen, S, Baranov, MV, Mahajan, S, Dabral, D, Bianchi, F, van Hilten, N, Risselada, HJ, Roos, WH, Olsen, JV, Cano, LQ & van den Bogaart, G 2024, 'Atypical cofilin signaling drives dendritic cell migration through the extracellular matrix via nuclear deformation', Cell Reports, bind 43, nr. 3, 113866. https://doi.org/10.1016/j.celrep.2024.113866

APA

Warner, H., Franciosa, G., van der Borg, G., Coenen, B., Faas, F., Koenig, C., de Boer, R., Classens, R., Maassen, S., Baranov, M. V., Mahajan, S., Dabral, D., Bianchi, F., van Hilten, N., Risselada, H. J., Roos, W. H., Olsen, J. V., Cano, L. Q., & van den Bogaart, G. (2024). Atypical cofilin signaling drives dendritic cell migration through the extracellular matrix via nuclear deformation. Cell Reports, 43(3), [113866]. https://doi.org/10.1016/j.celrep.2024.113866

Vancouver

Warner H, Franciosa G, van der Borg G, Coenen B, Faas F, Koenig C o.a. Atypical cofilin signaling drives dendritic cell migration through the extracellular matrix via nuclear deformation. Cell Reports. 2024;43(3). 113866. https://doi.org/10.1016/j.celrep.2024.113866

Author

Warner, Harry ; Franciosa, Giulia ; van der Borg, Guus ; Coenen, Britt ; Faas, Felix ; Koenig, Claire ; de Boer, Rinse ; Classens, René ; Maassen, Sjors ; Baranov, Maksim V. ; Mahajan, Shweta ; Dabral, Deepti ; Bianchi, Frans ; van Hilten, Niek ; Risselada, Herre Jelger ; Roos, Wouter H. ; Olsen, Jesper Velgaard ; Cano, Laia Querol ; van den Bogaart, Geert. / Atypical cofilin signaling drives dendritic cell migration through the extracellular matrix via nuclear deformation. I: Cell Reports. 2024 ; Bind 43, Nr. 3.

Bibtex

@article{fbd73cac64dc472889db0eb7c3311c9a,
title = "Atypical cofilin signaling drives dendritic cell migration through the extracellular matrix via nuclear deformation",
abstract = "To mount an adaptive immune response, dendritic cells must migrate to lymph nodes to present antigens to T cells. Critical to 3D migration is the nucleus, which is the size-limiting barrier for migration through the extracellular matrix. Here, we show that inflammatory activation of dendritic cells leads to the nucleus becoming spherically deformed and enables dendritic cells to overcome the typical 2- to 3-μm diameter limit for 3D migration through gaps in the extracellular matrix. We show that the nuclear shape change is partially attained through reduced cell adhesion, whereas improved 3D migration is achieved through reprogramming of the actin cytoskeleton. Specifically, our data point to a model whereby the phosphorylation of cofilin-1 at serine 41 drives the assembly of a cofilin-actomyosin ring proximal to the nucleus and enhances migration through 3D collagen gels. In summary, these data describe signaling events through which dendritic cells deform their nucleus and enhance their migratory capacity.",
keywords = "cofilin, CP: Cell biology, dendritic cell, mechanosensing, nucleus, phosphoproteomics",
author = "Harry Warner and Giulia Franciosa and {van der Borg}, Guus and Britt Coenen and Felix Faas and Claire Koenig and {de Boer}, Rinse and Ren{\'e} Classens and Sjors Maassen and Baranov, {Maksim V.} and Shweta Mahajan and Deepti Dabral and Frans Bianchi and {van Hilten}, Niek and Risselada, {Herre Jelger} and Roos, {Wouter H.} and Olsen, {Jesper Velgaard} and Cano, {Laia Querol} and {van den Bogaart}, Geert",
note = "Publisher Copyright: {\textcopyright} 2024 The Author(s)",
year = "2024",
doi = "10.1016/j.celrep.2024.113866",
language = "English",
volume = "43",
journal = "Cell Reports",
issn = "2211-1247",
publisher = "Cell Press",
number = "3",

}

RIS

TY - JOUR

T1 - Atypical cofilin signaling drives dendritic cell migration through the extracellular matrix via nuclear deformation

AU - Warner, Harry

AU - Franciosa, Giulia

AU - van der Borg, Guus

AU - Coenen, Britt

AU - Faas, Felix

AU - Koenig, Claire

AU - de Boer, Rinse

AU - Classens, René

AU - Maassen, Sjors

AU - Baranov, Maksim V.

AU - Mahajan, Shweta

AU - Dabral, Deepti

AU - Bianchi, Frans

AU - van Hilten, Niek

AU - Risselada, Herre Jelger

AU - Roos, Wouter H.

AU - Olsen, Jesper Velgaard

AU - Cano, Laia Querol

AU - van den Bogaart, Geert

N1 - Publisher Copyright: © 2024 The Author(s)

PY - 2024

Y1 - 2024

N2 - To mount an adaptive immune response, dendritic cells must migrate to lymph nodes to present antigens to T cells. Critical to 3D migration is the nucleus, which is the size-limiting barrier for migration through the extracellular matrix. Here, we show that inflammatory activation of dendritic cells leads to the nucleus becoming spherically deformed and enables dendritic cells to overcome the typical 2- to 3-μm diameter limit for 3D migration through gaps in the extracellular matrix. We show that the nuclear shape change is partially attained through reduced cell adhesion, whereas improved 3D migration is achieved through reprogramming of the actin cytoskeleton. Specifically, our data point to a model whereby the phosphorylation of cofilin-1 at serine 41 drives the assembly of a cofilin-actomyosin ring proximal to the nucleus and enhances migration through 3D collagen gels. In summary, these data describe signaling events through which dendritic cells deform their nucleus and enhance their migratory capacity.

AB - To mount an adaptive immune response, dendritic cells must migrate to lymph nodes to present antigens to T cells. Critical to 3D migration is the nucleus, which is the size-limiting barrier for migration through the extracellular matrix. Here, we show that inflammatory activation of dendritic cells leads to the nucleus becoming spherically deformed and enables dendritic cells to overcome the typical 2- to 3-μm diameter limit for 3D migration through gaps in the extracellular matrix. We show that the nuclear shape change is partially attained through reduced cell adhesion, whereas improved 3D migration is achieved through reprogramming of the actin cytoskeleton. Specifically, our data point to a model whereby the phosphorylation of cofilin-1 at serine 41 drives the assembly of a cofilin-actomyosin ring proximal to the nucleus and enhances migration through 3D collagen gels. In summary, these data describe signaling events through which dendritic cells deform their nucleus and enhance their migratory capacity.

KW - cofilin

KW - CP: Cell biology

KW - dendritic cell

KW - mechanosensing

KW - nucleus

KW - phosphoproteomics

U2 - 10.1016/j.celrep.2024.113866

DO - 10.1016/j.celrep.2024.113866

M3 - Journal article

C2 - 38416638

AN - SCOPUS:85187779819

VL - 43

JO - Cell Reports

JF - Cell Reports

SN - 2211-1247

IS - 3

M1 - 113866

ER -

ID: 387834130