X inactivation of the OCNC1 channel gene reveals a role for activity-dependent competition in the olfactory system

Cell. 2001 Mar 9;104(5):651-60. doi: 10.1016/s0092-8674(01)00262-8.

Abstract

The organization of neuronal systems is often dependent on activity and competition between cells. In olfaction, the X-linked OCNC1 channel subunit is subject to random inactivation and is essential for odorant-evoked activity. Reporter-tagged OCNC1 mutant mice permit the visualization of OCNC1-deficient olfactory neurons and their projections. In heterozygous females, X inactivation creates a mosaic with two populations of genetically distinct neurons. OCNC1-deficient neurons are slowly and specifically depleted from the olfactory epithelium and display unusual patterns of projection to the olfactory bulb. Remarkably, this depletion is dependent on odorant exposure and is reversed by odorant deprivation. This suggests that odorants and the activity they evoke are critical for neuronal survival in a competitive environment and implicate evoked activity in the organization and maintenance of the olfactory system.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Age Factors
  • Alleles
  • Animals
  • Cell Count
  • Cyclic Nucleotide-Gated Cation Channels
  • Dosage Compensation, Genetic*
  • Female
  • Gene Expression / physiology
  • Genes, Reporter
  • Green Fluorescent Proteins
  • Heterozygote
  • Indicators and Reagents / metabolism
  • Ion Channels / genetics*
  • Ion Channels / metabolism*
  • Lac Operon
  • Luminescent Proteins / genetics
  • Mice
  • Mice, Knockout
  • Odorants
  • Olfactory Receptor Neurons / cytology
  • Olfactory Receptor Neurons / physiology
  • Smell / genetics*

Substances

  • Cyclic Nucleotide-Gated Cation Channels
  • Indicators and Reagents
  • Ion Channels
  • Luminescent Proteins
  • Green Fluorescent Proteins