Glutamate Regulates Kainate-binding Protein Expression in
Cultured Chick Bergmann Glia through an Activator Protein-1 Binding
Site*
Adán
Aguirre
,
Tomás
López,
Esther
López-Bayghen, and
Arturo
Ortega§
From the Departamento de Genética y Biología
Molecular, Centro de Investigación y de Estudios Avanzados del
Instituto Politécnico Nacional, Apartado Postal 14-740, México D.F. 07000, México
The expression of the chick kainate-binding
protein, a member of the ionotropic glutamate receptor family, is
restricted to the cerebellum, specifically to Bergmann glia. Glutamate
induces a membrane to nuclei signaling involved in gene expression
regulation. Exposure of cultured chick Bergmann glia cells to glutamate
leads to an increase in kainate binding protein and mRNA levels,
suggesting a transcriptional level of regulation. The 5' proximal
region of the chick kainate binding gene was cloned and transfected
4into Bergmann glia cells. Three main regulatory regions could be
defined, a minimal promoter region, a negative regulatory region, and
interestingly, a glutamate-responsive element. Deletion of this element
abolishes the agonist effect. Moreover, electrophoretic mobility shift
assays, cotransfection experiments, and site-directed mutagenesis
clearly suggest that the glutamate effect is mediated through an AP-1 site by a Fos/Jun heterodimer. The present results favor the notion of
a functional role of kainate-binding protein in glutamatergic cerebellar neurotransmission.
*
This work was supported by Grant 26316-N from Consejo
Nacional de Ciencia y Tecnologia (CONACYT)-México (to A. O.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
The nucleotide sequence(s) reported in this paper has been submitted to the GenBankTM/EMBL Data Bank with accession number(s) AF208519.