Transcriptional repression by REST: recruitment of Sin3A and histone
deacetylase to neuronal genes
Yunfei Huang, Scott J. Myers
& Raymond Dingledine
Department of Pharmacology and Biochemistry, Cell and
Developmental Biology Graduate Program, Emory University School of Medicine,
Atlanta, Georgia 30322, USA
Many genes whose expression is restricted to neurons in the brain contain
a silencer element (RE1/NRSE) that limits transcription in nonneuronal cells
by binding the transcription factor REST (also named NRSF or XBR). Although
two independent domains of REST are known to confer repression, the mechanisms
of transcriptional repression by REST remain obscure. We provide multiple
lines of evidence that the N-terminal domain of REST represses transcription
of the GluR2 and type II sodium-channel genes by recruiting the corepressor
Sin3A and histone deacetylase (HDAC) to the promoter region in nonneuronal
cells. These results identify a general mechanism for controlling the neuronal
expression pattern of a specific set of genes via the RE1 silencer element.
