HeyL regulates the number of TrkC neurons in dorsal root ganglia

Abhishek Mukhopadhyay*, Jennifer Jarrett, Timothy Chlon, John A. Kessler

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

15 Scopus citations

Abstract

The basic-helix-loop-helix transcription factor HeyL is expressed at high levels by neural crest progenitor cells (NCPs) that give rise to neurons and glia in dorsal root ganglia (DRG). Since HeyL expression was observed in these NCPs during the period of neurogenesis, we generated HeyL null mutants to help examine the factor's role in ganglion neuronal specification. Homozygous null mutation of HeyL reduced the number of TrkC+ neurons in DRG at birth including the subpopulation that expresses the ETS transcription factor ER81. Conversely, null mutation of the Hey paralog, Hey1, increased the number of TrkC+ neurons. Null mutation of HeyL increased expression of the Hey paralogs Hey1 and Hey2, suggesting that HeyL normally inhibits their expression. Double null mutation of both Hey1 and HeyL rescued TrkC+ neuron numbers to control levels. Thus, the balance between HeyL and Hey1 expression regulates the differentiation of a subpopulation of TrkC+ neurons in the DRG.

Original languageEnglish (US)
Pages (from-to)142-151
Number of pages10
JournalDevelopmental Biology
Volume334
Issue number1
DOIs
StatePublished - Oct 1 2009

Keywords

  • Differentiation
  • Dorsal root ganglion
  • Hey1
  • HeyL
  • TrkC

ASJC Scopus subject areas

  • Molecular Biology
  • Developmental Biology
  • Cell Biology

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