12 th. Annual Pediatric Critical Care Colloquium
Session/Time Basic Sciences / 11:45 - 12:00 Paper No. 52
Title IDENTIFICATION OF A NEURON-RESTRICTIVE SILENCING ELEMENT IN THE KCC2 COTRANSPORTER GENE.
Author M.F. Karadsheh, J. Lu and E. Delpire
Affiliation Pediatric Critical Care & Anesthesiology Research Divisions, Vanderbilt University Medical Center, Nashville, Tennessee
KCC2 is a neuronal-specific isoform of the K-Cl cotransporter. It plays a role in GABAergic and glycinergic neurotransmission through its effect on intracellular Cl- in neurons. To understand the molecular basis for neuronal specificity of KCC2 expression, we isolated and sequenced portions of the KCC2 gene, including its 5' flanking (promoter) region. We found a 21 bp sequence within intron 1 that shares 80% homology to the consensus site for NRSF (neuron-restrictive silencing factor) binding. We demonstrated that this specific sequence of the KCC2 gene promotes transcriptional regulation, by 1) showing that nuclear proteins isolated from rat brain interact with this 21 bp element and 2) establishing that this element is able to silence reporter gene expression in non-neuronal cells. Electrophoretic mobility shift assay was performed using nuclear protein isolated from rat brain and 32P-labeled double-stranded NRSE oligonucleotide. We demonstrated the presence of a protein/NRSE DNA complex that could be displaced with an excess of cold NRSE oligonucleotide but not with unspecific DNA. This results supports the idea that the short KCC2 sequence interacts with nuclear proteins or transcription factors. We then analyzed the function of the 21 bp KCC2 element on transcriptional activity by using a reporter gene. C17 progenitor neural cells were transfected with 1) a promoterless luciferase vector, 2) a luciferase vector containing 1.5 kb of 5' flanking region of the KCC2 gene, and 3) a vector of same composition but also containing the 21 bp neuronal-restrictive silencing element found in inton 1. We showed that the presence of the 1.5 kb fragment upstream of exon 1 significantly increased luciferase activity when compared to the promoterless vector. Addition of the NRS element returned the activity of luciferase to baseline values. Taken together, these results suggest that the 21 bp sequence found in intron 1 of the KCC2 gene is a potential target for the neuron-restrictive silencer factor and the thus the putative site for KCC2 transcriptional repression in non-neuronal cells.

originally published in Clinical Intensive Care 1999;10(4)


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Document created October 2, 1999