Inactivation of Yeast Isw2 Chromatin Remodeling Enzyme Mimics Longevity Effect of Calorie Restriction via Induction of Genotoxic Stress Response

Dang, Weiwei; Sutphin, George L.; Dorsey, Jean; Otte, Gabriel; Cao, Kajia; Perry, Rocco; Wanat, Jennifer J.; Saviolaki, Dimitra; Murakami, Christopher J.; Tsuchiyama, Scott; Robison, Brett; Gregory, Brian D.; Vermeulen, Michiel; Shiekhattar, Ramin; Johnson, F. Brad; Kennedy, Brian K.; Kaeberlein, Matt; Berger, Shelley L.

doi:10.1016/j.cmet.2014.04.004

Cited by 71 publications

(77 citation statements)

References 67 publications

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“…For instance, ATP-dependent remodeling complexes have been implicated in longevity in yeast (Isw2) 110 and in worms (SWI/SNF Switch/Sucrose Non-fermentable), which colocalizes with DAF-16/FOXO at the promoters of longevity-promoting genes). 111 Among the histone-modifying enzymes, the NAD-dependent deacetylase SIRT1 (sirtuin 1) KAT8/MOF/MYST1/YBF2).…”

Section: Chromatin-modifying Enzymesmentioning

confidence: 99%

Transcriptional and epigenetic regulation of autophagy in aging

et al. 2015

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Macroautophagy is a major intracellular degradation process recognized as playing a central role in cell survival and longevity. This multistep process is extensively regulated at several levels, including post-translationally through the action of conserved longevity factors such as the nutrient sensor TOR. More recently, transcriptional regulation of autophagy genes has emerged as an important mechanism for ensuring the somatic maintenance and homeostasis necessary for a long life span. Autophagy is increased in many long-lived model organisms and contributes significantly to their longevity. In turn, conserved transcription factors, particularly the helix-loop-helix transcription factor TFEB and the forkhead transcription factor FOXO, control the expression of many autophagy-related genes and are important for life-span extension. In this review, we discuss recent progress in understanding the contribution of these transcription factors to macroautophagy regulation in the context of aging. We also review current research on epigenetic changes, such as histone modification by the deacetylase SIRT1, that influence autophagy-related gene expression and additionally affect aging. Understanding the molecular regulation of macroautophagy in relation to aging may offer new avenues for the treatment of age-related diseases.

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Section: Chromatin-modifying Enzymesmentioning

confidence: 99%

Transcriptional and epigenetic regulation of autophagy in aging

et al. 2015

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“…We reasoned that if the short life span effect of H3K36me3 loss is mediated through one of these pathways, disruption of the recruited enzyme should phenocopy the aging phenotype of the set2Δ and H3K36 mutants. Since deletion of ISW1 or CHD1 does not shorten life span (Dang et al 2014), we focused on the Rpd3S complex. The loss of H3K36me3 over the gene bodies of the cryptic genes likely causes inefficient recruitment of the Rpd3S complex and hyperacetylation, leading to spurious initiation of internal transcripts (Carrozza et al 2005).…”

Section: Genes Showing Cryptic Transcript Up-regulation With Age Losementioning

confidence: 99%

“…Up to 4 × 10 8 replicatively aged yeast mother cells (20-25 generations old on average) were purified as described (Dang et al 2014) for the life span screen, RNA-seq, or ChIP-seq.…”

Section: Purification Of Old Yeast Mother Cellsmentioning

confidence: 99%

“…Other factors include chromatin remodelers that function in calorie restriction pathways to promote life span. In yeast, nutrient depletion deactivates the ISW2 complex conferring life span extension by up-regulating the stress response pathway (Dang et al 2014). In worms, nutrient depletion reduces insulin-like signaling allowing for nuclear localization of DAF16/FOXO transcription factors that cooperate with SWI/SNF to promote stress response and longevity (Riedel et al 2013).…”

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confidence: 99%

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H3K36 methylation promotes longevity by enhancing transcriptional fidelity

et al. 2015

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Epigenetic mechanisms, including histone post-translational modifications, control longevity in diverse organisms. Relatedly, loss of proper transcriptional regulation on a global scale is an emerging phenomenon of shortened life span, but the specific mechanisms linking these observations remain to be uncovered. Here, we describe a life span screen in Saccharomyces cerevisiae that is designed to identify amino acid residues of histones that regulate yeast replicative aging. Our results reveal that lack of sustained histone H3K36 methylation is commensurate with increased cryptic transcription in a subset of genes in old cells and with shorter life span. In contrast, deletion of the K36me2/3 demethylase Rph1 increases H3K36me3 within these genes, suppresses cryptic transcript initiation, and extends life span. We show that this aging phenomenon is conserved, as cryptic transcription also increases in old worms. We propose that epigenetic misregulation in aging cells leads to loss of transcriptional precision that is detrimental to life span, and, importantly, this acceleration in aging can be reversed by restoring transcriptional fidelity.

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“…In this case, Isw2-dependent nucleosome remodeling represses stress response genes, whereas deletion of Isw2, which partially mimics the effect of CR through the up-regulation of stress response genes, extends life span. This is a conserved life span regulatory pathway in yeast and worms, and reduction of the orthologous complexes also extends life span (Dang et al 2014). …”

Section: Calorie Restriction Life Span Extension and Epigenetic Regmentioning

confidence: 99%

Metabolic Signaling to Chromatin

Berger

Sassone–Corsi

2015

Cold Spring Harb Perspect Biol

120

101

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There is a dynamic interplay between metabolic processes and gene regulation via the remodeling of chromatin. Most chromatin-modifying enzymes use cofactors, which are products of metabolic processes. This article explores the biosynthetic pathways of the cofactors nicotinamide adenine dinucleotide (NAD), acetyl coenzyme A (acetyl-CoA), S-adenosyl methionine (SAM), α-ketoglutarate, and flavin adenine dinucleotide (FAD), and their role in metabolically regulating chromatin processes. A more detailed look at the interaction between chromatin and the metabolic processes of circadian rhythms and aging is described as a paradigm for this emerging interdisciplinary field.

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Inactivation of Yeast Isw2 Chromatin Remodeling Enzyme Mimics Longevity Effect of Calorie Restriction via Induction of Genotoxic Stress Response

Cited by 71 publications

References 67 publications

Transcriptional and epigenetic regulation of autophagy in aging

Transcriptional and epigenetic regulation of autophagy in aging

H3K36 methylation promotes longevity by enhancing transcriptional fidelity

Metabolic Signaling to Chromatin

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