The PDGF beta-receptor expression is tightly regulated during embryonic development and in several physiological and pathological situations. To determine the regulatory mechanism of the receptor, a 1.9 kb 5' flanking genomic fragment of the mouse PDGF beta-receptor gene was cloned and analyzed by functional promoter assays. The fragment was shown to exert promoter activity in the luciferase expression vector system in mouse NIH 3T3 fibroblast and NB41 neuroblastoma cell lines as well as rat ST15A cerebellar cell lines. Functional studies on deletion mutants revealed several putative regulatory sequences. The deletion mutants acted similarly in NB41 cells and in ST15A cells, both of neuronal origin, but differently in the NIH 3T3 fibroblasts. No TATA box was found in the analyzed promoter region, however, site directed mutagenesis of a CCAAT motif, located 60 basepair upstream of the transcriptional start site, almost completely abolished the promoter activity in all cell types.