Evidence map›Paper›PMID 30053203›Full record

ArticleNucleic acids research2018

Lytic gene expression in the temperate bacteriophage GIL01 is activated by a phage-encoded LexA homologue.

Nadine Fornelos, Douglas F Browning, Anja Pavlin, Zdravko Podlesek, Vesna Hodnik, Margarita Salas, Matej Butala

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.8field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 22 citations in OpenAlex.

  1. Revisiting the life cycle of temperate phages.Nature reviews. Microbiology · 2026
    Review
  2. Article
  3. Repression ofJournal of bacteriology · 2024
    Article
  4. Article
  5. Characteristics and Whole-Genome Analysis ofFoods (Basel, Switzerland) · 2023
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Unraveling Protein Interactions between the Temperate Virus Bam35 and ItsInternational journal of molecular sciences · 2021
    Article
  11. Review
  12. Article
  13. Article
  14. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 3 countries.

Nadine FornelosInstituto de Biología Molecular 'Eladio Viñuela' (CSIC), Centro de Biología Molecular 'Severo Ochoa' (CSIC-Universidad Autónoma de Madrid), Cantoblanco, 28049 Madrid, Spain.
Douglas F BrowningInstitute of Microbiology and Infection, School of Biosciences, University of Birmingham, Birmingham B15 2TT, UK.
Anja PavlinDepartment of Biology, Biotechnical Faculty, University of Ljubljana, 1000 Ljubljana, Slovenia.
Zdravko PodlesekDepartment of Biology, Biotechnical Faculty, University of Ljubljana, 1000 Ljubljana, Slovenia.
Vesna HodnikDepartment of Biology, Biotechnical Faculty, University of Ljubljana, 1000 Ljubljana, Slovenia.
Margarita SalasInstituto de Biología Molecular 'Eladio Viñuela' (CSIC), Centro de Biología Molecular 'Severo Ochoa' (CSIC-Universidad Autónoma de Madrid), Cantoblanco, 28049 Madrid, Spain.
Matej ButalaDepartment of Biology, Biotechnical Faculty, University of Ljubljana, 1000 Ljubljana, Slovenia.
University of Ljubljana · SICentro de Biología Molecular Severo Ochoa · ESUniversity of Birmingham · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The GIL01 bacteriophage is a temperate phage that infects the insect pathogen Bacillus thuringiensis. During the lytic cycle, phage gene transcription is initiated from three promoters: P1 and P2, which control the expression of the early phage genes involved in genome replication and P3, which controls the expression of the late genes responsible for virion maturation and host lysis. Unlike most temperate phages, GIL01 lysogeny is not maintained by a dedicated phage repressor but rather by the host's regulator of the SOS response, LexA. Previously we showed that the lytic cycle was induced by DNA damage and that LexA, in conjunction with phage-encoded protein gp7, repressed P1. Here we examine the lytic/lysogenic switch in more detail and show that P3 is also repressed by a LexA-gp7 complex, binding to tandem LexA boxes within the promoter. We also demonstrate that expression from P3 is considerably delayed after DNA damage, requiring the phage-encoded DNA binding protein, gp6. Surprisingly, gp6 is homologous to LexA itself and, thus, is a rare example of a LexA homologue directly activating transcription. We propose that the interplay between these two LexA family members, with opposing functions, ensures the timely expression of GIL01 phage late genes.

Indexed as

Bacillus subtilisBacillus thuringiensisBacterial ProteinsBacteriophagesBase SequenceCytotoxinsGene Expression Regulation, ViralLexA Repressor ProteinLysogenyPromoter Regions, GeneticSequence HomologySerine EndopeptidasesTranscription, GeneticViral ProteinsBacterial ProteinsCytotoxinsLexA Repressor ProteinSerine EndopeptidasesViral Proteins

Identifiers

PMID30053203
PMCPMC6182141
OpenAlexW2883894119

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.