Evidence map›Paper›PMID 39558174›Full record

ArticleNucleic acids research2024

A deep mutational scanning platform to characterize the fitness landscape of anti-CRISPR proteins.

Tobias Stadelmann, Daniel Heid, Michael Jendrusch, Jan Mathony, Sabine Aschenbrenner, Stéphane Rosset, Bruno E Correia, Dominik Niopek

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 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Comprehensive deletion scan of anti-CRISPR AcrIIA4 reveals essential and dispensable domains for Cas9 inhibition.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  5. Article
  6. Article
  7. 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

8 authors.

Tobias StadelmannCenter for Synthetic Biology, Technical University of Darmstadt, Darmstadt 64287, Germany.
Daniel HeidHochschule Offenburg, Faculty of Mechanical & Process Engineering, 77652 Offenburg, Germany.
Michael JendruschEuropean Molecular Biology Laboratory (EMBL), 69117 Heidelberg, Germany.
Jan MathonyInstitute of Pharmacy and Molecular Biotechnology (IPMB), Faculty of Engineering Sciences, Heidelberg University, Heidelberg 69120, Germany.
Sabine AschenbrennerInstitute of Pharmacy and Molecular Biotechnology (IPMB), Faculty of Engineering Sciences, Heidelberg University, Heidelberg 69120, Germany.
Stéphane RossetInstitute of Bioengineering, École Polytechnique Fédérale de Lausanne, Lausanne, CH-1015, Switzerland.
Bruno E CorreiaInstitute of Bioengineering, École Polytechnique Fédérale de Lausanne, Lausanne, CH-1015, Switzerland.
Dominik NiopekInstitute of Pharmacy and Molecular Biotechnology (IPMB), Faculty of Engineering Sciences, Heidelberg University, Heidelberg 69120, Germany.ORCID 0000-0001-7479-530X

Funding

Aventis FoundationBiltema FoundationEuropean Research Council 716058German Academic Scholarship FoundationGerman Research Foundation 453202693National Center of Competence in Research Chemical BiologySwiss National Science Foundation
6 · The paper itself

Abstract

Deep mutational scanning is a powerful method for exploring the mutational fitness landscape of proteins. Its adaptation to anti-CRISPR proteins, which are natural CRISPR-Cas inhibitors and key players in the co-evolution of microbes and phages, facilitates their characterization and optimization. Here, we developed a robust anti-CRISPR deep mutational scanning pipeline in Escherichia coli that combines synthetic gene circuits based on CRISPR interference with flow cytometry coupled sequencing and mathematical modeling. Using this pipeline, we characterized comprehensive single point mutation libraries for AcrIIA4 and AcrIIA5, two potent inhibitors of CRISPR-Cas9. The resulting mutational fitness landscapes revealed considerable mutational tolerance for both Acrs, suggesting an intrinsic redundancy with respect to Cas9 inhibitory features, and - for AcrIIA5 - indicated mutations that boost Cas9 inhibition. Subsequent in vitro characterization suggested that the observed differences in inhibitory potency between mutant inhibitors were mostly due to changes in binding affinity rather than protein expression levels. Finally, to demonstrate that our pipeline can inform Acrs-based genome editing applications, we employed a selected subset of mutant inhibitors to increase CRISPR-Cas9 target specificity by modulating Cas9 activity. Taken together, our work establishes deep mutational scanning as a powerful method for anti-CRISPR protein characterization and optimization.

Indexed as

CRISPR-Cas SystemsEscherichia coliGene EditingClustered Regularly Interspaced Short Palindromic RepeatsCRISPR-Associated Protein 9CRISPR-Associated ProteinsMutationCRISPR-Associated Protein 9CRISPR-Associated Proteins

Identifiers

PMID39558174
PMCPMC11662660

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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.