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Volume 16, Number 18, Issue of September 15, 1996 pp. 5704-5714
Copyright ©1996 Society for Neuroscience

Retinoic Acid Stimulates -CAMKII Gene Expression in PC12 Cells at a Distinct Transcription Initiation Site

Received Feb. 9, 1996; revised June 20, 1996; accepted June 24, 1996.

Jing Chen and Paul T. Kelly

Department of Neurobiology and Anatomy, University of Texas Medical School at Houston, Houston, Texas 77225

The promoter region of the -subunit of the calcium/calmodulin-dependent protein kinase II (-CaMKII) gene was inserted into a -galactosidase (-gal) reporter plasmid, and -gal activities were examined in neuroblastoma (NB2a) and pheochromocytoma (PC12) cells after transient or stable transfections. The -CaMKII promoter was 12- to 45-fold more active in NB2a compared with PC12 cells after transient or stable transfections. All-trans retinoic acid (RA) stimulated reporter gene expression at both protein and mRNA levels in transfected PC12 cells. RA increased the level of endogenous -CaMKII mRNA in untransfected PC12 cells by 4.4-fold. The transcription initiation site(s) (TIS) of the -CaMKII gene in PC12 cells and rat brain was examined by RNase protection assays (RPA) and reverse transcriptase PCRs. The TIS for the -CaMKII/-gal reporter gene in transfected PC12 cells was indistinguishable from the TIS₊₁ in rat hippocampus. In contrast, the only detectable TIS for the -CaMKII gene in untransfected PC12 cells was located near the ATG translation start codon, 147 nucleotides 3 to TIS₊₁ in hippocampus. This unusual TIS was also the predominant TIS in rat cerebellum. These results suggest that the -CaMKII promoter may contain sequences that respond directly or indirectly to RA. In addition, the unusual TIS of the -CaMKII gene in PC12 cells and rat cerebellum may contribute to the very low expression of this gene compared with that in hippocampus.

Key words: retinoic acid; transcription initiation site; Ca²⁺/calmodulin-dependent protein kinase II; CaMKII; RNase protection assay

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