Evidence map›Paper›PMID 26083367›Full record

ArticlePLoS pathogens2015

The Herpes Simplex Virus Protein pUL31 Escorts Nucleocapsids to Sites of Nuclear Egress, a Process Coordinated by Its N-Terminal Domain.

Christina Funk, Melanie Ott, Verena Raschbichler, Claus-Henning Nagel, Anne Binz, Beate Sodeik, Rudolf Bauerfeind, Susanne M Bailer

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

46 citing papers in PubMed, 66 citations in OpenAlex.

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  15. Nuclear Egress.Current issues in molecular biology · 2021
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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

8 authors at 3 institutions in 1 country.

Christina FunkInstitute for Interfacial Engineering and Plasma Technology (IGVP), University of Stuttgart, Stuttgart, Germany.
Melanie OttMax von Pettenkofer-Institut, Ludwig-Maximilians-University Munich, Munich, Germany.
Verena RaschbichlerMax von Pettenkofer-Institut, Ludwig-Maximilians-University Munich, Munich, Germany.
Claus-Henning NagelInstitute of Virology, Hannover Medical School, Hannover, Germany.
Anne BinzInstitute of Virology, Hannover Medical School, Hannover, Germany.
Beate SodeikInstitute of Virology, Hannover Medical School, Hannover, Germany.
Rudolf BauerfeindInstitute of Cell Biology, Hannover Medical School, Hannover, Germany.
Susanne M BailerInstitute for Interfacial Engineering and Plasma Technology (IGVP), University of Stuttgart, Stuttgart, Germany; Max von Pettenkofer-Institut, Ludwig-Maximilians-University Munich, Munich, Germany; Fraunhofer Institute for Interfacial Engineering and Biotechnology (IGB), Stuttgart, Germany.
Medizinische Hochschule Hannover · DELudwig-Maximilians-Universität München · DEUniversity of Stuttgart · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Progeny capsids of herpesviruses leave the nucleus by budding through the nuclear envelope. Two viral proteins, the membrane protein pUL34 and the nucleo-phosphoprotein pUL31 form the nuclear egress complex that is required for capsid egress out of the nucleus. All pUL31 orthologs are composed of a diverse N-terminal domain with 1 to 3 basic patches and a conserved C-terminal domain. To decipher the functions of the N-terminal domain, we have generated several Herpes simplex virus mutants and show here that the N-terminal domain of pUL31 is essential with basic patches being critical for viral propagation. pUL31 and pUL34 entered the nucleus independently of each other via separate routes and the N-terminal domain of pUL31 was required to prevent their premature interaction in the cytoplasm. Unexpectedly, a classical bipartite nuclear localization signal embedded in this domain was not required for nuclear import of pUL31. In the nucleus, pUL31 associated with the nuclear envelope and newly formed capsids. Viral mutants lacking the N-terminal domain or with its basic patches neutralized still associated with nucleocapsids but were unable to translocate them to the nuclear envelope. Replacing the authentic basic patches with a novel artificial one resulted in HSV1(17+)Lox-UL31-hbpmp1mp2, that was viable but delayed in nuclear egress and compromised in viral production. Thus, while the C-terminal domain of pUL31 is sufficient for the interaction with nucleocapsids, the N-terminal domain was essential for capsid translocation to sites of nuclear egress and a coordinated interaction with pUL34. Our data indicate an orchestrated sequence of events with pUL31 binding to nucleocapsids and escorting them to the inner nuclear envelope. We propose a common mechanism for herpesviral nuclear egress: pUL31 is required for intranuclear translocation of nucleocapsids and subsequent interaction with pUL34 thereby coupling capsid maturation with primary envelopment.

Indexed as

Active Transport, Cell NucleusAnimalsChlorocebus aethiopsHeLa CellsHerpesvirus 1, HumanHumansMicroscopy, FluorescenceMutagenesis, Site-DirectedNucleocapsid ProteinsVero CellsVirus AssemblyNucleocapsid Proteins

Identifiers

PMID26083367
PMCPMC4471197
OpenAlexW610657578

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.