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Start Over Descriptor "dosage imbalance" Journal trends in cell biology
2 results on '"dosage imbalance"'

1. Aging: Somatic Mutations, Epigenetic Drift and Gene Dosage Imbalance.

Author

Veitia, Reiner A., Govindaraju, Diddahally R., Bottani, Samuel, and Birchler, James A.

Subjects
*AGING, *SOMATIC mutation, *GENE dosage, *EPIGENETICS, *METABOLISM
Abstract

Aging involves a progressive decline of metabolic function and an increased incidence of late-onset degenerative disorders and cancer. To a large extent, these processes are influenced by alterations affecting the integrity of genome architecture and, ultimately, its phenotypic expression. Despite the progress made towards establishing causal links between genomic and epigenomic changes and aging, mechanisms underlying metabolic dysregulation and age-related phenotypes remain obscure. Here, we present a model linking genome-wide changes and their age-related phenotypic consequences via the alteration of macromolecular complexes and cellular networks. This approach may provide a better understanding of the dynamically changing genome–phenome map with age, but also deeper insights to developing more targeted therapies to prevent and/or manage late-onset degenerative disorders as well as decelerate aging. [ABSTRACT FROM AUTHOR]

Published
2017
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2. Aging: Somatic Mutations, Epigenetic Drift and Gene Dosage Imbalance

Author

James A. Birchler, Samuel Bottani, Reiner A. Veitia, Diddahally R. Govindaraju, Institut Jacques Monod (IJM (UMR_7592)), Université Paris Diderot - Paris 7 (UPD7)-Centre National de la Recherche Scientifique (CNRS), Université Sorbonne Paris Cité (USPC), Matière et Systèmes Complexes (MSC (UMR_7057)), Centre National de la Recherche Scientifique (CNRS)-Université Paris Diderot - Paris 7 (UPD7), Department of Human Evolutionary Biology, Harvard University [Cambridge], Division of Biological Sciences [Columbia], University of Missouri [Columbia] (Mizzou), University of Missouri System-University of Missouri System, University Paris Diderot, Centre National de la Recherche Scientifique, Fondation pour le Recherche Medicale, National Science Foundation grant I05-1545780, ANR-10-BINF-0006,Iceberg,Des modèles de population aux populations de modèles: observation, modélisation et contrôle de l'expression génique au niveau de la cellule unique(2010), Department of Human Evolutionary Biology, Cambridge, University of Missouri [Columbia], and ANR-10-BINF-06-11,Iceberg,Des modèles de population aux populations de modèles: observation, modélisation et contrôle de l’expression génique au niveau de la cellule unique(2011)

Subjects
0301 basic medicine, Senescence, Aging, senescence, Degenerative Disorder, Somatic cell, Gene Dosage, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, Biology, medicine.disease_cause, Gene dosage, Models, Biological, dosage imbalance, Epigenesis, Genetic, epigenetic drift, 03 medical and health sciences, medicine, Animals, Humans, Epigenetics, mutational load, Epigenomics, Genetics, genomic integrity, Mutation, [SDV.GEN]Life Sciences [q-bio]/Genetics, Cell Biology, Phenotype, 030104 developmental biology, epigenetic clock
Abstract

International audience; Aging involves a progressive decline of metabolic function and an increased incidence of late-onset degenerative disorders and cancer. To a large extent, these processes are influenced by alterations affecting the integrity of genome architecture and, ultimately, its phenotypic expression. Despite the progress made towards establishing causal links between genomic and epigenomic changes and aging, mechanisms underlying metabolic dysregulation and age-related phenotypes remain obscure. Here, we present a model linking genome-wide changes and their age-related phenotypic consequences via the alteration of macromolecular complexes and cellular networks. This approach may provide a better understanding of the dynamically changing genome-phenome map with age, but also deeper insights to developing more targeted therapies to prevent and/or manage late-onset degenerative disorders as well as decelerate aging.

Published
2016
Full Text
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