Evidence map›Paper›PMID 36947548›Full record

ArticlePLoS computational biology2023

Characterization of RNA polymerase II trigger loop mutations using molecular dynamics simulations and machine learning.

Bercem Dutagaci, Bingbing Duan, Chenxi Qiu, Craig D Kaplan, Michael Feig

Open access · goldAbstract read
In one paragraph

Article in PLoS computational biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

3 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Structural basis of transcription: RNA polymerase II substrate binding and metal coordination using a free-electron laser.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  3. 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

5 authors at 4 institutions in 1 country.

Bercem DutagaciDepartment of Molecular and Cell Biology, University of California Merced, Merced, California, United States of America.
Bingbing DuanDepartment of Biological Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.
Chenxi QiuDepartment of Genetics, Harvard Medical School, Boston, Massachusetts, United States of America.
Craig D KaplanDepartment of Biological Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.ORCID 0000-0002-7518-695X
Michael FeigDepartment of Biochemistry and Molecular Biology, Michigan State University, East Lansing, Michigan, United States of America.ORCID 0000-0001-9380-6422
University of Pittsburgh · USHarvard University · USMichigan United · USUniversity of California, Merced · US

Funding

Mechanisms of RNA Polymerase II transcriptionR35GM144116 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Craig Kaplan · 2022 to 2026
$3.4M
Mechanism and Regulation of RNA Polymerase II ElongationR01GM097260 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KAPLAN, CRAIG · 2011 to 2020
$3.3M
Modeling and dynamics of biomolecules on cellular scalesR35GM126948 · NIGMS · MICHIGAN STATE UNIVERSITY · PI Michael Feig · 2018 to 2026
$3.2M
NIGMS NIH HHS R01 GM097260NIGMS NIH HHS R35 GM126948NIGMS NIH HHS R35 GM144116
6 · The paper itself

Abstract

Catalysis and fidelity of multisubunit RNA polymerases rely on a highly conserved active site domain called the trigger loop (TL), which achieves roles in transcription through conformational changes and interaction with NTP substrates. The mutations of TL residues cause distinct effects on catalysis including hypo- and hyperactivity and altered fidelity. We applied molecular dynamics simulation (MD) and machine learning (ML) techniques to characterize TL mutations in the Saccharomyces cerevisiae RNA Polymerase II (Pol II) system. We did so to determine relationships between individual mutations and phenotypes and to associate phenotypes with MD simulated structural alterations. Using fitness values of mutants under various stress conditions, we modeled phenotypes along a spectrum of continual values. We found that ML could predict the phenotypes with 0.68 R2 correlation from amino acid sequences alone. It was more difficult to incorporate MD data to improve predictions from machine learning, presumably because MD data is too noisy and possibly incomplete to directly infer functional phenotypes. However, a variational auto-encoder model based on the MD data allowed the clustering of mutants with different phenotypes based on structural details. Overall, we found that a subset of loss-of-function (LOF) and lethal mutations tended to increase distances of TL residues to the NTP substrate, while another subset of LOF and lethal substitutions tended to confer an increase in distances between TL and bridge helix (BH). In contrast, some of the gain-of-function (GOF) mutants appear to cause disruption of hydrophobic contacts among TL and nearby helices.

Indexed as

RNA Polymerase IITranscription, GeneticDNA-Directed RNA PolymerasesMolecular Dynamics SimulationMutationSaccharomyces cerevisiaeDNA-Directed RNA PolymerasesRNA Polymerase II

Identifiers

PMID36947548
PMCPMC10069792
OpenAlexW4353016412

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.