Evidence map›Paper›PMID 26923786›Full record

ArticleCurrent biology : CB2016

The Effect of Local Sequence Context on Mutational Bias of Genes Encoded on the Leading and Lagging Strands.

Jeremy W Schroeder, William G Hirst, Gabriella A Szewczyk, Lyle A Simmons

Abstract read
In one paragraph

Article in Current biology : CB, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing 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

45 citing papers in PubMed.

  1. Article
  2. Ribonucleotide errors, RNase HII, and ribonucleotide excision repair.Critical reviews in biochemistry and molecular biology · 2026
    Review
  3. Extended sequence context shapes mutational bias inProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  4. DNA polymerase I: structure, activity, and function in bacterial DNA replication and repair.Critical reviews in biochemistry and molecular biology · 2026
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. 8-Oxoadenine: A «New» Player of the Oxidative Stress in Mammals?International journal of molecular sciences · 2024
    Review
  14. Mutation bias and adaptation in bacteria.Microbiology (Reading, England) · 2023
    Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Bacterial DNA excision repair pathways.Nature reviews. Microbiology · 2022
    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

4 authors.

Jeremy W SchroederDepartment of Molecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, MI 48109, USA.
William G HirstDepartment of Molecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, MI 48109, USA.
Gabriella A SzewczykDepartment of Molecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, MI 48109, USA.
Lyle A SimmonsDepartment of Molecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, MI 48109, USA. Electronic address: lasimm@umich.edu.

Funding

PREDOCTORAL TRAINING IN GENETICST32GM007544 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MORAN, JOHN V. · 1985 to 2022
$11.3M
Supplement: DNA REPLICATION AND GENOME STABILITYR01GM107312 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SIMMONS, LYLE · 2013 to 2017
$1.5M
NIGMS NIH HHS R01 GM107312NIGMS NIH HHS T32 GM007544
6 · The paper itself

Abstract

All organisms must replicate their genetic information accurately to ensure its faithful transmission. DNA polymerase errors provide an important source of genetic variation that can drive evolution. Understanding the origins of genetic variation will inform our understanding of evolution and the development of genetic diseases. A number of factors have been proposed to influence mutagenesis [1-10]. Here, we used mutation accumulation lines, whole-genome sequencing, and whole-transcriptome analysis to study the locations and rate at which mutations arise in bacteria with as little selection bias as possible [11, 12]. Our analysis of greater than 7,000 replication errors in over 180 sequenced lines that underwent a total of more than 370,000 generations has provided new insights into how DNA polymerase errors sculpt genetic variation and drive evolution. Homopolymer run enrichment outside of genes causes insertions and deletions in these regions. Genes encoded in the lagging strand are transcribed such that RNA polymerase and DNA polymerase collide head-on. Head-on genes have been proposed to mutate at a higher rate than genes transcribed codirectionally with DNA polymerase progression due to conflicts between transcription and DNA replication [6, 10]. We did not detect associations between the number of base pair substitutions in genes and their orientation or expression. Strikingly, any higher mutation rate for head-on genes can be explained by differing sequence composition between the leading and lagging strands and the error bias for DNA polymerase in specific sequence contexts. Therefore, we find local sequence context is the major determinant of mutagenesis in bacteria.

Indexed as

DNA ReplicationMutagenesisBacillus subtilisBacterial ProteinsDNA DamageDNA-Directed DNA PolymeraseDNA-Directed RNA PolymerasesSequence Analysis, DNABacterial ProteinsDNA-Directed DNA PolymeraseDNA-Directed RNA Polymerases

Identifiers

PMID26923786
PMCPMC4783269

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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.