Competition for binding to the cellular protein paxillin by the proteins Nudel and focal adhesion kinase is important for the proper regulation of cell adhesion and migration

A Gupta

A Hall

A Nayal

A Ponti

A Richardson

AD Bershadsky

B Geiger

C Huang

CD Nobes

CE Turner

CG Galbraith

CJ Echeverri

CK Choi

D Ilic

D Lietha

D Riveline

DA Lauffenburger

DJ Sieg

DJ Webb

DL Dujardin

Fubin Wang

GG Gundersen

HC Chen

I Hayashi

I Kaverina

J Chen

J Guo

JD Hildebrand

Jianfeng Chen

JK Burkhardt

K Burridge

KA Beningo

Kenneth M. Yamada

KH Martin

L Ma

L Yang

LB Smilenov

Lihou Yu

M Hagel

M Raftopoulou

MA Cooley

MA Schwartz

MC Brown

MS Duxbury

N Nishiya

NQ Balaban

Qiangge Zhang

R Kozma

R Zaidel-Bar

S Hirotsune

S Sasaki

SA Stehman

SK Mitra

SL Gupton

SL Stroschein

T Shu

TD Pollard

U Derewenda

WG Dirks

X Yan

Xueliang Zhu

Y Liang

Y Shen

Yan Li

Yongli Shan

Youdong Pan

Z Yang

English

PubMed

Crossref

Nudel and FAK as Antagonizing Strength Modulators of Nascent Adhesions through Paxillin

Adhesion and detachment are coordinated critical steps during cell migration. Conceptually, efficient migration requires both effective stabilization of membrane protrusions at the leading edge via nascent adhesions and their successful persistence during retraction of the trailing side via disruption of focal adhesions. As nascent adhesions are much smaller in size than focal adhesions, they are expected to exhibit a stronger adhesivity in order to achieve the coordination between cell front and back. Here, we show that Nudel knockdown by interference RNA (RNAi) resulted in cell edge shrinkage due to poor adhesions of membrane protrusions. Nudel bound to paxillin, a scaffold protein of focal contacts, and colocalized with it in areas of active membrane protrusions, presumably at nascent adhesions. The Nudel-paxillin interaction was disrupted by focal adhesion kinase (FAK) in a paxillin-binding-dependent manner. Forced localization of Nudel in all focal contacts by fusing it to paxillin markedly strengthened their adhesivity, whereas overexpression of structurally activated FAK or any paxillin-binding FAK mutant lacking the N-terminal autoinhibitory domain caused cell edge shrinkage. These results suggest a novel mechanism for selective reinforcement of nascent adhesions via interplays of Nudel and FAK with paxillin to facilitate cell migration

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PLoS Biology

Nudel and FAK as antagonizing strength modulators of nascent adhesions through paxillin.

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Hall A

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The relationship between force and focal complex development.

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Transmembrane crosstalk between the extracellular matrix and the cytoskeleton.

Two distinct actin networks drive the protrusion of migrating cells.

Wynshaw-Boris A

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2684528

Nudel and FAK as Antagonizing Strength Modulators of Nascent Adhesions through Paxillin

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