Phage T7 DNA mimic protein Ocr is a potent inhibitor of BREX defence

التفاصيل البيبلوغرافية
العنوان: Phage T7 DNA mimic protein Ocr is a potent inhibitor of BREX defence
المؤلفون: Alena Drobiazko, Nicolas Sierro, Konstantin Severinov, Artem Isaev, Udi Qimron, Julia Gordeeva, Ido Yosef, Nikolai V. Ivanov
المصدر: Nucleic Acids Research
بيانات النشر: Oxford University Press (OUP), 2020.
سنة النشر: 2020
مصطلحات موضوعية: Methyltransferase, AcademicSubjects/SCI00010, Gene regulation, Chromatin and Epigenetics, Methylation, DNA Methylation, Biology, biology.organism_classification, Bacteriophage, Viral Proteins, chemistry.chemical_compound, Plasmid, chemistry, Biochemistry, Bacteriophage T7, DNA methylation, Escherichia coli, Genetics, Nucleic acid, A-DNA, Corrigendum, Gene, DNA Modification Methylases, DNA, Plasmids
الوصف: BREX (for BacteRiophage EXclusion) is a superfamily of common bacterial and archaeal defence systems active against diverse bacteriophages. While the mechanism of BREX defence is currently unknown, self versus non-self differentiation requires methylation of specific asymmetric sites in host DNA by BrxX (PglX) methyltransferase. Here, we report that T7 bacteriophage Ocr, a DNA mimic protein that protects the phage from the defensive action of type I restriction–modification systems, is also active against BREX. In contrast to the wild–type phage, which is resistant to BREX defence, T7 lacking Ocr is strongly inhibited by BREX, and its ability to overcome the defence could be complemented by Ocr provided in trans. We further show that Ocr physically associates with BrxX methyltransferase. Although BREX+ cells overproducing Ocr have partially methylated BREX sites, their viability is unaffected. The result suggests that, similar to its action against type I R–M systems, Ocr associates with as yet unidentified BREX system complexes containing BrxX and neutralizes their ability to both methylate and exclude incoming phage DNA.
تدمد: 1362-4962
0305-1048
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::06f517449e73a2bdf50e8d9268e6ac92
https://doi.org/10.1093/nar/gkaa510
حقوق: OPEN
رقم الأكسشن: edsair.doi.dedup.....06f517449e73a2bdf50e8d9268e6ac92
قاعدة البيانات: OpenAIRE