Evidence map›Paper›PMID 37028419›Full record

ArticleMolecular cell2023

Structural and functional properties of mSWI/SNF chromatin remodeling complexes revealed through single-cell perturbation screens.

Jordan E Otto, Oana Ursu, Alexander P Wu, Evan B Winter, Michael S Cuoco, Sai Ma, Kristin Qian, Brittany C Michel, Jason D Buenrostro, Bonnie Berger and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Molecular cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
6.8field-weighted citation impact, top 3% 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

29 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. Article
  3. Mapping the dialogue: Decoding alveolar stem-niche interactions.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  4. SMARCD1 and Its Functional Relevance in SWI/SNF and Cancer.International journal of molecular sciences · 2026
    Review
  5. Article
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  8. The SMARCA4-TMEM47 axis plays an essential role in chikungunya virus RNA replication.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
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  11. Article
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  13. Article
  14. Review
  15. Article
  16. Article
  17. R-loops: a key driver of inflammatory responses in cancer.Experimental & molecular medicine · 2025
    Review
  18. Article
  19. Article
  20. 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

12 authors at 1 institution in 1 country.

Jordan E OttoDepartment of Pediatric Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA, USA; Broad Institute of MIT and Harvard, Cambridge, MA, USA; Chemical Biology Program, Harvard University, Cambridge, MA, USA.
Oana UrsuBroad Institute of MIT and Harvard, Cambridge, MA, USA; Department of Biology, Massachusetts Institute of Technology, Cambridge, MA, USA.
Alexander P WuBroad Institute of MIT and Harvard, Cambridge, MA, USA; Computer Science and Artificial Intelligence Laboratory, Massachusetts Institute of Technology, Cambridge, MA, USA; Department of Mathematics, Massachusetts Institute of Technology, Cambridge, MA, USA.
Evan B WinterDepartment of Pediatric Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA, USA; Broad Institute of MIT and Harvard, Cambridge, MA, USA.
Michael S CuocoBroad Institute of MIT and Harvard, Cambridge, MA, USA.
Sai MaBroad Institute of MIT and Harvard, Cambridge, MA, USA; Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA, USA.
Kristin QianDepartment of Pediatric Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA, USA; Broad Institute of MIT and Harvard, Cambridge, MA, USA; Biological and Biomedical Sciences Program, Harvard Medical School, Boston, MA, USA.
Brittany C MichelDepartment of Pediatric Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA, USA; Broad Institute of MIT and Harvard, Cambridge, MA, USA; Biological and Biomedical Sciences Program, Harvard Medical School, Boston, MA, USA.
Jason D BuenrostroBroad Institute of MIT and Harvard, Cambridge, MA, USA; Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA, USA.
Bonnie BergerBroad Institute of MIT and Harvard, Cambridge, MA, USA; Computer Science and Artificial Intelligence Laboratory, Massachusetts Institute of Technology, Cambridge, MA, USA; Department of Mathematics, Massachusetts Institute of Technology, Cambridge, MA, USA.
Aviv RegevBroad Institute of MIT and Harvard, Cambridge, MA, USA; Department of Biology, Massachusetts Institute of Technology, Cambridge, MA, USA; Howard Hughes Medical Institute, Chevy Chase, MD, UA. Electronic address: aviv.regev.sc@gmail.com.
Cigall KadochDepartment of Pediatric Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA, USA; Broad Institute of MIT and Harvard, Cambridge, MA, USA; Chemical Biology Program, Harvard University, Cambridge, MA, USA; Howard Hughes Medical Institute, Chevy Chase, MD, UA. Electronic address: cigall_kadoch@dfci.harvard.edu.
Broad Institute · US

Funding

Developing high-throughput genetic perturbation strategies for single cells in cancer organoidsU01CA250554 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI BERGER, BONNIE, YILMAZ, OMER · 2020 to 2022
$2.8M
Reversing Oncogenic BAF Complex Structure & Function: New Therapeutic ApproachesDP2CA195762 · NCI · DANA-FARBER CANCER INST · PI KADOCH, CIGALL · 2014 to 2014
$2.6M
Howard Hughes Medical InstituteNCI NIH HHS DP2 CA195762NCI NIH HHS U01 CA250554
6 · The paper itself

Abstract

The mammalian SWI/SNF (mSWI/SNF or BAF) family of chromatin remodeling complexes play critical roles in regulating DNA accessibility and gene expression. The three final-form subcomplexes-cBAF, PBAF, and ncBAF-are distinct in biochemical componentry, chromatin targeting, and roles in disease; however, the contributions of their constituent subunits to gene expression remain incompletely defined. Here, we performed Perturb-seq-based CRISPR-Cas9 knockout screens targeting mSWI/SNF subunits individually and in select combinations, followed by single-cell RNA-seq and SHARE-seq. We uncovered complex-, module-, and subunit-specific contributions to distinct regulatory networks and defined paralog subunit relationships and shifted subcomplex functions upon perturbations. Synergistic, intra-complex genetic interactions between subunits reveal functional redundancy and modularity. Importantly, single-cell subunit perturbation signatures mapped across bulk primary human tumor expression profiles both mirror and predict cBAF loss-of-function status in cancer. Our findings highlight the utility of Perturb-seq to dissect disease-relevant gene regulatory impacts of heterogeneous, multi-component master regulatory complexes.

Indexed as

Chromatin Assembly and DisassemblyNeoplasmsAnimalsChromatinChromosomal Proteins, Non-HistoneHumansMammalsTranscription FactorsChromatinChromosomal Proteins, Non-HistoneTranscription FactorsATAC-seqATP-dependent chromatin remodelingBAF complexcancerchromatin accessibilitygene expressionmammalian SWI/SNF complexespediatric cancerPerturb-seqrare diseasesSHARE-Seq

Identifiers

PMID37028419
PMCPMC12593249
OpenAlexW4362694632

What OpenQuestion holds

Textmetadata
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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.