Mechanism of cell cycle-dependent transcriptional control of RNA polymerase I Mechanismus Zellzyklus-abhängiger Transkriptionskontrolle von RNA-Polymerase I

• Antragstellerin: Professorin Dr. Ingrid Grummt
• Fachliche Zuordnung: Grundlagen der Biologie und Medizin
• Förderung: Förderung von 1995 bis 2002
• Projektkennung: Deutsche Forschungsgemeinschaft (DFG) - Projektnummer 5224735

Cell cycle-dependent fluctuations of transcription have been observed for all three classes of nuclear RNA polymerases. The numerous biological events that are associated with the periodicity of the cell cycle make it an attractive model for the study of regulatory mechanism that link gene activity to cell cycle control. Ribosomal RNA genes (rDNA) represent an attractive model to investigate such fundamental processes, because their activity oscillates during the cell cycle. rDNA transcription is maximal in S and G2 phase, shuts down in mitosis and slowly recovers in G1. Transcriptional inactivation is accompanied by reversible phosphorylation of two basal Pol I transcription factors, e.g. SL1 and UBF. The goal of this research project is a detailed analysis of the molecular mechanisms that inactivate the basal factors SL1 and UBF, the identification of the cellular protein phosphatase(s) that counteract mitotic inactivation of transcription factors, mapping of phosphorylated amino acids, and the analysis of functional consequences of specific mutation of the respective target sites. We will study the influence of specific protein kinases and phosphatases on the activity of RNA polymerase I-specific transcription factors as well as their effects on protein-protein interactions that are involved in transcription complex assembly at the rDNA promoter. Moreover, we are going to investigate the physiological significance of pRb- and p130-mediated repression of Pol I transcription.

• DFG-Verfahren: Schwerpunktprogramme
• Teilprojekt zu: SPP 314: Kontrolle des Zellzyklus bei Eukaryonten