RapamycinFungusV1, Main, Exploration, bibRecord, 000220

TOP2β-Dependent Nuclear DNA Damage Shapes Extracellular Growth Factor Responses via Dynamic AKT Phosphorylation to Control Virus Latency.

Identifieur interne : 000220 ( Main/Exploration ); précédent : 000219; suivant : 000221

TOP2β-Dependent Nuclear DNA Damage Shapes Extracellular Growth Factor Responses via Dynamic AKT Phosphorylation to Control Virus Latency.

Auteurs : Hui-Lan Hu [États-Unis] ; Lora A. Shiflett [États-Unis] ; Mariko Kobayashi [États-Unis] ; Moses V. Chao [États-Unis] ; Angus C. Wilson [États-Unis] ; Ian Mohr [États-Unis] ; Tony T. Huang [États-Unis]

Source :

Molecular cell [ 1097-4164 ] ; 2019.

RBID : pubmed:30930055

Descripteurs français

English descriptors

KwdEn :
- Animals (MeSH), DNA Breaks, Double-Stranded (MeSH), DNA Damage (genetics), DNA End-Joining Repair (genetics), DNA Repair (genetics), DNA Repair Enzymes (genetics), DNA Topoisomerases, Type II (genetics), DNA-Binding Proteins (genetics), Herpesvirus 1, Human (genetics), Herpesvirus 1, Human (pathogenicity), Humans (MeSH), MRE11 Homologue Protein (genetics), Mechanistic Target of Rapamycin Complex 1 (genetics), Neurons (metabolism), Neurons (virology), Nuclear Proteins (genetics), Phosphorylation (MeSH), Proto-Oncogene Proteins c-akt (genetics), Rats (MeSH), Signal Transduction (genetics), TOR Serine-Threonine Kinases (genetics), Virus Latency (genetics).
MESH :
- chemical , genetics : DNA Repair Enzymes, DNA Topoisomerases, Type II, DNA-Binding Proteins, MRE11 Homologue Protein, Mechanistic Target of Rapamycin Complex 1, Nuclear Proteins, Proto-Oncogene Proteins c-akt, TOR Serine-Threonine Kinases.
- genetics : DNA Damage, DNA End-Joining Repair, DNA Repair, Herpesvirus 1, Human, Signal Transduction, Virus Latency.
- metabolism : Neurons.
- pathogenicity : Herpesvirus 1, Human.
- virology : Neurons.
- Animals, DNA Breaks, Double-Stranded, Humans, Phosphorylation, Rats.

Abstract

The mTOR pathway integrates both extracellular and intracellular signals and serves as a central regulator of cell metabolism, growth, survival, and stress responses. Neurotropic viruses, such as herpes simplex virus-1 (HSV-1), also rely on cellular AKT-mTORC1 signaling to achieve viral latency. Here, we define a novel genotoxic response whereby spatially separated signals initiated by extracellular neurotrophic factors and nuclear DNA damage are integrated by the AKT-mTORC1 pathway. We demonstrate that endogenous DNA double-strand breaks (DSBs) mediated by Topoisomerase 2β-DNA cleavage complex (TOP2βcc) intermediates are required to achieve AKT-mTORC1 signaling and maintain HSV-1 latency in neurons. Suppression of host DNA-repair pathways that remove TOP2βcc trigger HSV-1 reactivation. Moreover, perturbation of AKT phosphorylation dynamics by downregulating the PHLPP1 phosphatase led to AKT mis-localization and disruption of DSB-induced HSV-1 reactivation. Thus, the cellular genome integrity and environmental inputs are consolidated and co-opted by a latent virus to balance lifelong infection with transmission.

DOI: 10.1016/j.molcel.2019.02.032
PubMed: 30930055
PubMed Central: PMC6499694

Affiliations:

Links toward previous steps (curation, corpus...)

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Le document en format XML

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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term>
<term>DNA Breaks, Double-Stranded (MeSH)</term>
<term>DNA Damage (genetics)</term>
<term>DNA End-Joining Repair (genetics)</term>
<term>DNA Repair (genetics)</term>
<term>DNA Repair Enzymes (genetics)</term>
<term>DNA Topoisomerases, Type II (genetics)</term>
<term>DNA-Binding Proteins (genetics)</term>
<term>Herpesvirus 1, Human (genetics)</term>
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<term>Mechanistic Target of Rapamycin Complex 1 (genetics)</term>
<term>Neurons (metabolism)</term>
<term>Neurons (virology)</term>
<term>Nuclear Proteins (genetics)</term>
<term>Phosphorylation (MeSH)</term>
<term>Proto-Oncogene Proteins c-akt (genetics)</term>
<term>Rats (MeSH)</term>
<term>Signal Transduction (genetics)</term>
<term>TOR Serine-Threonine Kinases (genetics)</term>
<term>Virus Latency (genetics)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>ADN topoisomérases de type II (génétique)</term>
<term>Altération de l'ADN (génétique)</term>
<term>Animaux (MeSH)</term>
<term>Cassures double-brin de l'ADN (MeSH)</term>
<term>Complexe-1 cible mécanistique de la rapamycine (génétique)</term>
<term>Enzymes de réparation de l'ADN (génétique)</term>
<term>Herpèsvirus humain de type 1 (génétique)</term>
<term>Herpèsvirus humain de type 1 (pathogénicité)</term>
<term>Humains (MeSH)</term>
<term>Latence virale (génétique)</term>
<term>Neurones (métabolisme)</term>
<term>Neurones (virologie)</term>
<term>Phosphorylation (MeSH)</term>
<term>Protéine homologue de MRE11 (génétique)</term>
<term>Protéines de liaison à l'ADN (génétique)</term>
<term>Protéines nucléaires (génétique)</term>
<term>Protéines proto-oncogènes c-akt (génétique)</term>
<term>Rats (MeSH)</term>
<term>Réparation de l'ADN (génétique)</term>
<term>Réparation de l'ADN par jonction d'extrémités (génétique)</term>
<term>Sérine-thréonine kinases TOR (génétique)</term>
<term>Transduction du signal (génétique)</term>
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<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>DNA Repair Enzymes</term>
<term>DNA Topoisomerases, Type II</term>
<term>DNA-Binding Proteins</term>
<term>MRE11 Homologue Protein</term>
<term>Mechanistic Target of Rapamycin Complex 1</term>
<term>Nuclear Proteins</term>
<term>Proto-Oncogene Proteins c-akt</term>
<term>TOR Serine-Threonine Kinases</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>DNA Damage</term>
<term>DNA End-Joining Repair</term>
<term>DNA Repair</term>
<term>Herpesvirus 1, Human</term>
<term>Signal Transduction</term>
<term>Virus Latency</term>
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<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>ADN topoisomérases de type II</term>
<term>Altération de l'ADN</term>
<term>Complexe-1 cible mécanistique de la rapamycine</term>
<term>Enzymes de réparation de l'ADN</term>
<term>Herpèsvirus humain de type 1</term>
<term>Latence virale</term>
<term>Protéine homologue de MRE11</term>
<term>Protéines de liaison à l'ADN</term>
<term>Protéines nucléaires</term>
<term>Protéines proto-oncogènes c-akt</term>
<term>Réparation de l'ADN</term>
<term>Réparation de l'ADN par jonction d'extrémités</term>
<term>Sérine-thréonine kinases TOR</term>
<term>Transduction du signal</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Neurons</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Neurones</term>
</keywords>
<keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Herpesvirus 1, Human</term>
</keywords>
<keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Herpèsvirus humain de type 1</term>
</keywords>
<keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Neurones</term>
</keywords>
<keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Neurons</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>DNA Breaks, Double-Stranded</term>
<term>Humans</term>
<term>Phosphorylation</term>
<term>Rats</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Cassures double-brin de l'ADN</term>
<term>Humains</term>
<term>Phosphorylation</term>
<term>Rats</term>
</keywords>
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<front><div type="abstract" xml:lang="en">The mTOR pathway integrates both extracellular and intracellular signals and serves as a central regulator of cell metabolism, growth, survival, and stress responses. Neurotropic viruses, such as herpes simplex virus-1 (HSV-1), also rely on cellular AKT-mTORC1 signaling to achieve viral latency. Here, we define a novel genotoxic response whereby spatially separated signals initiated by extracellular neurotrophic factors and nuclear DNA damage are integrated by the AKT-mTORC1 pathway. We demonstrate that endogenous DNA double-strand breaks (DSBs) mediated by Topoisomerase 2β-DNA cleavage complex (TOP2βcc) intermediates are required to achieve AKT-mTORC1 signaling and maintain HSV-1 latency in neurons. Suppression of host DNA-repair pathways that remove TOP2βcc trigger HSV-1 reactivation. Moreover, perturbation of AKT phosphorylation dynamics by downregulating the PHLPP1 phosphatase led to AKT mis-localization and disruption of DSB-induced HSV-1 reactivation. Thus, the cellular genome integrity and environmental inputs are consolidated and co-opted by a latent virus to balance lifelong infection with transmission.</div>
</front>
</TEI>
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<DateCompleted><Year>2019</Year>
<Month>10</Month>
<Day>22</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>05</Month>
<Day>02</Day>
</DateRevised>
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<Issue>3</Issue>
<PubDate><Year>2019</Year>
<Month>05</Month>
<Day>02</Day>
</PubDate>
</JournalIssue>
<Title>Molecular cell</Title>
<ISOAbbreviation>Mol Cell</ISOAbbreviation>
</Journal>
<ArticleTitle>TOP2β-Dependent Nuclear DNA Damage Shapes Extracellular Growth Factor Responses via Dynamic AKT Phosphorylation to Control Virus Latency.</ArticleTitle>
<Pagination><MedlinePgn>466-480.e4</MedlinePgn>
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<Abstract><AbstractText>The mTOR pathway integrates both extracellular and intracellular signals and serves as a central regulator of cell metabolism, growth, survival, and stress responses. Neurotropic viruses, such as herpes simplex virus-1 (HSV-1), also rely on cellular AKT-mTORC1 signaling to achieve viral latency. Here, we define a novel genotoxic response whereby spatially separated signals initiated by extracellular neurotrophic factors and nuclear DNA damage are integrated by the AKT-mTORC1 pathway. We demonstrate that endogenous DNA double-strand breaks (DSBs) mediated by Topoisomerase 2β-DNA cleavage complex (TOP2βcc) intermediates are required to achieve AKT-mTORC1 signaling and maintain HSV-1 latency in neurons. Suppression of host DNA-repair pathways that remove TOP2βcc trigger HSV-1 reactivation. Moreover, perturbation of AKT phosphorylation dynamics by downregulating the PHLPP1 phosphatase led to AKT mis-localization and disruption of DSB-induced HSV-1 reactivation. Thus, the cellular genome integrity and environmental inputs are consolidated and co-opted by a latent virus to balance lifelong infection with transmission.</AbstractText>
<CopyrightInformation>Copyright © 2019 Elsevier Inc. All rights reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hu</LastName>
<ForeName>Hui-Lan</ForeName>
<Initials>HL</Initials>
<AffiliationInfo><Affiliation>Department of Biochemistry & Molecular Pharmacology, NYU School of Medicine, New York, NY 10016, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Shiflett</LastName>
<ForeName>Lora A</ForeName>
<Initials>LA</Initials>
<AffiliationInfo><Affiliation>Department of Microbiology, NYU School of Medicine, New York, NY 10016, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kobayashi</LastName>
<ForeName>Mariko</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of Microbiology, NYU School of Medicine, New York, NY 10016, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chao</LastName>
<ForeName>Moses V</ForeName>
<Initials>MV</Initials>
<AffiliationInfo><Affiliation>Skirball Institute of Biomolecular Medicine, Departments of Cell Biology, Physiology & Neuroscience and Psychiatry, NYU School of Medicine, New York, NY 10016, USA; NYU Neuroscience Institute, NYU School of Medicine, New York, NY 10016, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wilson</LastName>
<ForeName>Angus C</ForeName>
<Initials>AC</Initials>
<AffiliationInfo><Affiliation>Department of Microbiology, NYU School of Medicine, New York, NY 10016, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Mohr</LastName>
<ForeName>Ian</ForeName>
<Initials>I</Initials>
<AffiliationInfo><Affiliation>Department of Microbiology, NYU School of Medicine, New York, NY 10016, USA; Laura and Isaac Perlmutter Cancer Institute, NYU School of Medicine, New York, NY 10016, USA. Electronic address: ian.mohr@med.nyu.edu.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Huang</LastName>
<ForeName>Tony T</ForeName>
<Initials>TT</Initials>
<AffiliationInfo><Affiliation>Department of Biochemistry & Molecular Pharmacology, NYU School of Medicine, New York, NY 10016, USA; Laura and Isaac Perlmutter Cancer Institute, NYU School of Medicine, New York, NY 10016, USA. Electronic address: tony.huang@nyumc.org.</Affiliation>
</AffiliationInfo>
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<Language>eng</Language>
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<Acronym>GM</Acronym>
<Agency>NIGMS NIH HHS</Agency>
<Country>United States</Country>
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<Grant><GrantID>R56 NS021072</GrantID>
<Acronym>NS</Acronym>
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   |area=    RapamycinFungusV1
   |flux=    Main
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   |type=    RBID
   |clé=     pubmed:30930055
   |texte=   TOP2β-Dependent Nuclear DNA Damage Shapes Extracellular Growth Factor Responses via Dynamic AKT Phosphorylation to Control Virus Latency.
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	Serveur d'exploration sur la rapamycine et les champignons
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.

Serveur d'exploration sur la rapamycine et les champignons

TOP2β-Dependent Nuclear DNA Damage Shapes Extracellular Growth Factor Responses via Dynamic AKT Phosphorylation to Control Virus Latency.

TOP2β-Dependent Nuclear DNA Damage Shapes Extracellular Growth Factor Responses via Dynamic AKT Phosphorylation to Control Virus Latency.

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