Skip to main navigation Skip to search Skip to main content

The laminin-keratin link shields the nucleus from mechanical deformation and signalling

  • Zanetta Kechagia*
  • , Pablo Sáez
  • , Manuel Gómez-González
  • , Brenda Canales
  • , Srivatsava Viswanadha
  • , Martín Zamarbide
  • , Ion Andreu
  • , Thijs Koorman
  • , Amy E M Beedle
  • , Alberto Elosegui-Artola
  • , Patrick W B Derksen
  • , Xavier Trepat
  • , Marino Arroyo
  • , Pere Roca-Cusachs*
  • *Corresponding author for this work

Research output: Contribution to journal › Article › Academic › peer-review

10 Downloads (Pure)

Abstract

The mechanical properties of the extracellular matrix dictate tissue behaviour. In epithelial tissues, laminin is a very abundant extracellular matrix component and a key supporting element. Here we show that laminin hinders the mechanoresponses of breast epithelial cells by shielding the nucleus from mechanical deformation. Coating substrates with laminin-111-unlike fibronectin or collagen I-impairs cell response to substrate rigidity and YAP nuclear localization. Blocking the laminin-specific integrin β4 increases nuclear YAP ratios in a rigidity-dependent manner without affecting the cell forces or focal adhesions. By combining mechanical perturbations and mathematical modelling, we show that β4 integrins establish a mechanical linkage between the substrate and keratin cytoskeleton, which stiffens the network and shields the nucleus from actomyosin-mediated mechanical deformation. In turn, this affects the nuclear YAP mechanoresponses, chromatin methylation and cell invasion in three dimensions. Our results demonstrate a mechanism by which tissues can regulate their sensitivity to mechanical signals.

Original languageEnglish
Pages (from-to)1409-1420
Number of pages12
JournalNature materials
Volume22
Issue number11
Early online date14 Sept 2023
DOIs
Publication statusPublished - Nov 2023

Fingerprint

Dive into the research topics of 'The laminin-keratin link shields the nucleus from mechanical deformation and signalling'. Together they form a unique fingerprint.

Cite this