April 2009
Volume 50, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2009
Recruitment of -Catenin, Cortactin and Arp3 to N-Cadherin Junctions as Regulators of Actin Dynamics in Lens Cell Differentiation
Author Affiliations & Notes
  • M. Leonard
    Pathology Anatomy & Cell Biol, Thomas Jefferson University, Philadelphia, Pennsylvania
  • A. S. Menko
    Pathology Anatomy & Cell Biol, Thomas Jefferson University, Philadelphia, Pennsylvania
  • Footnotes
    Commercial Relationships  M. Leonard, None; A.S. Menko, None.
  • Footnotes
    Support  NIH Grant EY10577; NEI Grant EY014258; NIH/NIEHS Training Grant T32E5007282
Investigative Ophthalmology & Visual Science April 2009, Vol.50, 1222. doi:
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      M. Leonard, A. S. Menko; Recruitment of -Catenin, Cortactin and Arp3 to N-Cadherin Junctions as Regulators of Actin Dynamics in Lens Cell Differentiation. Invest. Ophthalmol. Vis. Sci. 2009;50(13):1222.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: : Lens fiber cell differentiation requires both the formation of N-cadherin junctions and the assembly of cortically arranged actin filaments. We now have investigated the in vivo recruitment of molecular regulators of actin dynamics to N-cadherin junctions as the means by which N-cadherin junction formation directs lens fiber cell differentiation and morphogenesis.

Methods: : Differentiation-specific changes in the recruitment of -catenin, cortactin and Arp3 to N-cadherin junctions was determined by co-immunoprecipitation analysis of microdissected E10 chick embryo lenses. Localization of these proteins to N-cadherin junctions in E10 chick lens sections was determined by confocal microscopy of immunostained sections.

Results: : We have previously demonstrated that the assembly of cortically arranged actin filaments is dependent on formation of mature N-cadherin junctions and necessary for lens cell differentiation. Here, by examining the differentiation-state specific recruitment of actin regulators to N-cadherin junctions in vivo, we have revealed the mechanisms by which these junctions regulate assembly of actin filaments for lens cell differentiation. The recruitment of -catenin to cadherin junctions is known to block lamellipodial extension. In the developing lens -catenin became linked to N-cadherin just as the cells establish close cell-cell appositions. Cortactin, an activator of actin filament nucleation, became associated with N-cadherin junctions as lens cells initiated their differentiation, but prior to lens fiber cell morphogenesis. Arp3, a nucleator of actin filament assembly that binds to and is activated by cortactin, was recruited to N-cadherin junctions coincident with rapid cortical actin assembly and fiber cell elongation.

Conclusions: : We propose a model whereby recruitment of -catenin to N-cadherin regulates junctional maturation necessary for the initiation of lens fiber cell differentiation, while the N-cadherin/cortactin/Arp3 pathway directs the assembly of actin that extends N-cadherin cell-cell adhesions and generates the forces that drive fiber cell elongation for the establishment of lens cytoarchitecture.

Keywords: cell adhesions/cell junctions • differentiation 
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