<i>Drosophila</i> longevity is not affected by heterochromatin‐mediated gene silencing

Frankel, Stewart; Rogina, Blanka

doi:10.1111/j.1474-9726.2005.00143.x

Cited by 17 publications

(17 citation statements)

References 31 publications

(28 reference statements)

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“…A previous study has shown that Drosophila life span was only slightly reduced in Su(var)205 heterozygotes and was not affected by a chromosomal duplication that encompasses the Su(var)205 locus and many other genes [31]. Using chromosomal duplication, any effects associated with higher levels of Su(var)205 might be masked by higher levels of other neighboring genes.…”

Section: Resultsmentioning

confidence: 99%

“…It has also been shown that HP1 mutations disrupt epigenetic reprogramming, causing transgenerational inheritance of epigenetic information [33], [34]. Thus, in the aging study by Frankel and Rogina (2005) [31], the presence or absence of the Su(var)205 2 mutation in the test flies may not have been accurately determined. In our current studies, we confirmed the presence of Su(var)205 mutations in the coisogenic strains by both suppression of PEV and homozygous lethality (see Materials and Methods).…”

Section: Resultsmentioning

confidence: 99%

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Heterochromatin Formation Promotes Longevity and Represses Ribosomal RNA Synthesis

et al. 2012

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Organismal aging is influenced by a multitude of intrinsic and extrinsic factors, and heterochromatin loss has been proposed to be one of the causes of aging. However, the role of heterochromatin in animal aging has been controversial. Here we show that heterochromatin formation prolongs lifespan and controls ribosomal RNA synthesis in Drosophila. Animals with decreased heterochromatin levels exhibit a dramatic shortening of lifespan, whereas increasing heterochromatin prolongs lifespan. The changes in lifespan are associated with changes in muscle integrity. Furthermore, we show that heterochromatin levels decrease with normal aging and that heterochromatin formation is essential for silencing rRNA transcription. Loss of epigenetic silencing and loss of stability of the rDNA locus have previously been implicated in aging of yeast. Taken together, these results suggest that epigenetic preservation of genome stability, especially at the rDNA locus, and repression of unnecessary rRNA synthesis, might be an evolutionarily conserved mechanism for prolonging lifespan.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Heterochromatin Formation Promotes Longevity and Represses Ribosomal RNA Synthesis

et al. 2012

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“…Although the Rpd3 findings are similar to yeast, Drosophila longevity is not mediated through heterochromatic gene silencing. Together, these data suggest that in flies, different deacetylases (dSir2 and Rpd3) function in opposite ways at euchromatin to affect longevity by influencing specific gene expression patterns (Frankel and Rogina, 2005). The disparity may stem from the multiple substrates targeted by these proteins but nevertheless underscore the importance of specific gene regulation in longevity, which, as discussed above, may be a more dominant mechanism regulating lifespan in some models.…”

Section: Nutrient Signaling and Its Effects On The Chromatinmentioning

confidence: 94%

“…For one, different deacetylases, dSir2 and Rpd3, have different effects on lifespan. Second, increased H3K9ac achieved by mutation of Su (var) 2-1 has no effect on lifespan (Frankel and Rogina, 2005). Third, administration of different HDAC inhibitors like sodium butyrate, TSA, PBA and SAHA result in different changes in mean lifespan.…”

Section: Nutrient Signaling and Its Effects On The Chromatinmentioning

confidence: 99%

Epigenetic Mechanisms of Longevity and Aging

Sen

Shah

Nativio

et al. 2016

Cell

727

591

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Summary Aging is an inevitable outcome of life, characterized by progressive decline in tissue and organ function and increased risk of mortality. Accumulating evidence links aging to genetic and epigenetic alterations. Given the reversible nature of epigenetic mechanisms, these pathways provide promising avenues for therapeutics against age-related decline and disease. In this review, we provide a comprehensive overview of epigenetic studies from invertebrate organisms, vertebrate models, tissue and in vitro systems. We establish links between common operative aging pathways and hallmark chromatin signatures that can be used to identify “druggable” targets to counter human aging and age-related disease.

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“…Experimental tests of the role of heterochromatin formation in aging, however, have produced controversial results. It was shown that mutations at Su(var)2-1 and Su(var)205 loci have virtually no effect on life span (Rogina et al 2002;Frankel and Rogina 2005). At the same time, increasing and decreasing HP1 levels shortens and prolongs life span, respectively (Larson et al 2012).…”

Section: Global Regulatorsmentioning

confidence: 97%

Neuronal Genes and Developmental Neuronal Pathways in Drosophila Life Span Control

Pasyukova

Symonenko

Roshina

et al. 2015

Healthy Ageing and Longevity

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The nervous system has long been suggested as a key tissue that defines life span. The identity of neuronal cell types is established during development and maintained throughout adulthood due to the expression of specific neuronal genes coding for ion channels, neurotransmitters and neuropeptides, G-protein-coupled receptors, motor proteins, recognition and adhesion molecules. In this paper, we review data on the role of neuronal genes in Drosophila melanogaster life span control. Several pathways responsible for life span regulation are also important for the development of the nervous system. Genes involved in insulin-like, Target of Rapamycin, Janus Kinase/Signal Transducer and Activator of Transcription and cell polarity pathways, a number of global regulators and transcription factors play key roles both in aging and longevity control and in shaping the nervous system as a network of specialized neuronal cells in early development. Is their impact on life span related, at least partially, to their developmental functions or is it explained by other pleiotropic influences later in life? In this paper, we address this question based on the published data and our own findings.

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Drosophila longevity is not affected by heterochromatin‐mediated gene silencing

Cited by 17 publications

References 31 publications

Heterochromatin Formation Promotes Longevity and Represses Ribosomal RNA Synthesis

Heterochromatin Formation Promotes Longevity and Represses Ribosomal RNA Synthesis

Epigenetic Mechanisms of Longevity and Aging

Neuronal Genes and Developmental Neuronal Pathways in Drosophila Life Span Control

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