Diversification of C. elegans Motor Neuron Identity via Selective Effector Gene Repression

Neuron. 2017 Jan 4;93(1):80-98. doi: 10.1016/j.neuron.2016.11.036.

Abstract

A common organizational feature of nervous systems is the existence of groups of neurons that share common traits but can be divided into individual subtypes based on anatomical or molecular features. We elucidate the mechanistic basis of neuronal diversification processes in the context of C.elegans ventral cord motor neurons that share common traits that are directly activated by the terminal selector UNC-3. Diversification of motor neurons into different classes, each characterized by unique patterns of effector gene expression, is controlled by distinct combinations of phylogenetically conserved, class-specific transcriptional repressors. These repressors are continuously required in postmitotic neurons to prevent UNC-3, which is active in all neuron classes, from activating class-specific effector genes in specific motor neuron subsets via discrete cis-regulatory elements. The strategy of antagonizing the activity of broadly acting terminal selectors of neuron identity in a subtype-specific fashion may constitute a general principle of neuron subtype diversification.

Keywords: C. elegans; combinatorial code; maintenance; motor neuron; neuron diversification; neuron subtype; repressor; selective repression; terminal selector; transcription factor.

MeSH terms

  • Animals
  • Caenorhabditis elegans
  • Caenorhabditis elegans Proteins / genetics*
  • Cell Differentiation / genetics
  • Epithelial Sodium Channels / genetics
  • Gene Expression Regulation, Developmental*
  • Motor Neurons / cytology
  • Motor Neurons / metabolism*
  • Neurogenesis / genetics*
  • Receptors, AMPA / genetics
  • Receptors, Nicotinic / genetics
  • Transcription Factors / genetics*
  • Transforming Growth Factor beta / genetics

Substances

  • Caenorhabditis elegans Proteins
  • Epithelial Sodium Channels
  • Receptors, AMPA
  • Receptors, Nicotinic
  • Transcription Factors
  • Transforming Growth Factor beta
  • UNC-129 protein, C elegans
  • acr-16 protein, C elegans
  • glutamate receptor ionotropic, AMPA 4
  • unc-3 protein, C elegans