LENS GAP JUNCTIONS: IDENTITY AND PROPERTIES

Project: Research project

Project Details

Description

DESCRIPTION (adapted from applicant's abstract): Gap junctions provide a
pathway for intercellular communication influencing tissue homeostasis. In
the lens, gap junctions are particularly important for the maintenance of
proper tissue functioning. The fiber cells, which constitute most of the
lens tissue, are devoid of intracellular organelles and therefore most of
the transport properties of the lens are located in the anterior epithelial
cell layer. To exchange metabolites and maintain cellular volume the fiber
cells depend heavily on the diffusional pathway created by gap junctions
between lens fiber cells and between fiber and epithelial cells. Until
recently intercellular communication in the lens was thought to be mediated
by the main intrinsic protein of the lens (MIP), but evidence has been
presented showing that MIP, although present in junctional areas, is not
the gap junction forming protein. The applicant proposes to elucidate the
role played by this ubiquitous protein in lens physiology by studying MIP
channel properties in liposomes, bilayers, MIP transfected cells and in
isolated fiber cells. Two newly identified proteins (M, 70 and 46 kD) are
gap junction candidates, although there is at present no evidence that
either protein forms gap junction channels. The applicant proposes to
reconstitute MP70 into liposomes and planar bilayers and to transfect a
communication deficient cell line with connexin46 cDNA to study their
channel forming capacities. By comparing the properties of channels formed
by these methods to those of the junctional membrane conductance between
pairs of freshly dissociated lens fiber cells the applicant would be able
to address the question of which protein(s) is(are) responsible for gap
junction channel formation in the fiber cells. Through these studies the
applicant expects to gain insights into the role of gap junctions and MIP
channels in the homeostasis of lens tissue, and particularly into the
possibility that disruption of function of these channels leads to
pathological consequences.
StatusFinished
Effective start/end date2/1/911/31/92

Funding

  • NATIONAL EYE INSTITUTE

ASJC

  • Physiology

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