Evidence map›Paper›PMID 34732717›Full record

ArticleNature communications2021

BEAR reveals that increased fidelity variants can successfully reduce the mismatch tolerance of adenine but not cytosine base editors.

András Tálas, Dorottya A Simon, Péter I Kulcsár, Éva Varga, Sarah L Krausz, Ervin Welker

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

15 citing papers in PubMed, 20 citations in OpenAlex.

  1. Base Editing: Mechanisms and Therapeutic Applications.Methods in molecular biology (Clifton, N.J.) · 2027
    Review
  2. Article
  3. Article
  4. Article
  5. Prime editing in mammals: From promise to practicalities.Molecular therapy. Nucleic acids · 2025
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Enrichment strategies to enhance genome editing.Journal of biomedical science · 2023
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. 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

6 authors at 4 institutions in 1 country.

András TálasInstitute of Enzymology, Research Centre for Natural Sciences, Budapest, Hungary. talas.andras@ttk.hu.ORCID http://orcid.org/0000-0003-0851-8333
Dorottya A SimonInstitute of Enzymology, Research Centre for Natural Sciences, Budapest, Hungary.
Péter I KulcsárInstitute of Enzymology, Research Centre for Natural Sciences, Budapest, Hungary.ORCID http://orcid.org/0000-0002-7783-5108
Éva VargaInstitute of Enzymology, Research Centre for Natural Sciences, Budapest, Hungary.
Sarah L KrauszInstitute of Enzymology, Research Centre for Natural Sciences, Budapest, Hungary.
Ervin WelkerInstitute of Enzymology, Research Centre for Natural Sciences, Budapest, Hungary. welker.ervin@ttk.hu.ORCID http://orcid.org/0000-0001-9874-8794
Semmelweis University · HUHUN-REN Szegedi Biológiai Kutatóközpont · HUInstitute of Molecular Life Sciences · HUUniversity of Szeged · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adenine and cytosine base editors (ABE, CBE) allow for precision genome engineering. Here, Base Editor Activity Reporter (BEAR), a plasmid-based fluorescent tool is introduced, which can be applied to report on ABE and CBE editing in a virtually unrestricted sequence context or to label base edited cells for enrichment. Using BEAR-enrichment, we increase the yield of base editing performed by nuclease inactive base editors to the level of the nickase versions while maintaining significantly lower indel background. Furthermore, by exploiting the semi-high-throughput potential of BEAR, we examine whether increased fidelity SpCas9 variants can be used to decrease SpCas9-dependent off-target effects of ABE and CBE. Comparing them on the same target sets reveals that CBE remains active on sequences, where increased fidelity mutations and/or mismatches decrease the activity of ABE. Our results suggest that the deaminase domain of ABE is less effective to act on rather transiently separated target DNA strands, than that of CBE explaining its lower mismatch tolerance.

Indexed as

Genetic EngineeringAdenineCRISPR-Associated Protein 9CRISPR-Cas SystemsCytosineDeoxyribonuclease IDNAGene EditingGenomeHEK293 CellsHumansMutationRNAAdenineCRISPR-Associated Protein 9CytosineDeoxyribonuclease IDNARNA

Identifiers

PMID34732717
PMCPMC8566456
OpenAlexW3110543729

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.