We will investigate the regulation of recA-dependent processes in E. coli, which include genetic recombination, radiation and chemical mutagenesis, inhibition of cell division, and the induction of temperate bacteriophage. A cellular signal elaborated when DNA is damaged or its synthesis is interrupted activates recA protein to attack repressors by proteolytic cleavage, leading to induction of these processes. We will attempt to identify this signal by studying the reaction in which recA protein attacks repressors and by examining conditions in induced cells that might affect this reaction. We also will study the mechanism of regulation of late gene expression during growth of bacteriophage lambda and its relative phi 82. We have partially purified the protein encoded by lambda gene Q, which positively regulates phage late genes, and we have shown that it is active to promote synthesis of a late gene product in vitro, in the crude coupled transcription-translation system. We will examine its mechanism of action by determining its effect on transcription in the crude extract, and we will derive from the extract a minimal system in which it is active. In particular, we will determine if it acts by anti-termination, as we suspect, or if it uses a different mechanism.
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