Evidence map›Paper›PMID 37425722›Full record

ArticlebioRxiv : the preprint server for biology2024

The interplay of DNA repair context with target sequence predictably biases Cas9-generated mutations.

Ananth Pallaseni, Elin Madli Peets, Gareth Girling, Luca Crepaldi, Ivan Kuzmin, Marilin Moor, Núria Muñoz-Subirana, Joost Schimmel, Özdemirhan Serçin, Balca R Mardin and 4 more

Open access · greenAbstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 6 institutions in 5 countries.

Ananth PallaseniWellcome Sanger Institute, Wellcome Genome Campus, Hinxton, United Kingdom.ORCID 0000-0002-4840-195X
Elin Madli PeetsWellcome Sanger Institute, Wellcome Genome Campus, Hinxton, United Kingdom.
Gareth GirlingWellcome Sanger Institute, Wellcome Genome Campus, Hinxton, United Kingdom.
Luca CrepaldiWellcome Sanger Institute, Wellcome Genome Campus, Hinxton, United Kingdom.
Ivan KuzminDepartment of Computer Science, University of Tartu, Tartu, Estonia.
Marilin MoorDepartment of Computer Science, University of Tartu, Tartu, Estonia.
Núria Muñoz-SubiranaDepartment of Human Genetics, Leiden University Medical Center, Leiden, The Netherlands.
Joost SchimmelDepartment of Human Genetics, Leiden University Medical Center, Leiden, The Netherlands.
Özdemirhan SerçinBioMed X Institute (GmbH), Im Neuenheimer Feld 515, Heidelberg, Germany.
Balca R MardinBioMed X Institute (GmbH), Im Neuenheimer Feld 515, Heidelberg, Germany.
Marcel TijstermanDepartment of Human Genetics, Leiden University Medical Center, Leiden, The Netherlands.
Hedi PetersonDepartment of Computer Science, University of Tartu, Tartu, Estonia.
Michael KosickiDepartment of Medicine, University of Cambridge, Cambridge, United Kingdom.ORCID 0000-0001-7173-8852
Leopold PartsWellcome Sanger Institute, Wellcome Genome Campus, Hinxton, United Kingdom.
Wellcome Sanger Institute · GBUniversity of Tartu · EEBioMed X Institute · DELeiden University Medical Center · NLLawrence Berkeley National Laboratory · USLeiden University · NL

Funding

Generation of an In Vivo Human Genome Transcriptional Enhancer DatasetR01HG003988 · NHGRI · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI Len Alexander Pennacchio · 2006 to 2026
$24.1M
NHGRI NIH HHS R01 HG003988Wellcome Trust
6 · The paper itself

Abstract

Mutagenic outcomes of CRISPR/Cas9-generated double-stranded breaks depend on both the sequence flanking the cut and cellular DNA damage repair. The interaction of these features has been largely unexplored, limiting our ability to understand and manipulate the outcomes. Here, we measured how the absence of 18 repair genes changed frequencies of 83,680 unique mutational outcomes generated by Cas9 double-stranded breaks at 2,838 synthetic target sequences in mouse embryonic stem cells. This large scale survey allowed us to classify the outcomes in an unbiased way, generating hypotheses about new modes of double-stranded break repair. Our data indicate a specialised role for

Identifiers

PMID37425722
PMCPMC10326969
OpenAlexW4382561571

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.