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

ABSTRACT: 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 φ80dlacZΔM15 prophage lysozyme encoding gene 19 (GenBank accession no. ACB02445.1, renamed it lysN, lysozyme nineteen), 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 grow

SUBMITTER: Tang Q 

PROVIDER: S-EPMC6715736 | biostudies-literature | 2019 Aug

REPOSITORIES: biostudies-literature