Disruption of a retinal guanylyl cyclase gene leads to cone-specific dystrophy and paradoxical rod behavior

Ruey Bing Yang, Susan W. Robinson, Wei Hong Xiong, King Wai Yau, David G. Birch, David L. Garbers

Research output: Contribution to journalArticlepeer-review

Abstract

One of two orphan photoreceptor guanylyl cyclases that are highly conserved from fish to mammals, GC-E (or retGC1) was eliminated by gene disruption. Expression of the second retinal cyclase (GC-F) as well as the numbers and morphology of rods remained unchanged in GC-E null mice. However, rods isolated from such mice, despite having a normal dark current, recovered from a light flash markedly faster. Unexpectedly, the a- and b-waves of electroretinograms (ERG) from dark-adapted null mice were suppressed markedly. Cones, initially present in normal numbers in the retina, disappeared by 5 weeks, based on ERG and histology. Thus, the GC-E-deficient mouse defines a model for cone dystrophy, but it also demonstrates that morphologically normal rods display paradoxical behavior in their responses to light.

Original languageEnglish (US)
Pages (from-to)5889-5897
Number of pages9
JournalJournal of Neuroscience
Volume19
Issue number14
DOIs
StatePublished - Jul 15 1999

Keywords

  • Cone dystrophy
  • Cyclic GMP
  • Gene disruption
  • Guanylyl cyclase-E
  • Guanylyl cyclases
  • Mice
  • Photoreceptors
  • Retina

ASJC Scopus subject areas

  • Neuroscience(all)

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