Evidence map›Paper›PMID 39051562›Full record

ArticleNucleic acids research2024

The translesion polymerase Pol Y1 is a constitutive component of the B. subtilis replication machinery.

McKayla E Marrin, Michael R Foster, Chloe M Santana, Yoonhee Choi, Avtar S Jassal, Sarah J Rancic, Carolyn R Greenwald, Madeline N Drucker, Denholm T Feldman, Elizabeth S Thrall

Abstract read
In one paragraph

Article in Nucleic acids research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. "ThebioRxiv : the preprint server for biology · 2026
    Article
  5. Review
  6. Article
  7. International journal of molecular sciences · 2025
    Article
  8. Article
  9. Article
  10. Germination and Outgrowth ofMicroorganisms · 2025
    Article
  11. Review
  12. 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

10 authors.

McKayla E MarrinDepartment of Chemistry and Biochemistry, Fordham University, Bronx, NY 10458, USA.
Michael R FosterDepartment of Chemistry and Biochemistry, Fordham University, Bronx, NY 10458, USA.
Chloe M SantanaDepartment of Chemistry and Biochemistry, Fordham University, Bronx, NY 10458, USA.
Yoonhee ChoiDepartment of Chemistry and Biochemistry, Fordham University, Bronx, NY 10458, USA.
Avtar S JassalDepartment of Chemistry and Biochemistry, Fordham University, Bronx, NY 10458, USA.
Sarah J RancicDepartment of Chemistry and Biochemistry, Fordham University, Bronx, NY 10458, USA.
Carolyn R GreenwaldDepartment of Chemistry and Biochemistry, Fordham University, Bronx, NY 10458, USA.
Madeline N DruckerDepartment of Chemistry and Biochemistry, Fordham University, Bronx, NY 10458, USA.
Denholm T FeldmanDepartment of Chemistry and Biochemistry, Fordham University, Bronx, NY 10458, USA.
Elizabeth S ThrallDepartment of Chemistry and Biochemistry, Fordham University, Bronx, NY 10458, USA.ORCID 0000-0002-7670-3939

Funding

Molecular Mechanisms of Y-Family Translesion Polymerase Activity in Bacillus subtilisR15GM151677 · NIGMS · FORDHAM UNIVERSITY · PI THRALL, ELIZABETH SIMMONS · 2023 to 2023
$495k
Fordham College at Rose Hill Undergraduate Research Grant programFordham University Clare Boothe Luce programFordham University Len Blavatnik STEM FellowshipNational Science Foundation 1833931NIGMS NIH HHS R15 GM151677NIGMS NIH HHS R15GM151677
6 · The paper itself

Abstract

Unrepaired DNA damage encountered by the cellular replication machinery can stall DNA replication, ultimately leading to cell death. In the DNA damage tolerance pathway translesion synthesis (TLS), replication stalling is alleviated by the recruitment of specialized polymerases to synthesize short stretches of DNA near a lesion. Although TLS promotes cell survival, most TLS polymerases are low-fidelity and must be tightly regulated to avoid harmful mutagenesis. The gram-negative bacterium Escherichia coli has served as the model organism for studies of the molecular mechanisms of bacterial TLS. However, it is poorly understood whether these same mechanisms apply to other bacteria. Here, we use in vivo single-molecule fluorescence microscopy to investigate the TLS polymerase Pol Y1 in the model gram-positive bacterium Bacillus subtilis. We find significant differences in the localization and dynamics of Pol Y1 in comparison to its E. coli homolog, Pol IV. Notably, Pol Y1 is constitutively enriched at or near sites of replication in the absence of DNA damage through interactions with the DnaN clamp; in contrast, Pol IV has been shown to be selectively enriched only upon replication stalling. These results suggest key differences in the roles and mechanisms of regulation of TLS polymerases across different bacterial species.

Indexed as

Bacillus subtilisBacterial ProteinsDNA DamageDNA-Directed DNA PolymeraseDNA ReplicationDNA, BacterialDNA Polymerase betaDNA RepairEscherichia coliSingle Molecule ImagingBacterial ProteinsDNA, BacterialDNA-Directed DNA PolymerasednaN protein, BacteriaDNA Polymerase beta

Identifiers

PMID39051562
PMCPMC11381352

What OpenQuestion holds

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LicenceCC BY
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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.