The FXR1 network acts as signaling scaffold for actomyosin remodeling.

Autor: Chen X; Cancer Biology and Genetics Program, Sloan Kettering Institute, New York, NY 10065, USA., Fansler MM; Cancer Biology and Genetics Program, Sloan Kettering Institute, New York, NY 10065, USA., Janjoš U; National Institute of Chemistry, Hajdrihova 19, 1001 Ljubljana, Slovenia.; Biosciences PhD Program, Biotechnical Faculty, University of Ljubljana, Ljubljana, Slovenia., Ule J; National Institute of Chemistry, Hajdrihova 19, 1001 Ljubljana, Slovenia.; UK Dementia Research Institute at King's College London, London, SE5 9NU, UK., Mayr C; Cancer Biology and Genetics Program, Sloan Kettering Institute, New York, NY 10065, USA.
Jazyk: angličtina
Zdroj: BioRxiv : the preprint server for biology [bioRxiv] 2024 May 25. Date of Electronic Publication: 2024 May 25.
DOI: 10.1101/2023.11.05.565677
Abstrakt: It is currently not known whether mRNAs fulfill structural roles in the cytoplasm. Here, we report the FXR1 network, an mRNA-protein (mRNP) network present throughout the cytoplasm, formed by FXR1-mediated packaging of exceptionally long mRNAs. These mRNAs serve as underlying condensate scaffold and concentrate FXR1 molecules. The FXR1 network contains multiple protein binding sites and functions as a signaling scaffold for interacting proteins. We show that it is necessary for RhoA signaling-induced actomyosin reorganization to provide spatial proximity between kinases and their substrates. Point mutations in FXR1, found in its homolog FMR1, where they cause Fragile X syndrome, disrupt the network. FXR1 network disruption prevents actomyosin remodeling-an essential and ubiquitous process for the regulation of cell shape, migration, and synaptic function. These findings uncover a structural role for cytoplasmic mRNA and show how the FXR1 RNA-binding protein as part of the FXR1 network acts as organizer of signaling reactions.
Competing Interests: Declaration of Interests Christine Mayr is a member of the Cell Advisory Board. The authors declare no other competing interests.
Databáze: MEDLINE