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Prophage enriched the prokaryotic genome, and their transcriptional factors improved the protein expression network of the host. In this study, we uncovered a new prophage-prophage interaction in  E. coli  JM83. The Rac prophage protein RacR (GenBank accession  no. AVI55875.1 ) directly activated the transcription of φ80 dlacZ Δ M15  prophage lysozyme encoding gene 19 (GenBank accession  no. ACB02445.1 , renamed it  lysN ,  lys ozyme  n ineteen), resulting in the growth defect of JM83. This phenomenon also occurred in DH5α, but not in BL21(DE3) and MG1655 due to the genotype differences. However, deletion of  lysN  could not completely rescued JM83 from the growth arrest, indicating that RacR may regulate other related targets. In addition, passivation of RacR regulation was found in the late period of growth of JM83, and it was transmissible to daughter cells. Altogether, our study revealed part of RacR regulatory network, which suggested some advanced genetic strategies in bacteria.

Prophage protein RacR activates lysozyme LysN, causing the growth defect of E. coli JM83