噬菌体蛋白 RacR 激活溶菌酶 LysN，导致大肠杆菌 JM83 的生长缺陷。
Prophage protein RacR activates lysozyme LysN, causing the growth defect of E. coli JM83.
机构信息
State Key Laboratory of Bioreactor Engineering, East China University of Science and Technology, Shanghai, China.
Department of Applied Biology, East China University of Science and Technology, Shanghai, China.
出版信息
Sci Rep. 2019 Aug 29;9(1):12537. doi: 10.1038/s41598-019-48690-4.
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 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.
噬菌体丰富了原核基因组，其转录因子改善了宿主的蛋白质表达网络。在本研究中，我们揭示了大肠杆菌 JM83 中的一种新的噬菌体-噬菌体相互作用。Rac 噬菌体蛋白 RacR（GenBank 登录号 AVI55875.1）直接激活 φ80dlacZΔM15 噬菌体溶菌酶编码基因 19（GenBank 登录号 ACB02445.1，重命名为 lysN）的转录，导致 JM83 的生长缺陷。这种现象也发生在 DH5α 中，但在 BL21(DE3)和 MG1655 中由于基因型差异而没有发生。然而，lysN 的缺失并不能完全挽救 JM83 的生长停滞，表明 RacR 可能调节其他相关靶标。此外，在 JM83 的生长后期发现 RacR 调节的失活，并且可以传递给子细胞。总之，我们的研究揭示了 RacR 部分调控网络，这表明细菌中存在一些先进的遗传策略。
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