Special Issue "The Epigenetics of Aging and Longevity"

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Human Genomics and Genetic Diseases".

Deadline for manuscript submissions: closed (31 October 2017)

Special Issue Editors

Guest Editor
Prof. Dr. Jessica Tyler

Weill Cornell Medicine, Department of Pathology and Laboratory Medicine, New York, NY, USA
Website | E-Mail
Interests: Chromatin assembly, histone modifications, chromatin remodeling, DNA double strand break repair, replicative aging
Guest Editor
Dr. Jay E. Johnson

Orentreich Foundation for the Advancement of Science, Cold Spring, NY, USA
Website | E-Mail
Interests: methionine restriction, chronological lifespan, Saccharomyces cerevisiae, budding yeast, aging, healthspan, longevity, senescence, autophagy

Special Issue Information

Dear Colleagues,

A growing body of evidence demonstrates that both genetic and epigenetic alterations contribute to aging. In contrast to genetic changes, the reversible nature of epigenetic mechanisms makes these pathways promising avenues for the development of regimens against age-related decline and disease.

With the advent of techniques for genome-wide analysis of histone modifications and DNA methylation, we are now learning that aging is accompanied by a wealth of changes to the epigenetic information. These age-associated changes in the epigenetic information alter the chromatin structure over time, in turn causing transcriptional changes, genomic instability and activation of transposons that drive the aging process. Furthermore, small molecules are being utilized to alter the epigenetic information in order to counter the aging process in model organisms. The best-characterized pathway connecting the environment to the epigenome is nutrient signaling. Exciting progress is being made in understanding how nutrients influence aging and how nutrients, including altered diets, can be utilized to promote longevity.

In this Special Issue, we would like to invite submissions of original research or review articles on topics relevant to “the epigenetics of aging and longevity”. We hope to gather together knowledge to empower efforts towards the effective and safe extension of lifespan and health span in humans. We look forward to receiving your contributions.

Prof. Dr. Jessica Tyler
Dr. Jay E. Johnson
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Genes is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • replicative lifespan
  • chronological lifespan
  • longevity
  • aging
  • health span
  • dietary restriction
  • methionine restriction
  • autophagy
  • epigenome
  • epigenetics

Published Papers (4 papers)

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Research

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Open AccessArticle Linking DNA Damage and Age-Related Promoter DNA Hyper-Methylation in the Intestine
Genes 2018, 9(1), 17; doi:10.3390/genes9010017
Received: 20 November 2017 / Revised: 21 December 2017 / Accepted: 21 December 2017 / Published: 5 January 2018
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Abstract
Aberrant DNA methylation in stem cells is a hallmark of aging and tumor development. Here, we explore whether and how DNA damage repair might impact on these time-dependent changes, in particular in proliferative intestinal stem cells. We introduce a 3D multiscale computer model
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Aberrant DNA methylation in stem cells is a hallmark of aging and tumor development. Here, we explore whether and how DNA damage repair might impact on these time-dependent changes, in particular in proliferative intestinal stem cells. We introduce a 3D multiscale computer model of intestinal crypts enabling simulation of aberrant DNA and histone methylation of gene promoters during aging. We assume histone state-dependent activity of de novo DNA methyltransferases (DNMTs) and methylation-dependent binding of maintenance DNMTs to CpGs. We simulate aging with and without repeated DNA repair. Motivated by recent findings on the histone demethylase KDM2b, we consider that DNA repair is associated with chromatin opening and improved recruitment of de novo DNMTs. Our results suggest that methylation-dependent binding of maintenance DNMTs to CpGs, establishing bistable DNA methylation states, is a prerequisite to promoter hyper-methylation following DNA repair. With this, the transient increase in de novo DNMT activity during repair can induce switches from low to high methylation states. These states remain stable after repair, leading to an epigenetic drift. The switches are most frequent in genes with H3K27me3 modified promoters. Our model provides a mechanistic explanation on how even successful DNA repair might confer long term changes of the epigenome. Full article
(This article belongs to the Special Issue The Epigenetics of Aging and Longevity)
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Review

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Open AccessReview Age-Related Epigenetic Derangement upon Reprogramming and Differentiation of Cells from the Elderly
Genes 2018, 9(1), 39; doi:10.3390/genes9010039
Received: 31 October 2017 / Revised: 22 December 2017 / Accepted: 10 January 2018 / Published: 16 January 2018
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Abstract
Aging is a complex multi-layered phenomenon. The study of aging in humans is based on the use of biological material from hard-to-gather tissues and highly specific cohorts. The introduction of cell reprogramming techniques posed promising features for medical practice and basic research. Recently,
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Aging is a complex multi-layered phenomenon. The study of aging in humans is based on the use of biological material from hard-to-gather tissues and highly specific cohorts. The introduction of cell reprogramming techniques posed promising features for medical practice and basic research. Recently, a growing number of studies have been describing the generation of induced pluripotent stem cells (iPSCs) from old or centenarian biologic material. Nonetheless, Reprogramming techniques determine a profound remodelling on cell epigenetic architecture whose extent is still largely debated. Given that cell epigenetic profile changes with age, the study of cell-fate manipulation approaches on cells deriving from old donors or centenarians may provide new insights not only on regenerative features and physiology of these cells, but also on reprogramming-associated and age-related epigenetic derangement. Full article
(This article belongs to the Special Issue The Epigenetics of Aging and Longevity)
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Open AccessReview Histone MacroH2A1: A Chromatin Point of Intersection between Fasting, Senescence and Cellular Regeneration
Genes 2017, 8(12), 367; doi:10.3390/genes8120367
Received: 26 October 2017 / Revised: 27 November 2017 / Accepted: 30 November 2017 / Published: 5 December 2017
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Abstract
Histone variants confer chromatin unique properties. They have specific genomic distribution, regulated by specific deposition and removal machineries. Histone variants, mostly of canonical histones H2A, H2B and H3, have important roles in early embryonic development, in lineage commitment of stem cells, in the
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Histone variants confer chromatin unique properties. They have specific genomic distribution, regulated by specific deposition and removal machineries. Histone variants, mostly of canonical histones H2A, H2B and H3, have important roles in early embryonic development, in lineage commitment of stem cells, in the converse process of somatic cell reprogramming to pluripotency and, in some cases, in the modulation of animal aging and life span. MacroH2A1 is a variant of histone H2A, present in two alternatively exon-spliced isoforms macroH2A1.1 and macroH2A1.2, regulating cell plasticity and proliferation, during pluripotency and tumorigenesis. Furthermore, macroH2A1 participates in the formation of senescence-associated heterochromatic foci (SAHF) in senescent cells, and multiple lines of evidence in genetically modified mice suggest that macroH2A1 integrates nutritional cues from the extracellular environment to transcriptional programs. Here, we review current molecular evidence based on next generation sequencing data, cell assays and in vivo models supporting different mechanisms that could mediate the function of macroH2A1 in health span and life span. We will further discuss context-dependent and isoform-specific functions. The aim of this review is to provide guidance to assess histone variant macroH2A1 potential as a therapeutic intervention point. Full article
(This article belongs to the Special Issue The Epigenetics of Aging and Longevity)
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Open AccessReview Epigenetic Basis of Cellular Senescence and Its Implications in Aging
Genes 2017, 8(12), 343; doi:10.3390/genes8120343
Received: 30 October 2017 / Revised: 18 November 2017 / Accepted: 21 November 2017 / Published: 24 November 2017
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Abstract
Cellular senescence is a tumor suppressive response that has become recognized as a major contributor of tissue aging. Senescent cells undergo a stable proliferative arrest that protects against neoplastic transformation, but acquire a secretory phenotype that has long-term deleterious effects. Studies are still
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Cellular senescence is a tumor suppressive response that has become recognized as a major contributor of tissue aging. Senescent cells undergo a stable proliferative arrest that protects against neoplastic transformation, but acquire a secretory phenotype that has long-term deleterious effects. Studies are still unraveling the effector mechanisms that underlie these senescence responses with the goal to identify therapeutic interventions. Such effector mechanisms have been linked to the dramatic remodeling in the epigenetic and chromatin landscape that accompany cellular senescence. We discuss these senescence-associated epigenetic changes and their impact on the senescence phenotypes, notably the proliferative arrest and senescence associated secretory phenotype (SASP). We also explore possible epigenetic targets to suppress the deleterious effects of senescent cells that contribute towards aging. Full article
(This article belongs to the Special Issue The Epigenetics of Aging and Longevity)
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