Evidence map›Paper›PMID 21573023›Full record

ArticlePloS one2011

Deep sequencing reveals direct targets of gammaherpesvirus-induced mRNA decay and suggests that multiple mechanisms govern cellular transcript escape.

Karen Clyde, Britt A Glaunsinger

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

41 citing papers in PubMed, 53 citations in OpenAlex.

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  10. The mProceedings of the National Academy of Sciences of the United States of America · 2022
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  15. The molecular virology of coronaviruses.The Journal of biological chemistry · 2020
    Review
  16. Global epigenomic analysis of KSHV-infected primary effusion lymphoma identifies functionalProceedings of the National Academy of Sciences of the United States of America · 2020
    Article
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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

2 authors at 1 institution in 1 country.

Karen ClydeDepartment of Plant and Microbial Biology, University of California, Berkeley, California, United States of America.
Britt A Glaunsinger
University of California, Berkeley · US

Funding

Viral evasion of global RNA turnover during gammaherpesvirus lytic infectionF32AI080082 · NIAID · UNIVERSITY OF CALIFORNIA BERKELEY · PI CLYDE, KAREN LEE · 2009 to 2010
$102k
NIAID NIH HHS F32 AI080082NIAID NIH HHS F32AI080082
6 · The paper itself

Abstract

One characteristic of lytic infection with gammaherpesviruses, including Kaposi's sarcoma-associated herpesvirus (KSHV), Epstein-Barr virus (EBV) and murine herpesvirus 68 (MHV68), is the dramatic suppression of cellular gene expression in a process known as host shutoff. The alkaline exonuclease proteins (KSHV SOX, MHV-68 muSOX and EBV BGLF5) have been shown to induce shutoff by destabilizing cellular mRNAs. Here we extend previous analyses of cellular mRNA abundance during lytic infection to characterize the effects of SOX and muSOX, in the absence of other viral genes, utilizing deep sequencing technology (RNA-seq). Consistent with previous observations during lytic infection, the majority of transcripts are downregulated in cells expressing either SOX or muSOX, with muSOX acting as a more potent shutoff factor than SOX. Moreover, most cellular messages fall into the same expression class in both SOX- and muSOX-expressing cells, indicating that both factors target similar pools of mRNAs. More abundant mRNAs are more efficiently downregulated, suggesting a concentration effect in transcript targeting. However, even among highly expressed genes there are mRNAs that escape host shutoff. Further characterization of select escapees reveals multiple mechanisms by which cellular genes can evade downregulation. While some mRNAs are directly refractory to SOX, the steady state levels of others remain unchanged, presumably as a consequence of downstream effects on mRNA biogenesis. Collectively, these studies lay the framework for dissecting the mechanisms underlying the susceptibility of mRNA to destruction during lytic gammaherpesvirus infection.

Indexed as

3' Untranslated RegionsBase SequenceCarrier ProteinsDeath Domain Receptor Signaling Adaptor ProteinsDown-RegulationExodeoxyribonucleasesExonucleasesGammaherpesvirinaeGreen Fluorescent ProteinsHEK293 CellsHerpesvirus 8, HumanHigh-Throughput Nucleotide SequencingHumansReproducibility of ResultsReverse Transcriptase Polymerase Chain ReactionRhadinovirus3' Untranslated RegionsAEN protein, humanCarrier ProteinsDeath Domain Receptor Signaling Adaptor ProteinsExodeoxyribonucleasesExonucleasesGreen Fluorescent ProteinsPIDD1 protein, humanRNA, Messenger

Identifiers

PMID21573023
PMCPMC3090416
OpenAlexW2006900344

What OpenQuestion holds

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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.