Atypical cofilin signaling drives dendritic cell migration through the extracellular matrix via nuclear deformation
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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.
In: Cell Reports, Vol. 43, No. 3, 113866, 2024.Research output: Contribution to journal › Journal article › Research › peer-review
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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