Evidence map›Paper›PMID 39386505›Full record

ArticlebioRxiv : the preprint server for biology2024

Transcription elongation factor ELOF1 is required for efficient somatic hypermutation and class switch recombination.

Lizhen Wu, Anurupa Devi Yadavalli, Gabriel Matos-Rodrigues, Dijin Xu, Andreas P Pintado-Urbanc, Matthew D Simon, Wei Wu, André Nussenzweig, David G Schatz

Abstract readPreprint
PubMed Full text at PMC Publisher
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.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors.

Lizhen WuDepartment of Immunobiology, Yale School of Medicine, 300 Cedar Street, Box 208011, New Haven, CT 06520-8011, USA.
Anurupa Devi YadavalliDepartment of Immunobiology, Yale School of Medicine, 300 Cedar Street, Box 208011, New Haven, CT 06520-8011, USA.
Gabriel Matos-RodriguesLaboratory of Genome Integrity, National Cancer Institute NIH, Bethesda, MD, USA.
Dijin XuDepartment of Microbial Pathogenesis, Yale University School of Medicine, New Haven, CT, USA.
Andreas P Pintado-UrbancDepartment of Molecular Biophysics & Biochemistry, Yale University, New Haven, CT, USA.
Matthew D SimonDepartment of Molecular Biophysics & Biochemistry, Yale University, New Haven, CT, USA.ORCID 0000-0001-7423-5265
Wei WuKey Laboratory of Multi-Cell Systems, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, Shanghai, China.
André NussenzweigLaboratory of Genome Integrity, National Cancer Institute NIH, Bethesda, MD, USA.
David G SchatzDepartment of Immunobiology, Yale School of Medicine, 300 Cedar Street, Box 208011, New Haven, CT 06520-8011, USA.

Funding

Yale Pathology Tissue Services Shared ResourceP30CA016359 · NCI · YALE UNIVERSITY · PI Eric P. Winer · 1985 to 2026
$85.0M
Targeting of somatic hypermutation in the genomeR01AI127642 · NIAID · YALE UNIVERSITY · PI SCHATZ, DAVID G. · 2017 to 2025
$4.6M
Revealing the dynamics of RNA metabolism with nucleotide recoding chemistryR01GM137117 · NIGMS · YALE UNIVERSITY · PI Matthew David Simon · 2020 to 2026
$2.6M
High Performance Computing Instrumentation for the Yale Center for Genome AnalysisS10OD030363 · OD · YALE UNIVERSITY · PI MANE, SHRIKANT M · 2022 to 2022
$1.2M
Pacific Bioscience Sequel II sequencing system for the Yale Center for Genome Analysis (YCGA)S10OD028669 · OD · YALE UNIVERSITY · PI MANE, SHRIKANT M · 2020 to 2020
$407k
NCI NIH HHS HHSN261201500003INCI NIH HHS P30 CA016359NIAID NIH HHS R01 AI127642NIGMS NIH HHS R01 GM137117NIH HHS S10 OD028669NIH HHS S10 OD030363
6 · The paper itself

Abstract

Somatic hypermutation (SHM) and class switch recombination (CSR) diversify immunoglobulin (Ig) genes and are initiated by the activation induced deaminase (AID), a single-stranded DNA cytidine deaminase that is thought to engage its substrate in the context of RNA polymerase II (RNAPII) transcription. Through a loss of function genetic screen, we identified numerous potential factors involved in SHM including ELOF1, a component of the RNAPII elongation complex that has been shown to function in DNA repair and transcription elongation. Loss of ELOF1 strongly compromises SHM, CSR, and AID targeting and alters RNAPII transcription by reducing RNAPII pausing downstream of transcription start sites and levels of serine 5 but not serine 2 phosphorylated RNAPII throughout transcribed genes. ELOF1 must bind to RNAPII to be a proximity partner for AID and to function in SHM and CSR. We propose that ELOF1 helps create the appropriate stalled RNAPII substrate on which AID acts.

Indexed as

AIDclass switch recombinationELOF1RNA polymerase IISomatic hypermutationtranscription

Identifiers

PMID39386505
PMCPMC11463689

What OpenQuestion holds

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Registered trials

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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.