Evidence map›Paper›PMID 32562709›Full record

ArticleJournal of molecular biology2020

The Structural Basis of T4 Phage Lysis Control: DNA as the Signal for Lysis Inhibition.

Inna V Krieger, Vladimir Kuznetsov, Jeng-Yih Chang, Junjie Zhang, Samir H Moussa, Ryland F Young, James C Sacchettini

Abstract read
In one paragraph

Article in Journal of molecular biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–field-weighted citation impact
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

23 citing papers in PubMed.

  1. Review
  2. Article
  3. Prophage: agent provocateur?Archives of microbiology · 2026
    Review
  4. The Lysis cassette of jumbophage PhiKZ.Scientific reports · 2026
    Article
  5. Review
  6. Phage N4 uses a SAR endolysin-holin system for host cell lysis.bioRxiv : the preprint server for biology · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. More than just pattern recognition: Prediction of uncommon protein structure features by AI methods.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Characterization ofFrontiers in microbiology · 2022
    Article
  20. Review
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.

Inna V KriegerDepartment of Biochemistry and Biophysics, Texas A&M University, College Station, TX 77843, USA.
Vladimir KuznetsovDepartment of Biochemistry and Biophysics, Texas A&M University, College Station, TX 77843, USA.
Jeng-Yih ChangDepartment of Biochemistry and Biophysics, Texas A&M University, College Station, TX 77843, USA; Center for Phage Technology, Department of Biochemistry and Biophysics.
Junjie ZhangDepartment of Biochemistry and Biophysics, Texas A&M University, College Station, TX 77843, USA; Center for Phage Technology, Department of Biochemistry and Biophysics.
Samir H MoussaDepartment of Biochemistry and Biophysics, Texas A&M University, College Station, TX 77843, USA; Center for Phage Technology, Department of Biochemistry and Biophysics.
Ryland F YoungDepartment of Biochemistry and Biophysics, Texas A&M University, College Station, TX 77843, USA; Center for Phage Technology, Department of Biochemistry and Biophysics.
James C SacchettiniDepartment of Biochemistry and Biophysics, Texas A&M University, College Station, TX 77843, USA. Electronic address: sacchett@tamu.edu.

Funding

CONTROL OF VIRUS-INDUCED LYSISR01GM027099 · NIGMS · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI YOUNG, RYLAND FLETCHER · 1985 to 2019
$4.6M
Phage LysisR35GM136396 · NIGMS · TEXAS A&M AGRILIFE RESEARCH · PI YOUNG, RYLAND FLETCHER · 2020 to 2024
$1.9M
NIGMS NIH HHS R01 GM027099NIGMS NIH HHS R35 GM136396
6 · The paper itself

Abstract

Optimal phage propagation depends on the regulation of the lysis of the infected host cell. In T4 phage infection, lysis occurs when the holin protein (T) forms lesions in the host membrane. However, the lethal function of T can be blocked by an antiholin (RI) during lysis inhibition (LIN). LIN sets if the infected cell undergoes superinfection, then the lysis is delayed until host/phage ratio becomes more favorable for the release of progeny. It has been thought that a signal derived from the superinfection is required to activate RI. Here we report structures that suggest a radically different model in which RI binds to T irrespective of superinfection, causing it to accumulate in a membrane as heterotetrameric 2RI-2T complex. Moreover, we show the complex binds non-specifically to DNA, suggesting that the gDNA from the superinfecting phage serves as the LIN signal and that stabilization of the complex by DNA binding is what defines LIN. Finally, we show that soluble domain of free RI crystallizes in a domain-swapped homotetramer, which likely works as a sink for RI molecules released from the RI-T complex to ensure efficient lysis. These results constitute the first structural basis and a new model not only for the historic LIN phenomenon but also for the temporal regulation of phage lysis in general.

Indexed as

Bacterial Physiological PhenomenaBacteriolysisBacteriophage T4Cell MembraneCryoelectron MicroscopyCrystallography, X-RayDNA, ViralModels, MolecularProtein ConformationProtein DomainsViral ProteinsDNA, Viralholin t protein, Enterobacteria phage T4Viral Proteinsantiholindomain swappingholinlysisSAR domain

Identifiers

PMID32562709
PMCPMC7394242

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Registered trials

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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.