Evidence map›Paper›PMID 25104019›Full record

ArticleNucleic acids research2014

Regulation of transcription termination by glucosylated hydroxymethyluracil, base J, in Leishmania major and Trypanosoma brucei.

David Reynolds, Laura Cliffe, Konrad U Förstner, Chung-Chau Hon, T Nicolai Siegel, Robert Sabatini

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

51 citing papers in PubMed, 83 citations in OpenAlex.

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  17. Localization of Epigenetic Markers inPathogens (Basel, Switzerland) · 2022
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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

6 authors at 3 institutions in 3 countries.

David ReynoldsDepartment of Biochemistry and Molecular Biology, University of Georgia, Davison Life Sciences Building, 120 Green Street, Athens, GA 30602-7229, USA.
Laura CliffeDepartment of Biochemistry and Molecular Biology, University of Georgia, Davison Life Sciences Building, 120 Green Street, Athens, GA 30602-7229, USA.
Konrad U FörstnerCore Unit Systems Medicine, University of Wuerzburg, Wuerzburg 97080, Germany.
Chung-Chau HonInstitut Pasteur, Unité Biologie Cellulaire du Parasitisme, Département Biologie cellulaire et infection, Paris 75015, France INSERM U786, Paris 75015, France.
T Nicolai SiegelResearch Center for Infectious Diseases, University of Wuerzburg, Wuerzburg 97080, Germany.
Robert SabatiniDepartment of Biochemistry and Molecular Biology, University of Georgia, Davison Life Sciences Building, 120 Green Street, Athens, GA 30602-7229, USA rsabatini@bmb.uga.edu.
University of Georgia · USInstitut Pasteur · FRUniversity of Würzburg · DE

Funding

Regulation of RNA polymerase II transcription in trypanosomatidsR01AI109108 · NIAID · UNIVERSITY OF GEORGIA · PI SABATINI, ROBERT S · 2014 to 2022
$3.7M
Biosynthesis and Function of Base JR01AI063523 · NIAID · UNIVERSITY OF GEORGIA · PI SABATINI, ROBERT S · 2006 to 2010
$1.6M
Biosynthesis and function of base J in T. bruceiR56AI063523 · NIAID · UNIVERSITY OF GEORGIA · PI SABATINI, ROBERT S · 2011 to 2011
$384k
NIAID NIH HHS AI063523-03NIAID NIH HHS R01 AI109108NIAID NIH HHS R56 AI063523
6 · The paper itself

Abstract

Base J, β-d-glucosyl-hydroxymethyluracil, is an epigenetic modification of thymine in the nuclear DNA of flagellated protozoa of the order Kinetoplastida. J is enriched at sites involved in RNA polymerase (RNAP) II initiation and termination. Reduction of J in Leishmania tarentolae via growth in BrdU resulted in cell death and indicated a role of J in the regulation of RNAP II termination. To further explore J function in RNAP II termination among kinetoplastids and avoid indirect effects associated with BrdU toxicity and genetic deletions, we inhibited J synthesis in Leishmania major and Trypanosoma brucei using DMOG. Reduction of J in L. major resulted in genome-wide defects in transcription termination at the end of polycistronic gene clusters and the generation of antisense RNAs, without cell death. In contrast, loss of J in T. brucei did not lead to genome-wide termination defects; however, the loss of J at specific sites within polycistronic gene clusters led to altered transcription termination and increased expression of downstream genes. Thus, J regulation of RNAP II transcription termination genome-wide is restricted to Leishmania spp., while in T. brucei it regulates termination and gene expression at specific sites within polycistronic gene clusters.

Indexed as

Gene Expression RegulationTranscription Termination, GeneticCell LineGlucosidesLeishmania majorRNA Polymerase IIRNA, ProtozoanTrypanosoma brucei bruceiUracil5-((glucopyranosyloxy)methyl)uracilGlucosidesRNA Polymerase IIRNA, ProtozoanUracil

Identifiers

PMID25104019
PMCPMC4150806
OpenAlexW1979858789

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.