Article
A role for Uracil DNA Glycosylase (UDG) in murine retina function?
Search Medline for
Authors
Published: | September 22, 2004 |
---|
Outline
Text
Objective
Retinal neurosensory function is limited by recessive inheritable defects of DNA repair (Cockayne syndrome). UDG is expressed in mouse retina where its function is initiation of Base Excision Repair (BER) of aberrant Uracil residues in mitochondrial or nuclear DNA. Recent publications indicated possible protection from photochemical and age-related retinal damage by BER (Gordon et al., 2002; Sparrow et al., 2003). Uracil accumulation in mitochondrial and/or nuclear DNA could lead to faulty transcripts and may impair cellular transmembrane potentials through hampered protein function. Here, we tested the hypothesis, whether or not UDG deletion might result in detectable retinal electrophysiologic changes.
Methods
Electroretinographic (ERG) tests were performed in UDG-/- and UDG+/+ mice strains.
Results
In our preliminary results, analysis of a-waves and b-waves failed to evince significant differences between UDG null vs. UDG wildtype mice.
Conclusions
In comparison, ERG tests of basal retinal function in UDG-/- and UDG+/+ mice so far show similar results. Further analysis of retinal function under certain stress conditions may uncover a role for BER of Uracil in maintaining neurosensory retinal function.