Evidence map›Paper›PMID 19176625›Full record

ArticleJournal of virology2009

Identification of functional domains in reovirus replication proteins muNS and mu2.

Takeshi Kobayashi, Laura S Ooms, James D Chappell, Terence S Dermody

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

37 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. Article
  3. Reovirus μ2 Protein Impairs Translation to Reduce U5 snRNP Protein Levels.International journal of molecular sciences · 2022
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. RNA regulatory processes in RNA virus biology.Wiley interdisciplinary reviews. RNA · 2019
    Review
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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

4 authors at 1 institution in 2 countries.

Takeshi KobayashiDepartment of Pediatrics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.
Laura S Ooms
James D Chappell
Terence S Dermody
Vanderbilt University · US

Funding

Tumor Immunology and Microenvironment Research ProgramP30CA068485 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MATTHEW J TYSKA · 1995 to 2026
$172.8M
Vanderbilt Diabetes Research CenterP30DK020593 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI OWEN P MCGUINNESS · 2012 to 2026
$29.3M
TRANSGENIC MOUSE/ ES CELL SHARES RESOURCESP60DK020593 · NIDDK · VANDERBILT UNIVERSITY · PI MCGUINNESS, OWEN P · 1986 to 2011
$28.1M
CELL ENTRY OF REOVIRUSR01AI032539 · NIAID · VANDERBILT UNIVERSITY MEDICAL CENTER · PI TERENCE S. DERMODY · 1998 to 2026
$12.3M
Mechanisims of Reovirus Translational RegulationK08AI062862 · NIAID · VANDERBILT UNIVERSITY · PI CHAPPELL, JAMES D · 2005 to 2007
$325k
NCI NIH HHS CA68485NCI NIH HHS P30 CA068485NIAID NIH HHS K08 AI062862NIAID NIH HHS R01 AI032539NIAID NIH HHS R01 AI32539NIDDK NIH HHS DK20593NIDDK NIH HHS P30 DK020593
6 · The paper itself

Abstract

Mammalian reoviruses are nonenveloped particles containing a genome of 10 double-stranded RNA (dsRNA) gene segments. Reovirus replication occurs within viral inclusions, which are specialized nonmembranous cytoplasmic organelles formed by viral nonstructural and structural proteins. Although these structures serve as sites for several major events in the reovirus life cycle, including dsRNA synthesis, gene segment assortment, and genome encapsidation, biochemical mechanisms of virion morphogenesis within inclusions have not been elucidated because much remains unknown about inclusion anatomy and functional organization. To better understand how inclusions support viral replication, we have used RNA interference (RNAi) and reverse genetics to define functional domains in two inclusion-associated proteins, muNS and mu2, which are interacting partners essential for inclusion development and viral replication. Removal of muNS N-terminal sequences required for association with mu2 or another muNS-binding protein, sigmaNS, prevented the capacity of muNS to support viral replication without affecting inclusion formation, indicating that muNS-mu2 and muNS-sigmaNS interactions are necessary for inclusion function but not establishment. In contrast, introduction of changes into the muNS C-terminal region, including sequences that form a putative oligomerization domain, precluded inclusion formation as well as viral replication. Mutational analysis of mu2 revealed a critical dependence of viral replication on an intact nucleotide/RNA triphosphatase domain and an N-terminal cluster of basic amino acid residues conforming to a nuclear localization motif. Another domain in mu2 governs the capacity of viral inclusions to affiliate with microtubules and thereby modulates inclusion morphology, either globular or filamentous. However, viral variants altered in inclusion morphology displayed equivalent replication efficiency. These studies reveal a modular functional organization of inclusion proteins muNS and mu2, define the importance of specific amino acid sequences and motifs in these proteins for viral replication, and demonstrate the utility of complementary RNAi-based and reverse genetic approaches for studies of reovirus replication proteins.

Indexed as

Virus ReplicationAnimalsCell LineDNA Mutational AnalysisGene SilencingHumansInclusion Bodies, ViralMiceReoviridaeRNA InterferenceSequence DeletionViral Nonstructural ProteinsViral Proteinsmu2 protein, ReovirusViral Nonstructural ProteinsViral Proteins

Identifiers

PMID19176625
PMCPMC2655549
OpenAlexW2014407475

What OpenQuestion holds

Textmetadata
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.