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  1. Artikel ; Online: Histone acetylation in neuronal (dys)function.

    Bonnaud, Emilie M / Suberbielle, Elsa / Malnou, Cécile E

    Biomolecular concepts

    2016  Band 7, Heft 2, Seite(n) 103–116

    Abstract: Cognitive functions require the expression of an appropriate pattern of genes in response to environmental stimuli. Over the last years, many studies have accumulated knowledge towards the understanding of molecular mechanisms that regulate neuronal gene ...

    Abstract Cognitive functions require the expression of an appropriate pattern of genes in response to environmental stimuli. Over the last years, many studies have accumulated knowledge towards the understanding of molecular mechanisms that regulate neuronal gene expression. Epigenetic modifications have been shown to play an important role in numerous neuronal functions, from synaptic plasticity to learning and memory. In particular, histone acetylation is a central player in these processes. In this review, we present the molecular mechanisms of histone acetylation and summarize the data underlying the relevance of histone acetylation in cognitive functions in normal and pathological conditions. In the last part, we discuss the different mechanisms underlying the dysregulation of histone acetylation associated with neurological disorders, with a particular focus on environmental causes (stress, drugs, or infectious agents) that are linked to impaired histone acetylation.
    Mesh-Begriff(e) Acetylation ; Animals ; Cognition ; Environment ; Epigenesis, Genetic ; Gene Expression Regulation ; Genetic Predisposition to Disease ; Histones/metabolism ; Humans ; Memory ; Mutation ; Neurodegenerative Diseases/etiology ; Neurodegenerative Diseases/metabolism ; Neuronal Plasticity ; Neurons/physiology
    Chemische Substanzen Histones
    Sprache Englisch
    Erscheinungsdatum 2016-05-01
    Erscheinungsland Germany
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2557908-3
    ISSN 1868-503X ; 1868-5021
    ISSN (online) 1868-503X
    ISSN 1868-5021
    DOI 10.1515/bmc-2016-0002
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Histone acetylation in neuronal (dys)function

    Bonnaud Emilie M. / Suberbielle Elsa / Malnou Cécile E.

    Biomolecular Concepts, Vol 7, Iss 2, Pp 103-

    2016  Band 116

    Abstract: Cognitive functions require the expression of an appropriate pattern of genes in response to environmental stimuli. Over the last years, many studies have accumulated knowledge towards the understanding of molecular mechanisms that regulate neuronal gene ...

    Abstract Cognitive functions require the expression of an appropriate pattern of genes in response to environmental stimuli. Over the last years, many studies have accumulated knowledge towards the understanding of molecular mechanisms that regulate neuronal gene expression. Epigenetic modifications have been shown to play an important role in numerous neuronal functions, from synaptic plasticity to learning and memory. In particular, histone acetylation is a central player in these processes. In this review, we present the molecular mechanisms of histone acetylation and summarize the data underlying the relevance of histone acetylation in cognitive functions in normal and pathological conditions. In the last part, we discuss the different mechanisms underlying the dysregulation of histone acetylation associated with neurological disorders, with a particular focus on environmental causes (stress, drugs, or infectious agents) that are linked to impaired histone acetylation.
    Schlagwörter cognition ; epigenetics ; histone acetylation ; histone acetyltransferase ; histone deacetylase ; neuron ; synaptic plasticity ; Biology (General) ; QH301-705.5
    Thema/Rubrik (Code) 572
    Sprache Englisch
    Erscheinungsdatum 2016-05-01T00:00:00Z
    Verlag De Gruyter
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  3. Artikel ; Online: Comparison of intra- and inter-host genetic diversity in rabies virus during experimental cross-species transmission.

    Bonnaud, Emilie M / Troupin, Cécile / Dacheux, Laurent / Holmes, Edward C / Monchatre-Leroy, Elodie / Tanguy, Marion / Bouchier, Christiane / Cliquet, Florence / Barrat, Jacques / Bourhy, Hervé

    PLoS pathogens

    2019  Band 15, Heft 6, Seite(n) e1007799

    Abstract: The development of high-throughput genome sequencing enables accurate measurements of levels of sub-consensus intra-host virus genetic diversity and analysis of the role played by natural selection during cross-species transmission. We analysed the ... ...

    Abstract The development of high-throughput genome sequencing enables accurate measurements of levels of sub-consensus intra-host virus genetic diversity and analysis of the role played by natural selection during cross-species transmission. We analysed the natural and experimental evolution of rabies virus (RABV), an important example of a virus that is able to make multiple host jumps. In particular, we (i) analyzed RABV evolution during experimental host switching with the goal of identifying possible genetic markers of host adaptation, (ii) compared the mutational changes observed during passage with those observed in natura, and (iii) determined whether the colonization of new hosts or tissues requires adaptive evolution in the virus. To address these aims, animal infection models (dog and fox) and primary cell culture models (embryo brain cells of dog and fox) were developed and viral variation was studied in detail through deep genome sequencing. Our analysis revealed a strong unidirectional host evolutionary effect, as dog-adapted rabies virus was able to replicate in fox and fox cells relatively easily, while dogs or neuronal dog cells were not easily susceptible to fox adapted-RABV. This suggests that dog RABV may be able to adapt to some hosts more easily than other host variants, or that when RABV switched from dogs to red foxes it lost its ability to adapt easily to other species. Although no difference in patterns of mutation variation between different host organs was observed, mutations were common following both in vitro and in vivo passage. However, only a small number of these mutations also appeared in natura, suggesting that adaptation during successful cross-species virus transmission is a complex, multifactorial evolutionary process.
    Mesh-Begriff(e) Animals ; Cell Line ; Dog Diseases/genetics ; Dog Diseases/immunology ; Dogs ; Evolution, Molecular ; Female ; Foxes/genetics ; Foxes/immunology ; Foxes/virology ; High-Throughput Nucleotide Sequencing ; Host-Parasite Interactions/genetics ; Host-Parasite Interactions/immunology ; Male ; Mutation ; Rabies/genetics ; Rabies/immunology ; Rabies virus/physiology
    Sprache Englisch
    Erscheinungsdatum 2019-06-20
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2205412-1
    ISSN 1553-7374 ; 1553-7366
    ISSN (online) 1553-7374
    ISSN 1553-7366
    DOI 10.1371/journal.ppat.1007799
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Hippocampal expression of a virus-derived protein impairs memory in mice.

    Bétourné, Alexandre / Szelechowski, Marion / Thouard, Anne / Abrial, Erika / Jean, Arnaud / Zaidi, Falek / Foret, Charlotte / Bonnaud, Emilie M / Charlier, Caroline M / Suberbielle, Elsa / Malnou, Cécile E / Granon, Sylvie / Rampon, Claire / Gonzalez-Dunia, Daniel

    Proceedings of the National Academy of Sciences of the United States of America

    2018  Band 115, Heft 7, Seite(n) 1611–1616

    Abstract: The analysis of the biology of neurotropic viruses, notably of their interference with cellular signaling, provides a useful tool to get further insight into the role of specific pathways in the control of behavioral functions. Here, we exploited the ... ...

    Abstract The analysis of the biology of neurotropic viruses, notably of their interference with cellular signaling, provides a useful tool to get further insight into the role of specific pathways in the control of behavioral functions. Here, we exploited the natural property of a viral protein identified as a major effector of behavioral disorders during infection. We used the phosphoprotein (P) of Borna disease virus, which acts as a decoy substrate for protein kinase C (PKC) when expressed in neurons and disrupts synaptic plasticity. By a lentiviral-based strategy, we directed the singled-out expression of P in the dentate gyrus of the hippocampus and we examined its impact on mouse behavior. Mice expressing the P protein displayed increased anxiety and impaired long-term memory in contextual and spatial memory tasks. Interestingly, these effects were dependent on P protein phosphorylation by PKC, as expression of a mutant form of P devoid of its PKC phosphorylation sites had no effect on these behaviors. We also revealed features of behavioral impairment induced by P protein expression but that were independent of its phosphorylation by PKC. Altogether, our findings provide insight into the behavioral correlates of viral infection, as well as into the impact of virus-mediated alterations of the PKC pathway on behavioral functions.
    Mesh-Begriff(e) Animals ; Borna Disease/metabolism ; Borna Disease/pathology ; Borna Disease/virology ; Borna disease virus/physiology ; Cells, Cultured ; Cognition Disorders/etiology ; Cognition Disorders/metabolism ; Cognition Disorders/pathology ; Dentate Gyrus/metabolism ; Dentate Gyrus/pathology ; Dentate Gyrus/virology ; Hippocampus/metabolism ; Hippocampus/pathology ; Hippocampus/virology ; Memory, Long-Term/physiology ; Mice ; Mutation ; Neuronal Plasticity ; Neurons/metabolism ; Neurons/pathology ; Neurons/virology ; Phosphoproteins/genetics ; Phosphoproteins/metabolism ; Phosphorylation ; Protein Kinase C/genetics ; Protein Kinase C/metabolism ; Viral Structural Proteins/genetics ; Viral Structural Proteins/metabolism
    Chemische Substanzen P protein, Borna disease virus ; Phosphoproteins ; Viral Structural Proteins ; Protein Kinase C (EC 2.7.11.13)
    Sprache Englisch
    Erscheinungsdatum 2018--13
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.1711977115
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1148: Hefte anzeigen Standort:
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  5. Artikel ; Online: Comparison of intra- and inter-host genetic diversity in rabies virus during experimental cross-species transmission.

    Emilie M Bonnaud / Cécile Troupin / Laurent Dacheux / Edward C Holmes / Elodie Monchatre-Leroy / Marion Tanguy / Christiane Bouchier / Florence Cliquet / Jacques Barrat / Hervé Bourhy

    PLoS Pathogens, Vol 15, Iss 6, p e

    2019  Band 1007799

    Abstract: The development of high-throughput genome sequencing enables accurate measurements of levels of sub-consensus intra-host virus genetic diversity and analysis of the role played by natural selection during cross-species transmission. We analysed the ... ...

    Abstract The development of high-throughput genome sequencing enables accurate measurements of levels of sub-consensus intra-host virus genetic diversity and analysis of the role played by natural selection during cross-species transmission. We analysed the natural and experimental evolution of rabies virus (RABV), an important example of a virus that is able to make multiple host jumps. In particular, we (i) analyzed RABV evolution during experimental host switching with the goal of identifying possible genetic markers of host adaptation, (ii) compared the mutational changes observed during passage with those observed in natura, and (iii) determined whether the colonization of new hosts or tissues requires adaptive evolution in the virus. To address these aims, animal infection models (dog and fox) and primary cell culture models (embryo brain cells of dog and fox) were developed and viral variation was studied in detail through deep genome sequencing. Our analysis revealed a strong unidirectional host evolutionary effect, as dog-adapted rabies virus was able to replicate in fox and fox cells relatively easily, while dogs or neuronal dog cells were not easily susceptible to fox adapted-RABV. This suggests that dog RABV may be able to adapt to some hosts more easily than other host variants, or that when RABV switched from dogs to red foxes it lost its ability to adapt easily to other species. Although no difference in patterns of mutation variation between different host organs was observed, mutations were common following both in vitro and in vivo passage. However, only a small number of these mutations also appeared in natura, suggesting that adaptation during successful cross-species virus transmission is a complex, multifactorial evolutionary process.
    Schlagwörter Immunologic diseases. Allergy ; RC581-607 ; Biology (General) ; QH301-705.5
    Thema/Rubrik (Code) 630
    Sprache Englisch
    Erscheinungsdatum 2019-06-01T00:00:00Z
    Verlag Public Library of Science (PLoS)
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  6. Artikel ; Online: Borna disease virus phosphoprotein modulates epigenetic signaling in neurons to control viral replication.

    Bonnaud, Emilie M / Szelechowski, Marion / Bétourné, Alexandre / Foret, Charlotte / Thouard, Anne / Gonzalez-Dunia, Daniel / Malnou, Cécile E

    Journal of virology

    2015  Band 89, Heft 11, Seite(n) 5996–6008

    Abstract: Unlabelled: Understanding the modalities of interaction of neurotropic viruses with their target cells represents a major challenge that may improve our knowledge of many human neurological disorders for which viral origin is suspected. Borna disease ... ...

    Abstract Unlabelled: Understanding the modalities of interaction of neurotropic viruses with their target cells represents a major challenge that may improve our knowledge of many human neurological disorders for which viral origin is suspected. Borna disease virus (BDV) represents an ideal model to analyze the molecular mechanisms of viral persistence in neurons and its consequences for neuronal homeostasis. It is now established that BDV ensures its long-term maintenance in infected cells through a stable interaction of viral components with the host cell chromatin, in particular, with core histones. This has led to our hypothesis that such an interaction may trigger epigenetic changes in the host cell. Here, we focused on histone acetylation, which plays key roles in epigenetic regulation of gene expression, notably for neurons. We performed a comparative analysis of histone acetylation patterns of neurons infected or not infected by BDV, which revealed that infection decreases histone acetylation on selected lysine residues. We showed that the BDV phosphoprotein (P) is responsible for these perturbations, even when it is expressed alone independently of the viral context, and that this action depends on its phosphorylation by protein kinase C. We also demonstrated that BDV P inhibits cellular histone acetyltransferase activities. Finally, by pharmacologically manipulating cellular acetylation levels, we observed that inhibiting cellular acetyl transferases reduces viral replication in cell culture. Our findings reveal that manipulation of cellular epigenetics by BDV could be a means to modulate viral replication and thus illustrate a fascinating example of virus-host cell interaction.
    Importance: Persistent DNA viruses often subvert the mechanisms that regulate cellular chromatin dynamics, thereby benefitting from the resulting epigenetic changes to create a favorable milieu for their latent and persistent states. Here, we reasoned that Borna disease virus (BDV), the only RNA virus known to durably persist in the nucleus of infected cells, notably neurons, might employ a similar mechanism. In this study, we uncovered a novel modality of virus-cell interaction in which BDV phosphoprotein inhibits cellular histone acetylation by interfering with histone acetyltransferase activities. Manipulation of cellular histone acetylation is accompanied by a modulation of viral replication, revealing a perfect adaptation of this "ancient" virus to its host that may favor neuronal persistence and limit cellular damage.
    Mesh-Begriff(e) Acetylation ; Animals ; Borna disease virus/physiology ; Cells, Cultured ; Epigenesis, Genetic ; Histones/metabolism ; Host-Pathogen Interactions ; Neurons/virology ; Phosphoproteins/metabolism ; Protein Processing, Post-Translational ; Rats, Sprague-Dawley ; Viral Structural Proteins/metabolism ; Virus Replication
    Chemische Substanzen Histones ; P protein, Borna disease virus ; Phosphoproteins ; Viral Structural Proteins
    Sprache Englisch
    Erscheinungsdatum 2015-06
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80174-4
    ISSN 1098-5514 ; 0022-538X
    ISSN (online) 1098-5514
    ISSN 0022-538X
    DOI 10.1128/JVI.00454-15
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel ; Online: Lyssavirus matrix protein cooperates with phosphoprotein to modulate the Jak-Stat pathway.

    Sonthonnax, Florian / Besson, Benoit / Bonnaud, Emilie / Jouvion, Grégory / Merino, David / Larrous, Florence / Bourhy, Hervé

    Scientific reports

    2019  Band 9, Heft 1, Seite(n) 12171

    Abstract: Phosphoprotein (P) and matrix protein (M) cooperate to undermine the immune response ... through the cytoplasmic retention of interferon (IFN)-activated STAT1 (pSTAT1), M interacts with the RelAp43-p105-ABIN2 ... protein-complementation assays, reverse genetics and DNA ChIP, we identified a role of M protein ...

    Abstract Phosphoprotein (P) and matrix protein (M) cooperate to undermine the immune response to rabies virus (RABV) infections. While P is involved in the modulation of the Jak-Stat pathway through the cytoplasmic retention of interferon (IFN)-activated STAT1 (pSTAT1), M interacts with the RelAp43-p105-ABIN2-TPL2 complex, to efficiently inhibit the nuclear factor-κB (NF-κB) pathway. Using transfections, protein-complementation assays, reverse genetics and DNA ChIP, we identified a role of M protein in the control of Jak-Stat signaling pathway, in synergy with the P protein. In unstimulated cells, both M and P proteins were found to interact with JAK1. Upon type-I IFN stimulation, the M switches toward pSTAT1 interaction, which results in an enhanced capacity of P protein to interact with pSTAT1 and restrain it in the cytoplasm. Furthermore, the role for M-protein positions 77, 100, 104 and 110 was also demonstrated in interaction with both JAK1 and pY-STAT1, and confirmed in vivo. Together, these data indicate that M protein cooperates with P protein to restrain in parallel, and sequentially, NF-κB and Jak-Stat pathways.
    Mesh-Begriff(e) Animals ; Cytoplasm/metabolism ; HeLa Cells ; Humans ; Immunity, Innate ; Interferon Type I/metabolism ; Janus Kinase 1/metabolism ; Lyssavirus/metabolism ; Lyssavirus/pathogenicity ; Mice ; Mice, Inbred BALB C ; Mutagenesis, Site-Directed ; NF-kappa B/metabolism ; Phosphoproteins/genetics ; Phosphoproteins/metabolism ; Promoter Regions, Genetic ; STAT1 Transcription Factor/genetics ; STAT1 Transcription Factor/metabolism ; Signal Transduction ; Th2 Cells/immunology ; Th2 Cells/metabolism ; Viral Matrix Proteins/genetics ; Viral Matrix Proteins/metabolism ; Viral Proteins/genetics ; Viral Proteins/metabolism ; Virulence
    Chemische Substanzen Interferon Type I ; NF-kappa B ; Phosphoproteins ; STAT1 Transcription Factor ; STAT1 protein, human ; Viral Matrix Proteins ; Viral Proteins ; JAK1 protein, human (EC 2.7.10.2) ; Janus Kinase 1 (EC 2.7.10.2)
    Sprache Englisch
    Erscheinungsdatum 2019-08-21
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-019-48507-4
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Artikel ; Online: Lyssavirus matrix protein cooperates with phosphoprotein to modulate the Jak-Stat pathway

    Florian Sonthonnax / Benoit Besson / Emilie Bonnaud / Grégory Jouvion / David Merino / Florence Larrous / Hervé Bourhy

    Scientific Reports, Vol 9, Iss 1, Pp 1-

    2019  Band 13

    Abstract: Abstract Phosphoprotein (P) and matrix protein (M) cooperate to undermine the immune response ... through the cytoplasmic retention of interferon (IFN)-activated STAT1 (pSTAT1), M interacts with the RelAp43-p105-ABIN2 ... protein-complementation assays, reverse genetics and DNA ChIP, we identified a role of M protein ...

    Abstract Abstract Phosphoprotein (P) and matrix protein (M) cooperate to undermine the immune response to rabies virus (RABV) infections. While P is involved in the modulation of the Jak-Stat pathway through the cytoplasmic retention of interferon (IFN)-activated STAT1 (pSTAT1), M interacts with the RelAp43-p105-ABIN2-TPL2 complex, to efficiently inhibit the nuclear factor-κB (NF-κB) pathway. Using transfections, protein-complementation assays, reverse genetics and DNA ChIP, we identified a role of M protein in the control of Jak-Stat signaling pathway, in synergy with the P protein. In unstimulated cells, both M and P proteins were found to interact with JAK1. Upon type-I IFN stimulation, the M switches toward pSTAT1 interaction, which results in an enhanced capacity of P protein to interact with pSTAT1 and restrain it in the cytoplasm. Furthermore, the role for M-protein positions 77, 100, 104 and 110 was also demonstrated in interaction with both JAK1 and pY-STAT1, and confirmed in vivo. Together, these data indicate that M protein cooperates with P protein to restrain in parallel, and sequentially, NF-κB and Jak-Stat pathways.
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Erscheinungsdatum 2019-08-01T00:00:00Z
    Verlag Nature Portfolio
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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