Evidence map›Paper›PMID 23825966›Full record

ArticlePLoS genetics2013

Heritable change caused by transient transcription errors.

Alasdair J E Gordon, Dominik Satory, Jennifer A Halliday, Christophe Herman

Abstract read
In one paragraph

Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing 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

33 citing papers in PubMed.

  1. Article
  2. Article
  3. Diversity inmBio · 2019
    Article
  4. Review
  5. Article
  6. How Acts of Infidelity Promote DNA Break Repair: Collision and Collusion Between DNA Repair and Transcription.BioEssays : news and reviews in molecular, cellular and developmental biology · 2018
    Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  12. Transcription fidelity and its roles in the cell.Current opinion in microbiology · 2018
    Review
  13. Article
  14. Article
  15. Accurate RNA consensus sequencing for high-fidelity detection of transcriptional mutagenesis-induced epimutations.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

4 authors.

Alasdair J E GordonDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA.
Dominik Satory
Jennifer A Halliday
Christophe Herman

Funding

Tumor BiologyP30CA125123 · NCI · BAYLOR COLLEGE OF MEDICINE · PI Michael T. Lewis · 2007 to 2026
$73.9M
Virology CoreP30AI036211 · NIAID · BAYLOR COLLEGE OF MEDICINE · PI BUTEL, JANET S · 1994 to 2015
$21.7M
PROGRAM IN HUMAN MOLECULAR GENETICST32GM008307 · NIGMS · BAYLOR COLLEGE OF MEDICINE · PI SHAULSKY, GAD · 1990 to 2020
$6.6M
Molecular Noise, Transcription Errors and Heritable Phenotypic ChangeR01GM088653 · NIGMS · BAYLOR COLLEGE OF MEDICINE · PI HERMAN, CHRISTOPHE · 2010 to 2019
$3.1M
BD Biosciences Special Order LSRIIS10RR024574 · NCRR · BAYLOR COLLEGE OF MEDICINE · PI LUMPKIN, ELLEN A · 2009 to 2009
$430k
NCI NIH HHS P30 CA125123NCI NIH HHS P30CA125123NCRR NIH HHS S10 RR024574NCRR NIH HHS S10RR024574NIAID NIH HHS AI036211NIAID NIH HHS P30 AI036211NIGMS NIH HHS 1R01GM088653NIGMS NIH HHS R01 GM088653NIGMS NIH HHS T32 GM008307
6 · The paper itself

Abstract

Transmission of cellular identity relies on the faithful transfer of information from the mother to the daughter cell. This process includes accurate replication of the DNA, but also the correct propagation of regulatory programs responsible for cellular identity. Errors in DNA replication (mutations) and protein conformation (prions) can trigger stable phenotypic changes and cause human disease, yet the ability of transient transcriptional errors to produce heritable phenotypic change ('epimutations') remains an open question. Here, we demonstrate that transcriptional errors made specifically in the mRNA encoding a transcription factor can promote heritable phenotypic change by reprogramming a transcriptional network, without altering DNA. We have harnessed the classical bistable switch in the lac operon, a memory-module, to capture the consequences of transient transcription errors in living Escherichia coli cells. We engineered an error-prone transcription sequence (A9 run) in the gene encoding the lac repressor and show that this 'slippery' sequence directly increases epigenetic switching, not mutation in the cell population. Therefore, one altered transcript within a multi-generational series of many error-free transcripts can cause long-term phenotypic consequences. Thus, like DNA mutations, transcriptional epimutations can instigate heritable changes that increase phenotypic diversity, which drives both evolution and disease.

Indexed as

Evolution, MolecularTranscription, GeneticDNA ReplicationEpigenesis, GeneticEscherichia coliGenetic VariationGreen Fluorescent ProteinsHumansLac OperonLac RepressorsMutationPhenotypeProtein ConformationRNA, MessengerGreen Fluorescent ProteinsLac RepressorsRNA, Messenger

Identifiers

PMID23825966
PMCPMC3694819

What Socratic 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 Socratic graph.