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The β-actin mRNA zipcode regulates epithelial adherens junction assembly but not maintenance
Journal article   Open access   Peer reviewed

The β-actin mRNA zipcode regulates epithelial adherens junction assembly but not maintenance

Natasha Gutierrez, Itua Eromobor, Ryan J. Petrie, Pavan Vedula, Lissette Cruz and Alexis J. Rodriguez
RNA (Cambridge), v 20(5), pp 689-701
01 May 2014
PMID: 24681968
url
http://rnajournal.cshlp.org/content/20/5/689.full.pdfView
Published, Version of Record (VoR) Open
url
https://doi.org/10.1261/rna.043208.113View
Published, Version of Record (VoR) Open

Abstract

actin cytoskeleton regulation actin mRNA zipcodes adherens junction assembly RhoA and Src signaling translation regulation
This paper examines requirements for cytoskeletal remodeling during epithelial cell-cell contact. Antisense oligonucleotides that inhibit β-actin mRNA zipcode/ZBP1 interactions cause defects in adherens junction assembly. Epithelial cell-cell contact stimulates actin cytoskeleton remodeling to down-regulate branched filament polymerization-driven lamellar protrusion and subsequently to assemble linear actin filaments required for E-cadherin anchoring during adherens junction complex assembly. In this manuscript, we demonstrate that de novo protein synthesis, the β-actin 3′ UTR, and the β-actin mRNA zipcode are required for epithelial adherens junction complex assembly but not maintenance. Specifically, we demonstrate that perturbing cell-cell contact-localized β-actin monomer synthesis causes epithelial adherens junction assembly defects. Consequently, inhibiting β-actin mRNA zipcode/ZBP1 interactions with β-actin mRNA zipcode antisense oligonucleotides, to intentionally delocalize β-actin monomer synthesis, is sufficient to perturb adherens junction assembly following epithelial cell-cell contact. Additionally, we demonstrate active RhoA, the signal required to drive zipcode-mediated β-actin mRNA targeting, is localized at epithelial cell-cell contact sites in a β-actin mRNA zipcode-dependent manner. Moreover, chemically inhibiting Src kinase activity prevents the local stimulation of β-actin monomer synthesis at cell-cell contact sites while inhibiting epithelial adherens junction assembly. Together, these data demonstrate that epithelial cell-cell contact stimulates β-actin mRNA zipcode-mediated monomer synthesis to spatially regulate actin filament remodeling, thereby controlling adherens junction assembly to modulate cell and tissue adhesion.

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Collaboration types
Domestic collaboration
Web of Science research areas
Biochemistry & Molecular Biology
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