Evidence map›Paper›PMID 21029433›Full record

ReviewVirology journal2010

Transcriptional control in the prereplicative phase of T4 development.

Deborah M Hinton

Open access · goldAbstract readReview
In one paragraph

Review in Virology journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
4.5field-weighted citation impact, top 6% 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

65 citing papers in PubMed, 87 citations in OpenAlex.

  1. How bacterial immune systems sense phage infection.Nature reviews. Microbiology · 2026
    Review
  2. Article
  3. Article
  4. Review
  5. Viral effectors trigger innate immunity across the tree of life.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Review
  6. Article
  7. Article
  8. Tevenvirinae phages encode a family of LSm-like fold proteins.Computational and structural biotechnology journal · 2025
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. An OmpW-dependent T4-like phage infectsMicrobial genomics · 2023
    Article
  14. Article
  15. Ribosome inactivation byFrontiers in microbiology · 2023
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

5 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

Deborah M HintonLaboratory of Molecular and Cellular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Building 8, Room 2A-13, Bethesda, MD 20892-0830, USA. dhinton@helix.nih.gov
National Institute of Diabetes and Digestive and Kidney Diseases · US

Funding

Intramural NIH HHS
6 · The paper itself

Abstract

Control of transcription is crucial for correct gene expression and orderly development. For many years, bacteriophage T4 has provided a simple model system to investigate mechanisms that regulate this process. Development of T4 requires the transcription of early, middle and late RNAs. Because T4 does not encode its own RNA polymerase, it must redirect the polymerase of its host, E. coli, to the correct class of genes at the correct time. T4 accomplishes this through the action of phage-encoded factors. Here I review recent studies investigating the transcription of T4 prereplicative genes, which are expressed as early and middle transcripts. Early RNAs are generated immediately after infection from T4 promoters that contain excellent recognition sequences for host polymerase. Consequently, the early promoters compete extremely well with host promoters for the available polymerase. T4 early promoter activity is further enhanced by the action of the T4 Alt protein, a component of the phage head that is injected into E. coli along with the phage DNA. Alt modifies Arg265 on one of the two α subunits of RNA polymerase. Although work with host promoters predicts that this modification should decrease promoter activity, transcription from some T4 early promoters increases when RNA polymerase is modified by Alt. Transcription of T4 middle genes begins about 1 minute after infection and proceeds by two pathways: 1) extension of early transcripts into downstream middle genes and 2) activation of T4 middle promoters through a process called sigma appropriation. In this activation, the T4 co-activator AsiA binds to Region 4 of σ⁷⁰, the specificity subunit of RNA polymerase. This binding dramatically remodels this portion of σ⁷⁰, which then allows the T4 activator MotA to also interact with σ⁷⁰. In addition, AsiA restructuring of σ⁷⁰ prevents Region 4 from forming its normal contacts with the -35 region of promoter DNA, which in turn allows MotA to interact with its DNA binding site, a MotA box, centered at the -30 region of middle promoter DNA. T4 sigma appropriation reveals how a specific domain within RNA polymerase can be remolded and then exploited to alter promoter specificity.

Indexed as

DNA ReplicationTranscription, GeneticVirus ReplicationBacteriophage T4Escherichia coliGene Expression Regulation, ViralHost-Parasite InteractionsPromoter Regions, GeneticRNA, MessengerRNA, ViralRNA, MessengerRNA, Viral

Identifiers

PMID21029433
PMCPMC2988021
OpenAlexW2110162745

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.