Prior
work
in
the Pevny lab has demonstrated
that in vitro conditional ablation of
SOX2, a regulator of stem cell pluripotency, in murine retinal Muller
Glia
cells results in an ectopic entrance into the cell cycle. Müller
Glia cells are
the principal glial cells of the vertebrate retina, providing
structural and
trophic support. They are the only glia cells that arise from
multipotent,
neuroepethelial derived retinal progenitor cells and recent evidence
suggests
that they may make up a population of quiescent progenitor cells in the
vertebrate
retina. The ectopic division of Muller glia upon the in vitro ablation
of SOX2
suggests that SOX2 may function to maintain these cells in a quiescent,
progenitor-like state by limiting their ability to enter the cell cycle
and
terminally differentiate. What role SOX2 plays in cell cycle
maintenance is
unclear, as is the long-term affect of conditional SOX2 ablation on the
postnatal eye. To address this question more directly I am developing a
protocol for in vivo retinal electroporation. Once perfected this
method will
enable us to conditionally ablate SOX2 in a portion of the P0 retina
and allow
for long-term study of cell cycle regulation and development of the
postnatal
SOX2 deficient retina.