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CYRI-B loss promotes enlarged mature focal adhesions and restricts microtubule and ERC1 access to the cell leading edge

  • Jamie A. Whitelaw
  • , Sayantika Ghosh
  • , Sergio Lilla
  • , Savvas Nikolaou
  • , Luke Tweedy
  • , Loic Fort
  • , Nikki R. Paul
  • , Sara Zanivan
  • , Nikolaj Gadegaard
  • , Robert H. Insall
  • , Laura M. Machesky

Research output: Contribution to journalArticlepeer-review

Abstract

CYRI proteins promote lamellipodial dynamics by opposing Rac1-mediated activation of the Scar/WAVE complex. This activity also supports resolution of macropinocytic cups, promoting internalisation of surface proteins, including integrins. Here, we show that CYRI-B also promotes focal adhesion maturation and dynamics. Focal adhesions in CYRI-B-depleted cells show accelerated maturation and become excessively large. We probed the composition of these enlarged focal adhesions, using a Bio-ID screen, with paxillin as bait. Our screen revealed changes in adhesion proteins proximal to paxillin suggesting early activation of stress fibre contraction and depletion of the integrin internalisation mediator ERC1. Lack of CYRI-B leads to more stable lamellipodia and accumulation of polymerised actin in stress fibres. This actin acts as a barrier to microtubule targeting for adhesion turnover. Thus, our studies reveal an important connection between lamellipodia dynamics controlled by CYRI-B and microtubule targeting of ERC1 to modulate adhesion maturation and turnover.

Original languageEnglish (US)
Article numberjcs263646
JournalJournal of cell science
Volume138
Issue number22
DOIs
StatePublished - Nov 1 2025
Externally publishedYes

Keywords

  • Actin cytoskeleton
  • Bio-ID
  • CYRI-B
  • ERC1
  • Focal adhesions
  • Integrins
  • Microtubules
  • Paxillin
  • Vinculin

ASJC Scopus subject areas

  • Cell Biology

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