Apoptosis, axonal growth defects, and degeneration of peripheral neurons in mice lacking CREB

Bonnie E. Lonze, Antonella Riccio, Sonia Cohen, David D. Ginty

Research output: Contribution to journalArticle

Abstract

CRE-binding protein (CREB) belongs to a family of transcription factors that mediates stimulus-dependent gene expression in neuronal and non-neuronal cells. Here we show that CREB is phosphorylated on its transcriptional regulatory site, Ser-133, in vivo in a neurotrophin-dependent manner. In mice harboring a null mutation in the Creb gene, sensory neurons exhibit excess apoptosis and degeneration, and display impaired axonal growth and projections. Interestingly, excess apoptosis is not observed in the central nervous system. CREB is required within sensory and sympathetic neurons for survival and axon extension since both of these neurotrophin-dependent processes are compromised in cultured neurons from CREB null mice. Thus, during their period of neurotrophin dependency, peripheral neurons require CREB-mediated gene expression for both survival and growth in vivo.

Original languageEnglish (US)
Pages (from-to)371-385
Number of pages15
JournalNeuron
Volume34
Issue number3
DOIs
StatePublished - Apr 25 2002

ASJC Scopus subject areas

  • Neuroscience(all)

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