Optineurin links Hace1-dependent Rac ubiquitylation 1 to integrin-mediated mechanotransduction to control bacterial invasion and cell divisionOptineurin links Hace1-dependent Rac ubiquitylation 1 to integrin-mediated mechanotransduction to control bacterial invasion and cell division
Ontology highlight
ABSTRACT: Extracellular matrix (ECM) elasticity is perceived by cells via focal adhesion structures, which transduce mechanical cues into chemical signaling to conform cell behavior. Although the contribution of ECM compliance to the control of cell migration or division has been extensively studied, little has been reported regarding whole proteome adaptation to changes of mechanical forces. Uropathogenic E. coli (UPEC) are responsible of 70-95% of the Urinary Tract Infections (UTIs), comprising cystitis, prostatitis and pyelonephritis. These are recurrent or chronic infections causing significant costs in public health. UPEC produce the Cytotoxic Necrotizing Factor1 (CNF1) toxin, targeting one of the major host mechano-sensor and -adaptor, namely the actin cytoskeleton. We have discovered that the CNF1 and integrin-dependent invasion of cells by UPEC is highly dependent on ECM stiffness. Here we aim to analyze primary human cells treated or not with CNF1 and cultured on a fibronectin ECM of variable stiffness by label free shotgun proteomics, to bring new concepts on the manipulation of host tissue mechanics by pathogens.
INSTRUMENT(S): Orbitrap Fusion Lumos
ORGANISM(S): Homo Sapiens (human)
TISSUE(S): Endothelial Cell Of Vascular Tree
SUBMITTER: Delphi Van Haver
LAB HEAD: Amel Mettouchi
PROVIDER: PXD035396 | Pride | 2022-10-25
REPOSITORIES: Pride
ACCESS DATA