JournalTOCs

Briefings in Functional Genomics
Journal Prestige (SJR): 2.15

Citation Impact (citeScore): 3
Number of Followers: 3

Hybrid journal (It can contain Open Access articles)
ISSN (Print) 2041-2649 - ISSN (Online) 2041-2657
Published by Oxford University Press

[419 journals]

Functional genomics of ageing: implications of chromatin landscape and
beyond
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  Authors: Kirmizis A.
  Pages: 1 - 3
  Abstract: Cyprus Cancer Research InstituteCCRI-2020-FUN-001-103Cyprus Research and Innovation Foundation1216/02151216/00360918/01050918/0081
  PubDate: Tue, 25 Jan 2022 00:00:00 GMT
  DOI: 10.1093/bfgp/elac001
  Issue No: Vol. 21, No. 1 (2022)
Genome-wide screens in yeast models towards understanding chronological
lifespan regulation
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  Authors: Legon L; Rallis C.
  Pages: 4 - 12
  Abstract: AbstractCellular models such as yeasts are a driving force in biogerontology studies. Their simpler genome, short lifespans and vast genetic and genomics resources make them ideal to characterise pro-ageing and anti-ageing genes and signalling pathways. Over the last three decades, yeasts have contributed to the understanding of fundamental aspects of lifespan regulation including the roles of nutrient response, global protein translation rates and quality, DNA damage, oxidative stress, mitochondrial function and dysfunction as well as autophagy. In this short review, we focus on approaches used for competitive and non-competitive cell-based screens using the budding yeast Saccharomyces cerevisiae, and the fission yeast Schizosaccharomyces pombe, for deciphering the molecular mechanisms underlying chronological ageing. Automation accompanied with appropriate computational tools allowed manipulation of hundreds of thousands of colonies, generation, processing and analysis of genome-wide lifespan data. Together with barcoding and modern mutagenesis technologies, these approaches have allowed to take decisive steps towards a global, comprehensive view of cellular ageing.
  PubDate: Wed, 17 Mar 2021 00:00:00 GMT
  DOI: 10.1093/bfgp/elab011
  Issue No: Vol. 21, No. 1 (2021)
From mutation to mechanism: deciphering the molecular function of genetic
variants linked to human ageing
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  Authors: Baghdadi M; Hinterding H, Partridge L, et al.
  Pages: 13 - 23
  Abstract: AbstractMany of the leading causes of death in humans, such as cardiovascular disease, type 2 diabetes and Alzheimer’s disease are influenced by biological mechanisms that become dysregulated with increasing age. Hence, by targeting these ageing-related mechanisms, we may be able to improve health in old age. Ageing is partly heritable and genetic studies have been moderately successful in identifying genetic variants associated with ageing-related phenotypes (lifespan, healthspan and longevity). To decipher the mechanisms by which the identified variants influence ageing, studies that focus on their functional validation are vital. In this perspective, we describe the steps that could be taken in the process of functional validation: (1) in silico characterisation using bioinformatic tools; (2) in vitro characterisation using cell lines or organoids; and (3) in vivo characterisation studies using model organisms. For the in vivo characterisation, it is important to focus on translational phenotypes that are indicative of both healthspan and lifespan, such as the frailty index, to inform subsequent intervention studies. The depth of functional validation of a genetic variant depends on its location in the genome and conservation in model organisms. Moreover, some variants may prove to be hard to characterise due to context-dependent effects related to the experimental environment or genetic background. Future efforts to functionally characterise the (newly) identified genetic variants should shed light on the mechanisms underlying ageing and will help in the design of targeted interventions to improve health in old age.
  PubDate: Fri, 05 Mar 2021 00:00:00 GMT
  DOI: 10.1093/bfgp/elab005
  Issue No: Vol. 21, No. 1 (2021)
The functional impact of nuclear reorganization in cellular senescence
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  Authors: Rocha A; Dalgarno A, Neretti N.
  Pages: 24 - 34
  Abstract: AbstractCellular senescence is the irreversible cell cycle arrest in response to DNA damage. Because senescent cells accumulate with age and contribute to chronic inflammation, they are promising therapeutic targets for healthspan extension. The senescent phenotype can vary depending on cell type and on the specific insults that induce senescence. This variability is also reflected in the extensive remodeling of the genome organization within the nucleus of senescent cells. Here, we give an overview of the nuclear changes that occur in different forms of senescence, including changes to chromatin state and composition and to the three-dimensional organization of the genome, as well as alterations to the nuclear envelope and to the accessibility of repetitive genomic regions. Many of these changes are shared across all forms of senescence, implicating nuclear organization as a fundamental driver of the senescent state and of how senescent cells interact with the surrounding tissue.
  PubDate: Tue, 23 Mar 2021 00:00:00 GMT
  DOI: 10.1093/bfgp/elab012
  Issue No: Vol. 21, No. 1 (2021)
Epigenetic alterations in stem cell ageing—a promising target for
age-reversing interventions'
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  Authors: Pouikli A; Tessarz P.
  Pages: 35 - 42
  Abstract: AbstractAgeing is accompanied by loss of tissue integrity and organismal homeostasis partly due to decline in stem cell function. The age-associated decrease in stem cell abundance and activity is often referred to as stem cell exhaustion and is considered one major hallmark of ageing. Importantly, stem cell proliferation and differentiation potential are tightly coupled to the cellular epigenetic state. Thus, research during the last years has started to investigate how the epigenome regulates stem cell function upon ageing. Here, we summarize the role of epigenetic regulation in stem cell fate decisions and we review the impact of age-related changes of the epigenome on stem cell activity. Finally, we discuss how targeted interventions on the epigenetic landscape might delay ageing and extend health-span.
  PubDate: Fri, 19 Mar 2021 00:00:00 GMT
  DOI: 10.1093/bfgp/elab010
  Issue No: Vol. 21, No. 1 (2021)
Functional genomics of inflamm-aging and immunosenescence
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  Authors: Lu R; Wang E, Benayoun B.
  Pages: 43 - 55
  Abstract: AbstractThe aging population is at a higher risk for age-related diseases and infections. This observation could be due to immunosenescence: the decline in immune efficacy of both the innate and the adaptive immune systems. Age-related immune decline also links to the concept of ‘inflamm-aging,’ whereby aging is accompanied by sterile chronic inflammation. Along with a decline in immune function, aging is accompanied by a widespread of ‘omics’ remodeling. Transcriptional landscape changes linked to key pathways of immune function have been identified across studies, such as macrophages having decreased expression of genes associated to phagocytosis, a major function of macrophages. Therefore, a key mechanism underlying innate immune cell dysfunction during aging may stem from dysregulation of youthful genomic networks. In this review, we discuss both molecular and cellular phenotypes of innate immune cells that contribute to age-related inflammation.
  PubDate: Fri, 05 Mar 2021 00:00:00 GMT
  DOI: 10.1093/bfgp/elab009
  Issue No: Vol. 21, No. 1 (2021)
Loosening chromatin and dysregulated transcription: a perspective on
cryptic transcription during mammalian aging
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  Authors: McCauley B; Dang W.
  Pages: 56 - 61
  Abstract: AbstractCryptic transcription, the initiation of transcription from non-promoter regions within a gene body, is a type of transcriptional dysregulation that occurs throughout eukaryotes. In mammals, cryptic transcription is normally repressed at the level of chromatin, and this process is increased upon perturbation of complexes that increase intragenic histone H3 lysine 4 methylation or decrease intragenic H3 lysine 36 methylation, DNA methylation, or nucleosome occupancy. Significantly, similar changes to chromatin structure occur during aging, and, indeed, recent work indicates that cryptic transcription is elevated during aging in mammalian stem cells. Although increased cryptic transcription is known to promote aging in yeast, whether elevated cryptic transcription also contributes to mammalian aging is unclear. There is ample evidence that perturbations known to increase cryptic transcription are deleterious in embryonic and adult stem cells, and in some cases phenocopy certain aging phenotypes. Furthermore, an increase in cryptic transcription requires or impedes pathways that are known to have reduced function during aging, potentially exacerbating other aging phenotypes. Thus, we propose that increased cryptic transcription contributes to mammalian stem cell aging.
  PubDate: Fri, 28 May 2021 00:00:00 GMT
  DOI: 10.1093/bfgp/elab026
  Issue No: Vol. 21, No. 1 (2021)