Cortical dynamics during cell motility are regulated by CRL3KLHL21 E3 ubiquitin ligase

Thibault Courtheoux (), Radoslav I. Enchev, Fabienne Lampert, Juan Gerez, Jochen Beck, Paola Picotti, Izabela Sumara and Matthias Peter ()
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Thibault Courtheoux: Institute of Biochemistry, ETH Zurich
Radoslav I. Enchev: Institute of Biochemistry, ETH Zurich
Fabienne Lampert: Institute of Biochemistry, ETH Zurich
Juan Gerez: Institute of Biochemistry, ETH Zurich
Jochen Beck: Institute of Biochemistry, ETH Zurich
Paola Picotti: Institute of Biochemistry, ETH Zurich
Izabela Sumara: Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), Centre National de la Recherche Scientifique UMR 7104, Institut National de la Santé et de la Recherche Médicale U964, Université de Strasbourg
Matthias Peter: Institute of Biochemistry, ETH Zurich

Nature Communications, 2016, vol. 7, issue 1, 1-13

Abstract: Abstract Directed cell movement involves spatial and temporal regulation of the cortical microtubule (Mt) and actin networks to allow focal adhesions (FAs) to assemble at the cell front and disassemble at the rear. Mts are known to associate with FAs, but the mechanisms coordinating their dynamic interactions remain unknown. Here we show that the CRL3KLHL21 E3 ubiquitin ligase promotes cell migration by controlling Mt and FA dynamics at the cell cortex. Indeed, KLHL21 localizes to FA structures preferentially at the leading edge, and in complex with Cul3, ubiquitylates EB1 within its microtubule-interacting CH-domain. Cells lacking CRL3KLHL21 activity or expressing a non-ubiquitylatable EB1 mutant protein are unable to migrate and exhibit strong defects in FA dynamics, lamellipodia formation and cortical plasticity. Our study thus reveals an important mechanism to regulate cortical dynamics during cell migration that involves ubiquitylation of EB1 at focal adhesions.

Date: 2016
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms12810

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DOI: 10.1038/ncomms12810

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