Evidence map›Paper›PMID 41387726›Full record

ArticleNature communications2025

Chemically-inducible CRISPR/Cas9 circuits for ultra-high dynamic range gene perturbation.

Rajini Srinivasan, Tao Sun, Azalia Sandles, Diana Wu, Liang Wang, Hetal Patel, Ryan Pabalate, Maram Bader, Amy Heidersbach, Clark Ho and 3 more

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Review
  5. 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

13 authors.

Rajini Srinivasan *Department of Molecular Biology, Genentech Inc., South San Francisco, CA, USA.
Tao Sun *Department of Molecular Biology, Genentech Inc., South San Francisco, CA, USA.
Azalia SandlesDepartment of Molecular Biology, Genentech Inc., South San Francisco, CA, USA.
Diana WuDepartment of Functional Genomics, Genentech Inc., South San Francisco, CA, USA.
Liang WangDepartment of Functional Genomics, Genentech Inc., South San Francisco, CA, USA.
Hetal PatelDepartment of Molecular Biology, Genentech Inc., South San Francisco, CA, USA.
Ryan PabalateDepartment of Molecular Biology, Genentech Inc., South San Francisco, CA, USA.
Maram BaderDepartment of Molecular Biology, Genentech Inc., South San Francisco, CA, USA.
Amy HeidersbachDepartment of Molecular Biology, Genentech Inc., South San Francisco, CA, USA.
Clark HoDepartment of Molecular Biology, Genentech Inc., South San Francisco, CA, USA.
Shiqi XieDepartment of Functional Genomics, Genentech Inc., South San Francisco, CA, USA.
Andrew NgDepartment of Molecular Biology, Genentech Inc., South San Francisco, CA, USA. ng.andrew.an1@gene.com.ORCID http://orcid.org/0000-0001-8044-1807
Benjamin HaleyDepartment of Molecular Biology, Genentech Inc., South San Francisco, CA, USA. benjamin.haley@umontreal.ca.ORCID http://orcid.org/0000-0002-0074-0020

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CRISPR/Cas9 technologies provide unique capabilities for modeling disease and understanding gene-to-phenotype connections. In cultured cells, chemical-mediated control of Cas9 activity can limit off-target effects and enable mechanistic study of essential genes. However, widely-used Tet-On systems often show leaky Cas9 expression, leading to unintended edits, as well as weak activity upon induction. Leakiness can be problematic in the context of Cas9 nuclease activity, which may result in cumulative DNA damage and degradation of the target cell genome over time. To overcome these deficiencies, we have established transgenic platforms that minimize Cas9 functionality in the OFF-state along with maximized and uncompromised ON-state gene editing efficiency. By combining conditional destabilization and inhibition of Cas9, we have developed an all-in-one (one or multiple guide RNAs and Cas9) ultra-tight, Tet-inducible system with exceptional dynamic range (ON vs. OFF-state) across various cell lines and targets. As an alternative to Tet-mediated induction, we have created a Branaplam-regulated splice switch module for low-baseline and robust Cas9 activity control. Lastly, for circumstances where DNA damage needs to be avoided, we have constructed a dual-control, Tet-inducible CRISPRi module for tight and potent transcriptional silencing. This upgraded suite of inducible CRISPR systems has broad applications for numerous cell types and experimental conditions.

Indexed as

CRISPR-Cas SystemsGene EditingCRISPR-Associated Protein 9HEK293 CellsHumansRNA, Guide, CRISPR-Cas SystemsCRISPR-Associated Protein 9RNA, Guide, CRISPR-Cas Systems

Identifiers

PMID41387726
PMCPMC12804943

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.