Abstract

Gamma-aminobutyric acid Type A (GABAA) receptors are the major sites of synaptic inhibition in the central nervous system. These receptors are thought to be pentameric complexes of homologous transmembrane glycoproteins. Molecular cloning has revealed a multiplicity of different GABAA receptor subunits divided into five classes, alpha, beta, gamma, delta, and rho, based on sequence homology. Within the proposed major intracellular domain of these subunits, there are numerous potential consensus sites for protein phosphorylation by a variety of protein kinases. We have used purified fusion proteins of the major intracellular domain of GABAA receptor subunits produced in Escherichia coli to examine the phosphorylation of these subunits by cAMP-dependent protein kinase (PKA) and protein kinase C (PKC). The purified fusion protein of the intracellular domain of the beta 1 subunit was an excellent substrate for both PKA and PKC. PKA and PKC phosphorylated the beta 1 subunit fusion protein on serine residues on a single tryptic phosphopeptide. Site-directed mutagenesis of serine 409 in the intracellular domain of the beta 1 subunit to an alanine residue eliminated the phosphorylation of the beta 1 subunit fusion protein by both protein kinases. The purified fusion proteins of the major intracellular domain of the gamma 2S and gamma 2L subunits of the GABAA receptor were rapidly and stoichiometrically phosphorylated by PKC but not by PKA. The phosphorylation of the gamma 2S subunit occurred on serine residues on a single tryptic phosphopeptide. Site-directed mutagenesis of serine 327 of the gamma 2S subunit fusion protein to an alanine residue eliminated the phosphorylation of the gamma 2S fusion protein by PKC. The gamma 2L subunit is an alternatively spliced form of the gamma 2S subunit that differs by the insertion of 8 amino acids (LLRMFSFK) within the major intracellular domain of the gamma 2S subunit. The PKC phosphorylation of the gamma 2L subunit occurred on serine residues on two tryptic phosphopeptides. Site-specific mutagenesis of serine 343 within the 8-amino acid insert to an alanine residue eliminated the PKC phosphorylation of the novel site in the gamma 2L subunit. No phosphorylation of a purified fusion protein of the major intracellular loop of the alpha 1 subunit was observed with either PKA or PKC. These results identify the specific amino acid residues within GABAA receptor subunits that are phosphorylated by PKA and PKC and suggest that protein phosphorylation of these sites may be important in regulating GABAA receptor function.(ABSTRACT TRUNCATED AT 400 WORDS)

Highlights

  • We have used purified fusion proteins of the major intracellular domain of GABAA receptor subunits produced in Escherichia coli to examine thephosphorylation of these subunits bCyAMPdependent protein kinase (PKA) and protein kinase C

  • Site-directed mutagenesis of of GABAA receptors purified by benzodiazepine affinity chroserine 409 in the intracelluladromain of the B1subunit matography originally suggested that GABAA receptors conto an alanine residue eliminated the phosphorylation sisted of two types of subunits termed a and B [2]

  • Molecular cloning has revealed a ation of the yzS subunit occurredon serine residueson large number of GABAAreceptor subunits thact an be divided a single tryptic phosphopeptide

Read more

Summary

Type A Receptor*

Howard Hu-ghes Medical Institute, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 y-Aminobutyric acid Type A(GABAA) receptors are was observed with either PKA or PKC These results the major sites of synaptic inhibition in the central identify thespecific amino acid residues witGhiAnBAA nervous system. The the major intracellular loops of the GABAAreceptor subunits [8].In addition, physiological studies using agents that regulate protein kinases have suggested that protein phosphorylation of GABAA receptors regulates their function [8, 11,12,13,14,15]. Fusion specific residues within GABAA receptor subunits that are protein kinase substrates and allow further analysis of the role of protein phosphorylation in the regulation ofGABAA receptor function. CAMP-dependent protein kinase inhibitor peptide (PKI 5-24 amide, Peninsula Laboratories, Inc.) was included

MATERIALS ANDMETHODS
Protein kinase C
DISCUSSION
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call