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Volume 272, Number 47, Issue of November 21, 1997 pp. 29560-29565
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.

Two Novel Brain-specific Splice Variants of the Murine C Gene of cAMP-dependent Protein Kinase

(Received for publication, July 30, 1997)

From the Department of Pharmacology, School of Medicine, University of Washington, Seattle, Washington 98195

We have previously characterized two murine cAMP-dependent protein kinase catalytic subunit genes, C and C1. Targeted disruption of the C1 promoter revealed two splice variants of the C catalytic subunit gene (designated C2 and C3) that continue to be expressed. These variants arise from unique promoters and are brain-specific. C2 is expressed in several discrete areas in the limbic system. These include the lateral septum, the bed nucleus of the stria terminalis, the ventral medial hypothalamus, and the amygdala. In the neocortex, expression is highest in cortical areas such as the prefrontal and insular cortex that are associated limbic structures. By contrast, C1 is most highly expressed in the cortex and hippocampus and is also present in all non-neuronal tissues examined. C3 is expressed at very low levels with wide distribution throughout the brain. Both the C2 and C3 variants are enzymatically active and induce gene expression in transient transfections with a cAMP response element-reporter construct. This activity is inhibited by protein kinase A regulatory subunits, the protein kinase inhibitor, and the chemical inhibitor H-89. We also demonstrate that C1 is myristoylated at the amino terminus like the C isoform, but neither C2 nor C3 is myristoylated. The discrete expression of C variants in the brain suggests specific functional roles in neuronal signaling.

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