AI Article Synopsis
- The bipartite repressor elements CDE/CCRE and CHR are crucial for regulating the growth-dependent transcription of key cell cycle genes like cyclin A and cdc2.
- A similar functional element has been found in the mouse RB2 (p130) gene promoter, which plays a role in controlling expression of the retinoblastoma protein family.
- Disabling the CDE or CHR regions significantly increases p130 promoter activity during cell growth, indicating their repressive role, and distinct protein complexes attach to these elements, potentially linking them to other cell cycle-related promoters.
Article Abstract
The bipartite repressor elements, termed cell cycle-dependent element (CDE)/cell cycle regulatory element (CCRE)-cell cycle homology region (CHR) control the growth-dependent transcription of the cyclin A, cdc25C, cdc2 genes. Here, we have identified a functional element displaying the signature of the CDE-CHR in the promoter of the mouse RB2 (p130) gene, encoding the retinoblastoma protein family (pRB)-related protein p130. This element locates close to the major transcription start site where it makes major groove contacts with proteins that can be detected in a cellular context using in vivo genomic footprinting techniques. Inactivation of either the CDE or CHR sequence strongly up-regulates the p130 promoter activity in exponentially growing cells, a situation where endogenous p130 gene expression is almost undetectable. Electrophoretic mobility shift assays suggest that two different protein complexes bind independently to the p130 CDE and CHR elements, and that the protein(s) bound to the CDE might be related to those bound on cyclin A and cdc2 promoters.
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| http://dx.doi.org/10.1016/s0014-5793(00)01363-6 | DOI Listing |
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