TY - JOUR
T1 - Tensin3 interaction with talin drives the formation of fibronectin-associated fibrillar adhesions
AU - Atherton, Paul
AU - Konstantinou, Rafaella
AU - Neo, Suat Peng
AU - Wang, Emily
AU - Balloi, Eleonora
AU - Ptushkina, Marina
AU - Bennett, Hayley
AU - Clark, Kath
AU - Gunaratne, Jayantha
AU - Critchley, David
AU - Barsukov, Igor
AU - Manser, Edward
AU - Ballestrem, Christoph
N1 - Funding Information:
C. Ballestrem acknowledges the Biotechnology and Biological Sciences Research Council (BBSRC) and the Wellcome Trust for funding this project. The Ballestrem laboratory is part of the Wellcome Trust Centre for Cell-Matrix Research, University of Manchester, which is supported by core funding from the Wellcome Trust (grant number 203128/Z/16/Z). P. Atherton was funded by BBSRC (BB/P000681/1 and BB/V016326/1); R. Kon-stantinou is supported by the Faculty of Biology, Medicine and Health and the University of Manchester and by the Agency of Science Technology and Research (A*STAR); E. Wang is funded by the BBSRC doctoral training program in Liverpool. The Bio-imaging Facility microscopes were purchased with grants from the BBSRC, the Wellcome Trust, and the University of Manchester Strategic Fund. The authors declare no competing financial interests.
Publisher Copyright:
© 2022 Atherton et al.
PY - 2022/10/3
Y1 - 2022/10/3
N2 - The formation of healthy tissue involves continuous remodeling of the extracellular matrix (ECM). Whilst it is known that this requires integrin-associated cell-ECM adhesion sites (CMAs) and actomyosin-mediated forces, the underlying mechanisms remain unclear. Here, we examine how tensin3 contributes to the formation of fibrillar adhesions (FBs) and fibronectin fibrillogenesis. Using BioID mass spectrometry and a mitochondrial targeting assay, we establish that tensin3 associates with the mechanosensors such as talin and vinculin. We show that the talin R11 rod domain binds directly to a helical motif within the central intrinsically disordered region (IDR) of tensin3, whilst vinculin binds indirectly to tensin3 via talin. Using CRISPR knock-out cells in combination with defined tensin3 mutations, we show (i) that tensin3 is critical for the formation of α5β1-integrin FBs and for fibronectin fibrillogenesis, and (ii) the talin/tensin3 interaction drives this process, with vinculin acting to potentiate it.
AB - The formation of healthy tissue involves continuous remodeling of the extracellular matrix (ECM). Whilst it is known that this requires integrin-associated cell-ECM adhesion sites (CMAs) and actomyosin-mediated forces, the underlying mechanisms remain unclear. Here, we examine how tensin3 contributes to the formation of fibrillar adhesions (FBs) and fibronectin fibrillogenesis. Using BioID mass spectrometry and a mitochondrial targeting assay, we establish that tensin3 associates with the mechanosensors such as talin and vinculin. We show that the talin R11 rod domain binds directly to a helical motif within the central intrinsically disordered region (IDR) of tensin3, whilst vinculin binds indirectly to tensin3 via talin. Using CRISPR knock-out cells in combination with defined tensin3 mutations, we show (i) that tensin3 is critical for the formation of α5β1-integrin FBs and for fibronectin fibrillogenesis, and (ii) the talin/tensin3 interaction drives this process, with vinculin acting to potentiate it.
U2 - 10.1083/jcb.202107022
DO - 10.1083/jcb.202107022
M3 - Article
C2 - 36074065
AN - SCOPUS:85138125787
SN - 0021-9525
VL - 221
JO - Journal of Cell Biology
JF - Journal of Cell Biology
IS - 10
M1 - e202107022
ER -