Evidence map›Paper›PMID 37164018›Full record

ArticleMolecular cell2023

Co-transcriptional genome surveillance by HUSH is coupled to termination machinery.

Andrew L Spencley, Shiran Bar, Tomek Swigut, Ryan A Flynn, Cameron H Lee, Liang-Fu Chen, Michael C Bassik, Joanna Wysocka

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 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
17.5field-weighted citation impact, top 1% 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

24 citing papers in PubMed, 44 citations in OpenAlex.

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  8. Reversing transgene silencing via targeted chromatin editing.bioRxiv : the preprint server for biology · 2025
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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 at 3 institutions in 1 country.

Andrew L SpencleyDepartment of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA, USA; Cancer Biology Program, Stanford University School of Medicine, Stanford, CA, USA.
Shiran BarDepartment of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA, USA.
Tomek SwigutDepartment of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA, USA.
Ryan A FlynnStem Cell Program, Boston Children's Hospital, Boston, MA, USA; Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA, USA.
Cameron H LeeDepartment of Genetics, Stanford University School of Medicine, Stanford, CA, USA.
Liang-Fu ChenDepartment of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA, USA.
Michael C BassikDepartment of Genetics, Stanford University School of Medicine, Stanford, CA, USA.
Joanna WysockaDepartment of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA, USA; Department of Developmental Biology, Stanford University School of Medicine, Stanford, CA, USA; Institute of Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA, USA; Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, CA, USA. Electronic address: wysocka@stanford.edu.
Stanford University · USBoston Children's Hospital · USCalifornia Institute for Regenerative Medicine · US

Funding

Uncovering fundamentals of gene regulation by enhancersR35GM131757 · NIGMS · STANFORD UNIVERSITY · PI Joanna Wysocka · 2019 to 2026
$3.1M
Howard Hughes Medical InstituteNIGMS NIH HHS R35 GM131757
6 · The paper itself

Abstract

The HUSH complex recognizes and silences foreign DNA such as viruses, transposons, and transgenes without prior exposure to its targets. Here, we show that endogenous targets of the HUSH complex fall into two distinct classes based on the presence or absence of H3K9me3. These classes are further distinguished by their transposon content and differential response to the loss of HUSH. A de novo genomic rearrangement at the Sox2 locus induces a switch from H3K9me3-independent to H3K9me3-associated HUSH targeting, resulting in silencing. We further demonstrate that HUSH interacts with the termination factor WDR82 and-via its component MPP8-with nascent RNA. HUSH accumulates at sites of high RNAPII occupancy including long exons and transcription termination sites in a manner dependent on WDR82 and CPSF. Together, our results uncover the functional diversity of HUSH targets and show that this vertebrate-specific complex exploits evolutionarily ancient transcription termination machinery for co-transcriptional chromatin targeting and genome surveillance.

Indexed as

Gene SilencingTranscription FactorsGenomeRNATranscription, GeneticRNATranscription FactorsCPSFgene silencingheterochromatinHUSH complexMPP8SETDB1TASORtranscription terminationtransposable elementsWDR82

Identifiers

PMID37164018
PMCPMC10915761
OpenAlexW4376132875

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.