April 2009
Volume 50, Issue 13
ARVO Annual Meeting Abstract  |   April 2009
MAPK Signaling Regulates Cx50 During Lens Development
Author Affiliations & Notes
  • M. Srinivas
    Biological Sciences, SUNY College of Optometry, New York, New York
  • C. Rubinos
    Biological Sciences, SUNY College of Optometry, New York, New York
  • L. Li
    Physiology, Stony Brook University, Stony Brook, New York
  • C. Sellitto
    Physiology, Stony Brook University, Stony Brook, New York
  • X. Gong
    School of Optometry, UC Berkeley, Berkeley, California
  • T. W. White
    Physiology, Stony Brook University, Stony Brook, New York
  • Footnotes
    Commercial Relationships  M. Srinivas, None; C. Rubinos, None; L. Li, None; C. Sellitto, None; X. Gong, None; T.W. White, None.
  • Footnotes
    Support  NIH Grants EY13869 and EY13163
Investigative Ophthalmology & Visual Science April 2009, Vol.50, 4764. doi:
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      M. Srinivas, C. Rubinos, L. Li, C. Sellitto, X. Gong, T. W. White; MAPK Signaling Regulates Cx50 During Lens Development. Invest. Ophthalmol. Vis. Sci. 2009;50(13):4764.

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

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Purpose: : Both connexins and signal transduction pathways have been shown to play critical roles in lens development, but little is known about interaction between these two intercellular communication systems. To investigate whether growth factor signaling modulates gap junctional communication during lens development, we examined the effect of MAPK signaling on coupling mediated by lens connexins.

Methods: : For in vitro studies, ERK signaling was stimulated by the expression of a constitutively active form of MEK1 (caMEK1), or by treatment of cells with FGF. For in vivo studies, genetically engineered mice expressing caMEK1 in the lens were crossed with animals lacking Cx46 (Cx46KO) or Cx50 (Cx50KO). Junctional conductance was measured by dual whole cell voltage clamp. ERK activation was measured using antibodies specific for phosphorylated ERK. Lenses were analyzed by light microscopy.

Results: : Activation of MAPK signaling increased coupling provided by Cx50, but not Cx46 in vitro. Activation of MAPK signaling in vivo also specifically increased Cx50 functional activity between lens cells. In vivo, constitutively active MAPK signaling caused macrophthalmia, the formation of vacuoles in the bow region of the lens fibers and lens rupture. Deletion of Cx50, but not Cx46, eliminated all three pathologies in caMEK1 transgenic mice.

Conclusions: : These results indicate that MAPK signaling specifically modulates Cx50, and that gap junctional communication and signal transduction pathways may act synergistically during lens development.

Keywords: gap junctions/coupling • cell-cell communication • cell adhesions/cell junctions 

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