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  1. Article ; Online: Evaluation of Chen et al.: Overexpression of Protein Complexes and Aneuploidy.

    Amon, Angelika

    Cell systems

    2019  Volume 9, Issue 2, Page(s) 107–108

    Abstract: One snapshot of the peer review process for "Overdosage of Balanced Protein Complexes Reduces Proliferation Rate in Aneuploid Cells" (Chen et al., 2019). ...

    Abstract One snapshot of the peer review process for "Overdosage of Balanced Protein Complexes Reduces Proliferation Rate in Aneuploid Cells" (Chen et al., 2019).
    MeSH term(s) Aneuploidy ; Cell Proliferation ; Humans
    Language English
    Publishing date 2019-08-28
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Comment
    ISSN 2405-4720
    ISSN (online) 2405-4720
    DOI 10.1016/j.cels.2019.08.004
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Decreasing mitochondrial RNA polymerase activity reverses biased inheritance of hypersuppressive mtDNA.

    Corbi, Daniel / Amon, Angelika

    PLoS genetics

    2021  Volume 17, Issue 10, Page(s) e1009808

    Abstract: Faithful inheritance of mitochondrial DNA (mtDNA) is crucial for cellular respiration/oxidative phosphorylation and mitochondrial membrane potential. However, how mtDNA is transmitted to progeny is not fully understood. We utilized hypersuppressive mtDNA, ...

    Abstract Faithful inheritance of mitochondrial DNA (mtDNA) is crucial for cellular respiration/oxidative phosphorylation and mitochondrial membrane potential. However, how mtDNA is transmitted to progeny is not fully understood. We utilized hypersuppressive mtDNA, a class of respiratory deficient Saccharomyces cerevisiae mtDNA that is preferentially inherited over wild-type mtDNA (rho+), to uncover the factors governing mtDNA inheritance. We found that some regions of rho+ mtDNA persisted while others were lost after a specific hypersuppressive takeover indicating that hypersuppressive preferential inheritance may partially be due to active destruction of rho+ mtDNA. From a multicopy suppression screen, we found that overexpression of putative mitochondrial RNA exonuclease PET127 reduced biased inheritance of a subset of hypersuppressive genomes. This suppression required PET127 binding to the mitochondrial RNA polymerase RPO41 but not PET127 exonuclease activity. A temperature-sensitive allele of RPO41 improved rho+ mtDNA inheritance over a specific hypersuppressive mtDNA at semi-permissive temperatures revealing a previously unknown role for rho+ transcription in promoting hypersuppressive mtDNA inheritance.
    MeSH term(s) DNA Replication/genetics ; DNA, Fungal/genetics ; DNA, Mitochondrial/genetics ; DNA-Directed RNA Polymerases/genetics ; Genes, Fungal/genetics ; Mitochondria/genetics ; RNA, Mitochondrial/genetics ; Replication Origin/genetics ; Saccharomyces cerevisiae/genetics ; Saccharomyces cerevisiae Proteins/genetics ; Transcription, Genetic/genetics
    Chemical Substances DNA, Fungal ; DNA, Mitochondrial ; RNA, Mitochondrial ; Saccharomyces cerevisiae Proteins ; DNA-Directed RNA Polymerases (EC 2.7.7.6)
    Language English
    Publishing date 2021-10-19
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2186725-2
    ISSN 1553-7404 ; 1553-7390
    ISSN (online) 1553-7404
    ISSN 1553-7390
    DOI 10.1371/journal.pgen.1009808
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  3. Article ; Online: A case for more curiosity-driven basic research.

    Amon, Angelika

    Molecular biology of the cell

    2015  Volume 26, Issue 21, Page(s) 3690–3691

    Abstract: Having been selected to be among the exquisitely talented scientists who won the Sandra K. Masur Senior Leadership Award is a tremendous honor. I would like to take this opportunity to make the case for a conviction of mine that I think many will ... ...

    Abstract Having been selected to be among the exquisitely talented scientists who won the Sandra K. Masur Senior Leadership Award is a tremendous honor. I would like to take this opportunity to make the case for a conviction of mine that I think many will consider outdated. I am convinced that we need more curiosity-driven basic research aimed at understanding the principles governing life. The reasons are simple: 1) we need to learn more about the world around us; and 2) a robust and diverse basic research enterprise will bring ideas and approaches essential for developing new medicines and improving the lives of humankind.
    MeSH term(s) Awards and Prizes ; Biomedical Research ; Exploratory Behavior ; Humans ; Knowledge
    Language English
    Publishing date 2015-11-01
    Publishing country United States
    Document type Journal Article ; Personal Narratives
    ZDB-ID 1098979-1
    ISSN 1939-4586 ; 1059-1524
    ISSN (online) 1939-4586
    ISSN 1059-1524
    DOI 10.1091/mbc.E15-06-0430
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  4. Article ; Online: Relevance and Regulation of Cell Density.

    Neurohr, Gabriel E / Amon, Angelika

    Trends in cell biology

    2020  Volume 30, Issue 3, Page(s) 213–225

    Abstract: Cell density shows very little variation within a given cell type. For example, in humans variability in cell density among cells of a given cell type is 100 times smaller than variation in cell mass. This tight control indicates that maintenance of a ... ...

    Abstract Cell density shows very little variation within a given cell type. For example, in humans variability in cell density among cells of a given cell type is 100 times smaller than variation in cell mass. This tight control indicates that maintenance of a cell type-specific cell density is important for cell function. Indeed, pathological conditions such as cellular senescence are accompanied by changes in cell density. Despite the apparent importance of cell-type-specific density, we know little about how cell density affects cell function, how it is controlled, and how it sometimes changes as part of a developmental process or in response to changes in the environment. The recent development of new technologies to accurately measure the cell density of single cells in suspension and in tissues is likely to provide answers to these important questions.
    MeSH term(s) Animals ; Cell Count ; Cells/cytology ; Cytological Techniques ; Humans ; Models, Biological
    Language English
    Publishing date 2020-01-21
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 30122-x
    ISSN 1879-3088 ; 0962-8924
    ISSN (online) 1879-3088
    ISSN 0962-8924
    DOI 10.1016/j.tcb.2019.12.006
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  5. Article ; Online: Context is everything: aneuploidy in cancer.

    Ben-David, Uri / Amon, Angelika

    Nature reviews. Genetics

    2019  Volume 21, Issue 1, Page(s) 44–62

    Abstract: Cancer is driven by multiple types of genetic alterations, which range in size from point mutations to whole-chromosome gains and losses, known as aneuploidy. Chromosome instability, the process that gives rise to aneuploidy, can promote tumorigenesis by ...

    Abstract Cancer is driven by multiple types of genetic alterations, which range in size from point mutations to whole-chromosome gains and losses, known as aneuploidy. Chromosome instability, the process that gives rise to aneuploidy, can promote tumorigenesis by increasing genetic heterogeneity and promoting tumour evolution. However, much less is known about how aneuploidy itself contributes to tumour formation and progression. Unlike some pan-cancer oncogenes and tumour suppressor genes that drive transformation in virtually all cell types and cellular contexts, aneuploidy is not a universal promoter of tumorigenesis. Instead, recent studies suggest that aneuploidy is a context-dependent, cancer-type-specific oncogenic event that may have clinical relevance as a prognostic marker and as a potential therapeutic target.
    MeSH term(s) Aneuploidy ; Animals ; Cell Transformation, Neoplastic/pathology ; Chromosomal Instability ; Humans ; Neoplasms/genetics ; Neoplasms/pathology ; Phenotype
    Language English
    Publishing date 2019-09-23
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 2035157-4
    ISSN 1471-0064 ; 1471-0056
    ISSN (online) 1471-0064
    ISSN 1471-0056
    DOI 10.1038/s41576-019-0171-x
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  6. Article ; Online: Why haploinsufficiency persists.

    Morrill, Summer A / Amon, Angelika

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

    2019  Volume 116, Issue 24, Page(s) 11866–11871

    Abstract: Haploinsufficiency describes the decrease in organismal fitness observed when a single copy of a gene is deleted in diploids. We investigated the origin of haploinsufficiency by creating a comprehensive dosage sensitivity data set for genes under their ... ...

    Abstract Haploinsufficiency describes the decrease in organismal fitness observed when a single copy of a gene is deleted in diploids. We investigated the origin of haploinsufficiency by creating a comprehensive dosage sensitivity data set for genes under their native promoters. We demonstrate that the expression of haploinsufficient genes is limited by the toxicity of their overexpression. We further show that the fitness penalty associated with excess gene copy number is not the only determinant of haploinsufficiency. Haploinsufficient genes represent a unique subset of genes sensitive to copy number increases, as they are also limiting for important cellular processes when present in one copy instead of two. The selective pressure to decrease gene expression due to the toxicity of overexpression, combined with the pressure to increase expression due to their fitness-limiting nature, has made haploinsufficient genes extremely sensitive to changes in gene expression. As a consequence, haploinsufficient genes are dosage stabilized, showing much more narrow ranges in cell-to-cell variability of expression compared with other genes in the genome. We propose a dosage-stabilizing hypothesis of haploinsufficiency to explain its persistence over evolutionary time.
    MeSH term(s) Cell Survival/genetics ; Gene Dosage/genetics ; Gene Expression/genetics ; Genome/genetics ; Haploinsufficiency/genetics ; Promoter Regions, Genetic/genetics ; Yeasts/genetics
    Language English
    Publishing date 2019-05-29
    Publishing country United States
    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.
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.1900437116
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  7. Article ; Online: More to the story. Interview by Kristie Nybo.

    Amon, Angelika

    BioTechniques

    2013  Volume 55, Issue 3, Page(s) 103

    MeSH term(s) Aneuploidy ; Animals ; Cell Cycle/physiology ; Cytological Techniques/methods ; Humans ; Meiosis/physiology ; Mitosis/physiology
    Language English
    Publishing date 2013-09
    Publishing country England
    Document type Interview
    ZDB-ID 48453-2
    ISSN 1940-9818 ; 0736-6205
    ISSN (online) 1940-9818
    ISSN 0736-6205
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  8. Article ; Online: Cross-compartment signal propagation in the mitotic exit network.

    Zhou, Xiaoxue / Li, Wenxue / Liu, Yansheng / Amon, Angelika

    eLife

    2021  Volume 10

    Abstract: In budding yeast, the mitotic exit network (MEN), a GTPase signaling cascade, integrates spatial and temporal cues to promote exit from mitosis. This signal integration requires transmission of a signal generated on the cytoplasmic face of spindle pole ... ...

    Abstract In budding yeast, the mitotic exit network (MEN), a GTPase signaling cascade, integrates spatial and temporal cues to promote exit from mitosis. This signal integration requires transmission of a signal generated on the cytoplasmic face of spindle pole bodies (SPBs; yeast equivalent of centrosomes) to the nucleolus, where the MEN effector protein Cdc14 resides. Here, we show that the MEN activating signal at SPBs is relayed to Cdc14 in the nucleolus through the dynamic localization of its terminal kinase complex Dbf2-Mob1. Cdc15, the protein kinase that activates Dbf2-Mob1 at SPBs, also regulates its nuclear access. Once in the nucleus, priming phosphorylation of Cfi1/Net1, the nucleolar anchor of Cdc14, by the Polo-like kinase Cdc5 targets Dbf2-Mob1 to the nucleolus. Nucleolar Dbf2-Mob1 then phosphorylates Cfi1/Net1 and Cdc14, activating Cdc14. The kinase-primed transmission of the MEN signal from the cytoplasm to the nucleolus exemplifies how signaling cascades can bridge distant inputs and responses.
    MeSH term(s) Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Mitosis/genetics ; Protein Tyrosine Phosphatases/genetics ; Protein Tyrosine Phosphatases/metabolism ; Saccharomyces cerevisiae/genetics ; Saccharomyces cerevisiae/physiology ; Saccharomyces cerevisiae Proteins/genetics ; Saccharomyces cerevisiae Proteins/metabolism ; Signal Transduction
    Chemical Substances CDC14 protein, S cerevisiae ; Cell Cycle Proteins ; Saccharomyces cerevisiae Proteins ; Protein Tyrosine Phosphatases (EC 3.1.3.48)
    Language English
    Publishing date 2021-01-22
    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.63645
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  9. Article ; Online: Angelika Amon.

    Amon, Angelika

    Current biology : CB

    2012  Volume 23, Issue 20, Page(s) R906–7

    MeSH term(s) Aneuploidy ; Animals ; Austria ; Boston ; Cell Cycle ; Chromosome Segregation ; Drosophila/genetics ; History, 20th Century ; History, 21st Century ; Research Design ; Saccharomycetales/cytology ; Saccharomycetales/genetics
    Language English
    Publishing date 2012-10-08
    Publishing country England
    Document type Biography ; Historical Article ; Interview ; Research Support, Non-U.S. Gov't
    ZDB-ID 1071731-6
    ISSN 1879-0445 ; 0960-9822
    ISSN (online) 1879-0445
    ISSN 0960-9822
    DOI 10.1016/j.cub.2013.09.022
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  10. Article ; Online: Unanticipated success stories: an interview with Angelika Amon.

    Amon, Angelika B

    Genetics

    2014  Volume 198, Issue 2, Page(s) 425–426

    Abstract: THE Genetics Society of America Medal is awarded to an individual for outstanding contributions to the field of genetics in the past 15 years. Recipients of the GSA Medal are recognized for elegant and highly meaningful contributions to modern genetics. ... ...

    Abstract THE Genetics Society of America Medal is awarded to an individual for outstanding contributions to the field of genetics in the past 15 years. Recipients of the GSA Medal are recognized for elegant and highly meaningful contributions to modern genetics. The 2014 recipient, Angelika B. Amon, has uncovered key principles governing the cell cycle and was the first to demonstrate a connection between the physical completion of anaphase and the initiation of mitotic exit. More recently, her research has focused on the consequences of aneuploidy. GENETICS spoke with Dr. Amon about her approach to science and what is next on the horizon.
    MeSH term(s) Awards and Prizes ; Cell Cycle ; Genes, Fungal ; Humans ; Yeasts/cytology ; Yeasts/genetics
    Language English
    Publishing date 2014-10-14
    Publishing country United States
    Document type Interview ; Portrait
    ZDB-ID 2167-2
    ISSN 1943-2631 ; 0016-6731
    ISSN (online) 1943-2631
    ISSN 0016-6731
    DOI 10.1534/genetics.114.169094
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