Evidence map›Paper›PMID 26138485›Full record

ArticleNucleic acids research2015

Bacteriophage GIL01 gp7 interacts with host LexA repressor to enhance DNA binding and inhibit RecA-mediated auto-cleavage.

Nadine Fornelos, Matej Butala, Vesna Hodnik, Gregor Anderluh, Jaana K Bamford, Margarita Salas

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

26 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Repression ofJournal of bacteriology · 2024
    Article
  10. Article
  11. DNA damage response coregulatorFrontiers in cellular and infection microbiology · 2023
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Unraveling Protein Interactions between the Temperate Virus Bam35 and ItsInternational journal of molecular sciences · 2021
    Article
  20. Homodimerization and heterodimerization requirements ofCanadian journal of microbiology · 2021
    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

6 authors at 3 institutions in 3 countries.

Nadine FornelosDepartment of Biological and Environmental Science and Nanoscience Center, University of Jyvaskyla, Centre of Excellence in Biological Interactions, PO Box 35, F-40014 Jyvaskyla, Finland Instituto de Biología Molecular 'Eladio Viñuela' (CSIC), Centro de Biología Molecular 'Severo Ochoa' (CSIC-Universidad Autónoma de Madrid), Cantoblanco, 28049 Madrid, Spain nadine.fornelos@jyu.fi.
Matej ButalaDepartment of Biology, Biotechnical Faculty, University of Ljubljana, Večna pot 111, 1000 Ljubljana, Slovenia.
Vesna HodnikDepartment of Biology, Biotechnical Faculty, University of Ljubljana, Večna pot 111, 1000 Ljubljana, Slovenia.
Gregor AnderluhDepartment of Biology, Biotechnical Faculty, University of Ljubljana, Večna pot 111, 1000 Ljubljana, Slovenia National Institute of Chemistry, Hajdrihova 19, 1000 Ljubljana, Slovenia.
Jaana K BamfordDepartment of Biological and Environmental Science and Nanoscience Center, University of Jyvaskyla, Centre of Excellence in Biological Interactions, PO Box 35, F-40014 Jyvaskyla, Finland.
Margarita SalasInstituto de Biología Molecular 'Eladio Viñuela' (CSIC), Centro de Biología Molecular 'Severo Ochoa' (CSIC-Universidad Autónoma de Madrid), Cantoblanco, 28049 Madrid, Spain.
University of Ljubljana · SIUniversity of Jyväskylä · FIUniversidad Autónoma de Madrid · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The SOS response in Eubacteria is a global response to DNA damage and its activation is increasingly associated with the movement of mobile genetic elements. The temperate phage GIL01 is induced into lytic growth using the host's SOS response to genomic stress. LexA, the SOS transcription factor, represses bacteriophage transcription by binding to a set of SOS boxes in the lysogenic promoter P1. However, LexA is unable to efficiently repress GIL01 transcription unless the small phage-encoded protein gp7 is also present. We found that gp7 forms a stable complex with LexA that enhances LexA binding to phage and cellular SOS sites and interferes with RecA-mediated auto-cleavage of LexA, the key step in the initiation of the SOS response. Gp7 did not bind DNA, alone or when complexed with LexA. Our findings suggest that gp7 induces a LexA conformation that favors DNA binding but disfavors LexA auto-cleavage, thereby altering the dynamics of the cellular SOS response. This is the first account of an accessory factor interacting with LexA to regulate transcription.

Indexed as

Gene Expression Regulation, ViralBacillus PhagesBacterial ProteinsDNALexA Repressor ProteinPromoter Regions, GeneticProtein BindingRec A RecombinasesRepressor ProteinsSerine EndopeptidasesSOS Response, GeneticsTranscription, GeneticViral ProteinsBacterial ProteinsDNALexA Repressor ProteinRec A RecombinasesRepressor ProteinsSerine EndopeptidasesViral Proteins

Identifiers

PMID26138485
PMCPMC4551915
OpenAlexW2104315317

What OpenQuestion holds

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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.