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  1. Article ; Online: Viral protein activates the NLRP1 inflammasome.

    Hartenian, Ella / Broz, Petr

    Nature immunology

    2022  Volume 23, Issue 6, Page(s) 822–824

    MeSH term(s) Adaptor Proteins, Signal Transducing/metabolism ; Apoptosis Regulatory Proteins/metabolism ; Inflammasomes/metabolism ; Viral Proteins/metabolism
    Chemical Substances Adaptor Proteins, Signal Transducing ; Apoptosis Regulatory Proteins ; Inflammasomes ; Viral Proteins
    Language English
    Publishing date 2022-05-26
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 2016987-5
    ISSN 1529-2916 ; 1529-2908
    ISSN (online) 1529-2916
    ISSN 1529-2908
    DOI 10.1038/s41590-022-01226-x
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  2. Article ; Online: NINJ1 induces plasma membrane rupture and release of damage-associated molecular pattern molecules during ferroptosis.

    Ramos, Saray / Hartenian, Ella / Santos, José Carlos / Walch, Philipp / Broz, Petr

    The EMBO journal

    2024  Volume 43, Issue 7, Page(s) 1164–1186

    Abstract: Ferroptosis is a regulated form of necrotic cell death caused by iron-dependent accumulation of oxidized phospholipids in cellular membranes, culminating in plasma membrane rupture (PMR) and cell lysis. PMR is also a hallmark of other types of programmed ...

    Abstract Ferroptosis is a regulated form of necrotic cell death caused by iron-dependent accumulation of oxidized phospholipids in cellular membranes, culminating in plasma membrane rupture (PMR) and cell lysis. PMR is also a hallmark of other types of programmed necrosis, such as pyroptosis and necroptosis, where it is initiated by dedicated pore-forming cell death-executing factors. However, whether ferroptosis-associated PMR is also actively executed by proteins or driven by osmotic pressure remains unknown. Here, we investigate a potential ferroptosis role of ninjurin-1 (NINJ1), a recently identified executor of pyroptosis-associated PMR. We report that NINJ1 oligomerizes during ferroptosis, and that Ninj1-deficiency protects macrophages and fibroblasts from ferroptosis-associated PMR. Mechanistically, we find that NINJ1 is dispensable for the initial steps of ferroptosis, such as lipid peroxidation, channel-mediated calcium influx, and cell swelling. In contrast, NINJ1 is required for early loss of plasma membrane integrity, which precedes complete PMR. Furthermore, NINJ1 mediates the release of cytosolic proteins and danger-associated molecular pattern (DAMP) molecules from ferroptotic cells, suggesting that targeting NINJ1 could be a therapeutic option to reduce ferroptosis-associated inflammation.
    MeSH term(s) Humans ; Alarmins ; Ferroptosis ; Necrosis/metabolism ; Cell Death ; Cell Membrane/metabolism ; Nerve Growth Factors/metabolism ; Cell Adhesion Molecules, Neuronal/metabolism
    Chemical Substances Alarmins ; NINJ1 protein, human ; Nerve Growth Factors ; Cell Adhesion Molecules, Neuronal
    Language English
    Publishing date 2024-02-23
    Publishing country England
    Document type Journal Article
    ZDB-ID 586044-1
    ISSN 1460-2075 ; 0261-4189
    ISSN (online) 1460-2075
    ISSN 0261-4189
    DOI 10.1038/s44318-024-00055-y
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    Zs.MG 100: Show issues

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  3. Article ; Online: Feedback to the central dogma: cytoplasmic mRNA decay and transcription are interdependent processes.

    Hartenian, Ella / Glaunsinger, Britt A

    Critical reviews in biochemistry and molecular biology

    2019  Volume 54, Issue 4, Page(s) 385–398

    Abstract: Transcription and RNA decay are key determinants of gene expression; these processes are typically considered as the uncoupled beginning and end of the messenger RNA (mRNA) lifecycle. Here we describe the growing number of studies demonstrating interplay ...

    Abstract Transcription and RNA decay are key determinants of gene expression; these processes are typically considered as the uncoupled beginning and end of the messenger RNA (mRNA) lifecycle. Here we describe the growing number of studies demonstrating interplay between these spatially disparate processes in eukaryotes. Specifically, cells can maintain mRNA levels by buffering against changes in mRNA stability or transcription, and can also respond to virally induced accelerated decay by reducing RNA polymerase II gene expression. In addition to these global responses, there is also evidence that mRNAs containing a premature stop codon can cause transcriptional upregulation of homologous genes in a targeted fashion. In each of these systems, RNA binding proteins (RBPs), particularly those involved in mRNA degradation, are critical for cytoplasmic to nuclear communication. Although their specific mechanistic contributions are yet to be fully elucidated, differential trafficking of RBPs between subcellular compartments are likely to play a central role in regulating this gene expression feedback pathway.
    MeSH term(s) Animals ; Cell Nucleus/genetics ; Cell Nucleus/metabolism ; Codon, Terminator/genetics ; Cytoplasm/genetics ; Cytoplasm/metabolism ; Exoribonucleases/metabolism ; Gene Expression ; Homeostasis/genetics ; Humans ; Infections/genetics ; Microtubule-Associated Proteins/metabolism ; RNA Polymerase II/genetics ; RNA Polymerase II/metabolism ; RNA Stability/genetics ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; RNA-Binding Proteins/genetics ; Transcription, Genetic
    Chemical Substances Codon, Terminator ; Microtubule-Associated Proteins ; RNA, Messenger ; RNA-Binding Proteins ; RNA Polymerase II (EC 2.7.7.-) ; Exoribonucleases (EC 3.1.-) ; XRN1 protein, human (EC 3.1.13.1)
    Keywords covid19
    Language English
    Publishing date 2019-10-27
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 1000977-2
    ISSN 1549-7798 ; 1381-3455 ; 1040-9238
    ISSN (online) 1549-7798
    ISSN 1381-3455 ; 1040-9238
    DOI 10.1080/10409238.2019.1679083
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    Zs.A 1024: Show issues Location:
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  4. Article ; Online: Cytoplasmic mRNA decay represses RNA polymerase II transcription during early apoptosis.

    Duncan-Lewis, Christopher / Hartenian, Ella / King, Valeria / Glaunsinger, Britt A

    eLife

    2021  Volume 10

    Abstract: RNA abundance is generally sensitive to perturbations in decay and synthesis rates, but crosstalk between RNA polymerase II transcription and cytoplasmic mRNA degradation often leads to compensatory changes in gene expression. Here, we reveal that ... ...

    Abstract RNA abundance is generally sensitive to perturbations in decay and synthesis rates, but crosstalk between RNA polymerase II transcription and cytoplasmic mRNA degradation often leads to compensatory changes in gene expression. Here, we reveal that widespread mRNA decay during early apoptosis represses RNAPII transcription, indicative of positive (rather than compensatory) feedback. This repression requires active cytoplasmic mRNA degradation, which leads to impaired recruitment of components of the transcription preinitiation complex to promoter DNA. Importin α/β-mediated nuclear import is critical for this feedback signaling, suggesting that proteins translocating between the cytoplasm and nucleus connect mRNA decay to transcription. We also show that an analogous pathway activated by viral nucleases similarly depends on nuclear protein import. Collectively, these data demonstrate that accelerated mRNA decay leads to the repression of mRNA transcription, thereby amplifying the shutdown of gene expression. This highlights a conserved gene regulatory mechanism by which cells respond to threats.
    MeSH term(s) Active Transport, Cell Nucleus ; Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Cytoplasm/genetics ; Cytoplasm/metabolism ; Feedback, Physiological ; Gene Expression Regulation, Neoplastic ; HCT116 Cells ; HEK293 Cells ; HeLa Cells ; Humans ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/pathology ; RNA Polymerase II/genetics ; RNA Polymerase II/metabolism ; RNA Stability ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; RNA, Neoplasm/genetics ; RNA, Neoplasm/metabolism ; Time Factors ; Transcription, Genetic ; alpha Karyopherins/metabolism ; beta Karyopherins/metabolism
    Chemical Substances Antineoplastic Agents ; RNA, Messenger ; RNA, Neoplasm ; alpha Karyopherins ; beta Karyopherins ; RNA Polymerase II (EC 2.7.7.-)
    Language English
    Publishing date 2021-06-04
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2687154-3
    ISSN 2050-084X ; 2050-084X
    ISSN (online) 2050-084X
    ISSN 2050-084X
    DOI 10.7554/eLife.58342
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  5. Article ; Online: DNA processing by the Kaposi's sarcoma-associated herpesvirus alkaline exonuclease SOX contributes to viral gene expression and infectious virion production.

    Hartenian, Ella / Mendez, Aaron S / Didychuk, Allison L / Khosla, Shivani / Glaunsinger, Britt A

    Nucleic acids research

    2022  Volume 51, Issue 1, Page(s) 182–197

    Abstract: Alkaline exonucleases (AE) are present in several large DNA viruses including bacteriophage λ and herpesviruses, where they play roles in viral DNA processing during genome replication. Given the genetic conservation of AEs across viruses infecting ... ...

    Abstract Alkaline exonucleases (AE) are present in several large DNA viruses including bacteriophage λ and herpesviruses, where they play roles in viral DNA processing during genome replication. Given the genetic conservation of AEs across viruses infecting different kingdoms of life, these enzymes likely assume central roles in the lifecycles of viruses where they have yet to be well characterized. Here, we applied a structure-guided functional analysis of the bifunctional AE in the oncogenic human gammaherpesvirus Kaposi's sarcoma-associated herpesvirus (KSHV), called SOX. In addition to identifying a preferred DNA substrate preference for SOX, we define key residues important for DNA binding and DNA processing, and how SOX activity on DNA partially overlaps with its functionally separable cleavage of mRNA. By engineering these SOX mutants into KSHV, we reveal roles for its DNase activity in viral gene expression and infectious virion production. Our results provide mechanistic insight into gammaherpesviral AE activity as well as areas of functional conservation between this mammalian virus AE and its distant relative in phage λ.
    MeSH term(s) Animals ; Humans ; DNA, Viral/metabolism ; Exonucleases/genetics ; Gene Expression ; Gene Expression Regulation, Viral ; Herpesvirus 8, Human/metabolism ; Mammals/genetics ; Virion/metabolism ; Virus Replication
    Chemical Substances DNA, Viral ; Exonucleases (EC 3.1.-)
    Language English
    Publishing date 2022-12-19
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 186809-3
    ISSN 1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
    ISSN (online) 1362-4962 ; 1362-4954
    ISSN 0301-5610 ; 0305-1048
    DOI 10.1093/nar/gkac1190
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    Zs.A 1067: Show issues Location:
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  6. Article ; Online: Cytoplasmic mRNA decay represses RNA polymerase II transcription during early apoptosis

    Christopher Duncan-Lewis / Ella Hartenian / Valeria King / Britt A Glaunsinger

    eLife, Vol

    2021  Volume 10

    Abstract: RNA abundance is generally sensitive to perturbations in decay and synthesis rates, but crosstalk between RNA polymerase II transcription and cytoplasmic mRNA degradation often leads to compensatory changes in gene expression. Here, we reveal that ... ...

    Abstract RNA abundance is generally sensitive to perturbations in decay and synthesis rates, but crosstalk between RNA polymerase II transcription and cytoplasmic mRNA degradation often leads to compensatory changes in gene expression. Here, we reveal that widespread mRNA decay during early apoptosis represses RNAPII transcription, indicative of positive (rather than compensatory) feedback. This repression requires active cytoplasmic mRNA degradation, which leads to impaired recruitment of components of the transcription preinitiation complex to promoter DNA. Importin α/β-mediated nuclear import is critical for this feedback signaling, suggesting that proteins translocating between the cytoplasm and nucleus connect mRNA decay to transcription. We also show that an analogous pathway activated by viral nucleases similarly depends on nuclear protein import. Collectively, these data demonstrate that accelerated mRNA decay leads to the repression of mRNA transcription, thereby amplifying the shutdown of gene expression. This highlights a conserved gene regulatory mechanism by which cells respond to threats.
    Keywords apoptosis ; RNA decay ; RNA polymerase II ; feedback ; PNPT1 ; dis3l2 ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
    Language English
    Publishing date 2021-06-01T00:00:00Z
    Publisher eLife Sciences Publications Ltd
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article ; Online: Xrn1 activity broadly represses RNA polymerase II occupancy at mammalian but not viral promoters during herpesvirus infection

    Hartenian, Ella N / Glaunsinger, Britt A

    bioRxiv

    Abstract: In mammalian cells, widespread acceleration of cytoplasmic mRNA degradation is linked to impaired RNA polymerase II (Pol II) transcription. This mRNA decay-induced transcriptional repression occurs during infection with gammaherpesviruses including ... ...

    Abstract In mammalian cells, widespread acceleration of cytoplasmic mRNA degradation is linked to impaired RNA polymerase II (Pol II) transcription. This mRNA decay-induced transcriptional repression occurs during infection with gammaherpesviruses including Kaposi’s sarcoma-associated herpesvirus (KSHV) and murine gammaherpesvirus 68 (MHV68), which encode an mRNA endonuclease that initiates widespread RNA decay. Here, we show that MHV68-induced mRNA decay leads to a genome-wide reduction of Pol II occupancy at mammalian promoters, which requires the cellular 5’-3’ exonuclease Xrn1. Viral genes, despite the fact that they require Pol II for transcription, escape this transcriptional repression. Protection is not governed by viral promoter sequences; instead, location on the viral genome is both necessary and sufficient to escape the transcriptional repression effects of mRNA decay. We hypothesize that the ability to escape from transcriptional repression is linked to the conformation of viral DNA in replication compartments, providing a means for these viruses to counteract decay-induced viral transcript loss.
    Keywords covid19
    Publisher BioRxiv; MedRxiv
    Document type Article ; Online
    DOI 10.1101/585984
    Database COVID19

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  8. Article ; Online: Herpesvirus infection reduces Pol II occupancy of host promoters but spares viral promoters

    Ella N Hartenian / Britt A Glaunsinger

    Abstract: AbstractIn mammalian cells, widespread acceleration of cytoplasmic mRNA degradation is linked to impaired RNA polymerase II (Pol II) transcription. This mRNA decay-induced transcriptional repression occurs during infection with gammaherpesviruses ... ...

    Abstract AbstractIn mammalian cells, widespread acceleration of cytoplasmic mRNA degradation is linked to impaired RNA polymerase II (Pol II) transcription. This mRNA decay-induced transcriptional repression occurs during infection with gammaherpesviruses including Kaposi’s sarcoma-associated herpesvirus (KSHV) and murine gammaherpesvirus 68 (MHV68), which encode an mRNA endonuclease that initiates widespread RNA decay. Here, we show that MHV68-induced mRNA decay leads to a genome-wide reduction of Pol II occupancy at mammalian promoters. Viral genes, despite the fact that they require Pol II for transcription, escape this transcriptional repression. Protection is not governed by viral promoter sequences; instead, location on the viral genome is both necessary and sufficient to escape the transcriptional repression effects of mRNA decay. We hypothesize that the ability to escape from transcriptional repression is linked to the localization of viral DNA in replication compartments, providing a means for these viruses to counteract decay-induced viral transcript loss.
    Keywords covid19
    Publisher biorxiv
    Document type Article ; Online
    DOI 10.1101/585984
    Database COVID19

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  9. Article ; Online: Genetic screens and functional genomics using CRISPR/Cas9 technology.

    Hartenian, Ella / Doench, John G

    The FEBS journal

    2015  Volume 282, Issue 8, Page(s) 1383–1393

    Abstract: Functional genomics attempts to understand the genome by perturbing the flow of information from DNA to RNA to protein, in order to learn how gene dysfunction leads to disease. CRISPR/Cas9 technology is the newest tool in the geneticist's toolbox, ... ...

    Abstract Functional genomics attempts to understand the genome by perturbing the flow of information from DNA to RNA to protein, in order to learn how gene dysfunction leads to disease. CRISPR/Cas9 technology is the newest tool in the geneticist's toolbox, allowing researchers to edit DNA with unprecedented ease, speed and accuracy, and representing a novel means to perform genome-wide genetic screens to discover gene function. In this review, we first summarize the discovery and characterization of CRISPR/Cas9, and then compare it to other genome engineering technologies. We discuss its initial use in screening applications, with a focus on optimizing on-target activity and minimizing off-target effects. Finally, we comment on future challenges and opportunities afforded by this technology.
    MeSH term(s) CRISPR-Associated Proteins/physiology ; Clustered Regularly Interspaced Short Palindromic Repeats/genetics ; Gene Expression Regulation ; Genetic Engineering/methods ; Genetic Testing ; Genome, Human ; Humans ; RNA Editing/genetics
    Chemical Substances CRISPR-Associated Proteins
    Language English
    Publishing date 2015-04
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2173655-8
    ISSN 1742-4658 ; 1742-464X
    ISSN (online) 1742-4658
    ISSN 1742-464X
    DOI 10.1111/febs.13248
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    Zs.A 260: Show issues Location:
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  10. Article ; Online: The molecular virology of coronaviruses.

    Hartenian, Ella / Nandakumar, Divya / Lari, Azra / Ly, Michael / Tucker, Jessica M / Glaunsinger, Britt A

    The Journal of biological chemistry

    2020  Volume 295, Issue 37, Page(s) 12910–12934

    Abstract: Few human pathogens have been the focus of as much concentrated worldwide attention as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the cause of COVID-19. Its emergence into the human population and ensuing pandemic came on the heels of ... ...

    Abstract Few human pathogens have been the focus of as much concentrated worldwide attention as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the cause of COVID-19. Its emergence into the human population and ensuing pandemic came on the heels of severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV), two other highly pathogenic coronavirus spillovers, which collectively have reshaped our view of a virus family previously associated primarily with the common cold. It has placed intense pressure on the collective scientific community to develop therapeutics and vaccines, whose engineering relies on a detailed understanding of coronavirus biology. Here, we present the molecular virology of coronavirus infection, including its entry into cells, its remarkably sophisticated gene expression and replication mechanisms, its extensive remodeling of the intracellular environment, and its multifaceted immune evasion strategies. We highlight aspects of the viral life cycle that may be amenable to antiviral targeting as well as key features of its biology that await discovery.
    MeSH term(s) Animals ; Antigens, Viral/immunology ; Coronavirus/genetics ; Coronavirus/immunology ; Coronavirus/physiology ; Coronavirus Infections/genetics ; Coronavirus Infections/immunology ; Coronavirus Infections/virology ; Gene Expression Regulation, Viral ; Host-Pathogen Interactions ; Humans ; Virus Physiological Phenomena
    Chemical Substances Antigens, Viral
    Keywords covid19
    Language English
    Publishing date 2020-07-13
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.REV120.013930
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