GC-rich elements flanking the transcription start site govern strong activation on the SNURF gene.

To study the regulation of the murine small nuclear RING finger protein SNURF (RNF4) gene, approximately 0.7 kb of its TATA-less promoter was isolated. This fragment conferred strong activation in reporter gene assays, yielding > or = 30% of the activity of the SV40 virus promoter/enhancer construct. Interestingly, the short region from -38 to +36 flanking the transcription start site was sufficient for potent basal promoter activity in various mammalian cell lines. Mutation of the conserved GC box at +9 abolished nuclear protein binding to the proximal promoter and severely compromised promoter activity, suggesting that this element is critical for the assembly of the transcription apparatus to regulate SNURF gene expression. Furthermore, our results show that the Wilms' tumor 1 gene product is one of the potential activators of the SNURF gene.