ArticleJournal of bacteriology2011
Phage-borne factors and host LexA regulate the lytic switch in phage GIL01.
Article in Journal of bacteriology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 40 citations in OpenAlex.
- Revisiting the life cycle of temperate phages.Nature reviews. Microbiology · 2026Review
- From hijackers to architects: the role of prophages in bacterial genome evolution.Journal of bacteriology · 2026Review
- Prophage: agent provocateur?Archives of microbiology · 2026Review
- Bacteriophage deploys a RecA-dependent nuclease to inhibit Staphylococcus aureus replication and promote phage propagation.Nucleic acids research · 2026Article
- Characteristics of phage-plasmids and their impact on microbial communities.Essays in biochemistry · 2024Review
- Autoregulation ensures vertical transmission of the linear prophage GIL01.Communications biology · 2024Article
- Globally distributed bacteriophage genomes reveal mechanisms of tripartite phage-bacteria-coral interactions.The ISME journal · 2024Article
- Engineered bacterial orthogonal DNA replication system for continuous evolution.Nature chemical biology · 2023Article
- A small bacteriophage protein determines the hierarchy over co-residential jumbo phage in Bacillus thuringiensis serovar israelensis.Communications biology · 2022Article
- The DdrR Coregulator of the Acinetobacter baumannii Mutagenic DNA Damage Response Potentiates UmuDAb Repression of Error-Prone Polymerases.Journal of bacteriology · 2022Article
- Locking down SOS Mutagenesis Repression in a Dynamic Pathogen.Journal of bacteriology · 2022Article
- Genomic analysis of a novel active prophage of Hafnia paralvei.Archives of virology · 2022Article
- The transcriptional regulator CtrA controls gene expression in Alphaproteobacteria phages: Evidence for a lytic deferment pathway.Frontiers in microbiology · 2022Article
- Non-canonical LexA proteins regulate the SOS response in the Bacteroidetes.Nucleic acids research · 2021Article
- Unraveling Protein Interactions between the Temperate Virus Bam35 and ItsInternational journal of molecular sciences · 2021Article
- Comparative Genomics of Prophages Sato and Sole Expands the Genetic Diversity Found in the GenusMicroorganisms · 2021Article
- A Novel Genus of Actinobacterial Tectiviridae.Viruses · 2019Article
- Role of plasmid plasticity and mobile genetic elements in the entomopathogen Bacillus thuringiensis serovar israelensis.FEMS microbiology reviews · 2018Article
- Lytic gene expression in the temperate bacteriophage GIL01 is activated by a phage-encoded LexA homologue.Nucleic acids research · 2018Article
- Bam35 Tectivirus Intraviral Interaction Map Unveils New Function and Localization of Phage ORFan Proteins.Journal of virology · 2017Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Bacillus thuringiensis temperate phage GIL01 does not integrate into the host chromosome but exists stably as an independent linear replicon within the cell. Similar to that of the lambdoid prophages, the lytic cycle of GIL01 is induced as part of the cellular SOS response to DNA damage. However, no CI-like maintenance repressor has been detected in the phage genome, suggesting that GIL01 uses a novel mechanism to maintain lysogeny. To gain insights into the GIL01 regulatory circuit, we isolated and characterized a set of 17 clear plaque (cp) mutants that are unable to lysogenize. Two phage-encoded proteins, gp1 and gp7, are required for stable lysogen formation. Analysis of cp mutants also identified a 14-bp palindromic dinBox1 sequence within the P1-P2 promoter region that resembles the known LexA-binding site of Gram-positive bacteria. Mutations at conserved positions in dinBox1 result in a cp phenotype. Genomic analysis identified a total of three dinBox sites within GIL01 promoter regions. To investigate the possibility that the host LexA regulates GIL01, phage induction was measured in a host carrying a noncleavable lexA (Ind(-)) mutation. GIL01 formed stable lysogens in this host, but lytic growth could not be induced by treatment with mitomycin C. Also, mitomycin C induced β-galactosidase expression from GIL01-lacZ promoter fusions, and induction was similarly blocked in the lexA (Ind(-)) mutant host. These data support a model in which host LexA binds to dinBox sequences in GIL01, repressing phage gene expression during lysogeny and providing the switch necessary to enter lytic development.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.