Log in

Relevant bibliographies by topics / Replicative longevity

Contents

Journal articles
Dissertations / Theses
Books
Book chapters

Academic literature on the topic 'Replicative longevity'

Author: Grafiati

Published: 4 June 2021

Last updated: 5 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Replicative longevity.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Replicative longevity"

1

Kirchman, Paul A., Sangkyu Kim, Chi-Yung Lai, and S. Michal Jazwinski. "Interorganelle Signaling Is a Determinant of Longevity in Saccharomyces cerevisiae." Genetics 152, no. 1 (1999): 179–90. http://dx.doi.org/10.1093/genetics/152.1.179.

Full text

Abstract:

Abstract Replicative capacity, which is the number of times an individual cell divides, is the measure of longevity in the yeast Saccharomyces cerevisiae. In this study, a process that involves signaling from the mitochondrion to the nucleus, called retrograde regulation, is shown to determine yeast longevity, and its induction resulted in postponed senescence. Activation of retrograde regulation, by genetic and environmental means, correlated with increased replicative capacity in four different S. cerevisiae strains. Deletion of a gene required for the retrograde response, RTG2, eliminated the increased replicative capacity. RAS2, a gene previously shown to influence longevity in yeast, interacts with retrograde regulation in setting yeast longevity. The molecular mechanism of aging elucidated here parallels the results of genetic studies of aging in nematodes and fruit flies, as well as the caloric restriction paradigm in mammals, and it underscores the importance of metabolic regulation in aging, suggesting a general applicability.

APA, Harvard, Vancouver, ISO, and other styles

2

Zandycke, Sylvie M. Van, and Katherine A. Smart. "GLUTATHIONE BIOSYNTHESIS INFLUENCES REPLICATIVE LONGEVITY IN SACCHAROMYCES CEREVISIAE." TheScientificWorldJOURNAL 1, S3 (2001): 133. http://dx.doi.org/10.1100/tsw.2001.23.231.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Zandycke, Sylvie M. Van, and Katherine A. Smart. "Glutathione Biosynthesis Influences Replicative Longevity in Saccharomyces Cerevisiae." Scientific World JOURNAL 1 (2001): 133. http://dx.doi.org/10.1100/tsw.2001.231.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Spivey, Eric C., and Ilya J. Finkelstein. "From cradle to grave: high-throughput studies of aging in model organisms." Mol. BioSyst. 10, no. 7 (2014): 1658–67. http://dx.doi.org/10.1039/c3mb70604d.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Wasko, Brian M., and Matt Kaeberlein. "Yeast replicative aging: a paradigm for defining conserved longevity interventions." FEMS Yeast Research 14, no. 1 (2013): 148–59. http://dx.doi.org/10.1111/1567-1364.12104.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Lord, Christopher L., Benjamin L. Timney, Michael P. Rout, and Susan R. Wente. "Altering nuclear pore complex function impacts longevity and mitochondrial function in S. cerevisiae." Journal of Cell Biology 208, no. 6 (2015): 729–44. http://dx.doi.org/10.1083/jcb.201412024.

Full text

Abstract:

The eukaryotic nuclear permeability barrier and selective nucleocytoplasmic transport are maintained by nuclear pore complexes (NPCs), large structures composed of ∼30 proteins (nucleoporins [Nups]). NPC structure and function are disrupted in aged nondividing metazoan cells, although it is unclear whether these changes are a cause or consequence of aging. Using the replicative life span (RLS) of Saccharomyces cerevisiae as a model, we find that specific Nups and transport events regulate longevity independent of changes in NPC permeability. Mutants lacking the GLFG domain of Nup116 displayed decreased RLSs, whereas longevity was increased in nup100-null mutants. We show that Nup116 mediates nuclear import of the karyopherin Kap121, and each protein is required for mitochondrial function. Both Kap121-dependent transport and Nup116 levels decrease in replicatively aged yeast. Overexpression of GSP1, the small GTPase that powers karyopherin-mediated transport, rescued mitochondrial and RLS defects in nup116 mutants and increased longevity in wild-type cells. Together, these studies reveal that specific NPC nuclear transport events directly influence aging.

APA, Harvard, Vancouver, ISO, and other styles

7

Lorenzini, Antonello, Maria Tresini, Steven N. Austad, and Vincent J. Cristofalo. "Cellular replicative capacity correlates primarily with species body mass not longevity." Mechanisms of Ageing and Development 126, no. 10 (2005): 1130–33. http://dx.doi.org/10.1016/j.mad.2005.05.004.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Bitterman, Kevin J., Oliver Medvedik, and David A. Sinclair. "Longevity Regulation in Saccharomyces cerevisiae: Linking Metabolism, Genome Stability, and Heterochromatin." Microbiology and Molecular Biology Reviews 67, no. 3 (2003): 376–99. http://dx.doi.org/10.1128/mmbr.67.3.376-399.2003.

Full text

Abstract:

SUMMARY When it was first proposed that the budding yeast Saccharomyces cerevisiae might serve as a model for human aging in 1959, the suggestion was met with considerable skepticism. Although yeast had proved a valuable model for understanding basic cellular processes in humans, it was difficult to accept that such a simple unicellular organism could provide information about human aging, one of the most complex of biological phenomena. While it is true that causes of aging are likely to be multifarious, there is a growing realization that all eukaryotes possess surprisingly conserved longevity pathways that govern the pace of aging. This realization has come, in part, from studies of S. cerevisiae, which has emerged as a highly informative and respected model for the study of life span regulation. Genomic instability has been identified as a major cause of aging, and over a dozen longevity genes have now been identified that suppress it. Here we present the key discoveries in the yeast-aging field, regarding both the replicative and chronological measures of life span in this organism. We discuss the implications of these findings not only for mammalian longevity but also for other key aspects of cell biology, including cell survival, the relationship between chromatin structure and genome stability, and the effect of internal and external environments on cellular defense pathways. We focus on the regulation of replicative life span, since recent findings have shed considerable light on the mechanisms controlling this process. We also present the specific methods used to study aging and longevity regulation in S. cerevisiae.

APA, Harvard, Vancouver, ISO, and other styles

9

Yu, Ruofan, Luyang Sun, Yu Sun, Xin Han, Lidong Qin, and Weiwei Dang. "Cellular response to moderate chromatin architectural defects promotes longevity." Science Advances 5, no. 7 (2019): eaav1165. http://dx.doi.org/10.1126/sciadv.aav1165.

Full text

Abstract:

Changes in chromatin organization occur during aging. Overexpression of histones partially alleviates these changes and promotes longevity. We report that deletion of the histone H3-H4 minor locus HHT1-HHF1 extended the replicative life span of Saccharomyces cerevisiae. This longevity effect was mediated through TOR signaling inhibition. We present evidence for evolutionarily conserved transcriptional and phenotypic responses to defects in chromatin structure, collectively termed the chromatin architectural defect (CAD) response. Promoters of the CAD response genes were sensitive to histone dosage, with HHT1-HHF1 deletion, nucleosome occupancy was reduced at these promoters allowing transcriptional activation induced by stress response transcription factors Msn2 and Gis1, both of which were required for the life-span extension of hht1-hhf1Δ. Therefore, we conclude that the CAD response induced by moderate chromatin defects promotes longevity.

APA, Harvard, Vancouver, ISO, and other styles

10

Kirkwood, Thomas B. L. "Systems biology of ageing and longevity." Philosophical Transactions of the Royal Society B: Biological Sciences 366, no. 1561 (2011): 64–70. http://dx.doi.org/10.1098/rstb.2010.0275.

Full text

Abstract:

Ageing is intrinsically complex, being driven by multiple causal mechanisms. Each mechanism tends to be partially supported by data indicating that it has a role in the overall cellular and molecular pathways underlying the ageing process. However, the magnitude of this role is usually modest. The systems biology approach combines (i) data-driven modelling, often using the large volumes of data generated by functional genomics technologies, and (ii) hypothesis-driven experimental studies to investigate causal pathways and identify their parameter values in an unusually quantitative manner, which enables the contributions of individual mechanisms and their interactions to be better understood, and allows for the design of experiments explicitly to test the complex predictions arising from such models. A clear example of the success of the systems biology approach in unravelling the complexity of ageing can be seen in recent studies on cell replicative senescence, revealing interactions between mitochondrial dysfunction, telomere erosion and DNA damage. An important challenge also exists in connecting the network of (random) damage-driven proximate mechanisms of ageing with the higher level (genetically specified) signalling pathways that influence longevity. This connection is informed by actions of natural selection on the determinants of ageing and longevity.

APA, Harvard, Vancouver, ISO, and other styles

Dissertations / Theses on the topic "Replicative longevity"

1

Ayling, Jonathan. "Epigenetic regulation of chronological and replicative longevity in Saccharomyces cerevisiae." Thesis, University of Oxford, 2012. https://ora.ox.ac.uk/objects/uuid:4f59670e-5783-4548-b553-abe1c1c0a9ab.

Full text

Abstract:

Ageing and senescence remain among the most intriguing questions in biology. Saccharomyces cerevisiae has become well established as a fertile model system for the investigation of ageing. Remarkable conservation has been found to exist between interventions extending lifespan in higher animals and yeast â genetic, chemical, and nutritional â suggesting a network of common regulatory pathways controlling large-scale shifts in gene expression involved in senescence. While it has been proposed that epigenetic regulation controls these shifts, evidence remains incomplete. To address this question, novel longevity mutants were isolated in S. cerevisiae using a purpose-designed high-precision screen based on ageing culture outgrowth. A novel long-lived mutant in uncharacterised gene YDR026C was discovered and found to participate in a pathway distinct from TOR signalling, but share epistasis with the histone deacetylase SIR2Δ, a well established regulator of replicative longevity and rDNA maintenance. Through equilibrium density centrifugal separation of culture subpopulations, SIR2Δ and Ydr026cΔ cultures were found to demonstrate reduced and improved maintenance of post-diauxic quiescence respectively, previously shown to underlie chronological survival in strains including snf1Δ. Development of a quantified TUNEL-based assay for genome fragmentation indicated early apoptotic-like behaviour in the SIR2Δ strain. Microdissection experiments and sectored-colony assays of strains containing an rDNA-embedded ADE2 reporter determined that Ydr026cΔ cells also exhibit extended replicative lifespan, and reduced recombination at the rDNA spacer region hotspot, abrogated in SIR2Δ strains. SIR2Δ is well established to repress RNA polymerase II-derived transcripts in the rDNA spacer region, including IGS1-R. Northern analysis determined Ydr026c also silences transcription in the spacer, possibly through preventing termination of the main rRNA transcript, interfering with IGS1-R expression. By transformation with a vector overexpressing IGS1-R, partial reconstitution of the SIR2Δ phenotype was observed, including rDNA hyperrecombination, shortened replicative longevity, and higher-order chromatin structure restoration. These data suggests a model whereby non-coding rDNA spacer transcripts epigenetically determine rDNA maintenance through recombination, leading to physiological phenotypes of replicative and chronological ageing.

APA, Harvard, Vancouver, ISO, and other styles

2

Maskell, Dawn Louise. "Influence of stress on replicative longevity in Saccharomyces cerevisiae (syn.S.pastorianus)." Thesis, Oxford Brookes University, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.271277.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Powers, Ralph Wilson. "Genome-wide screens reveal that reduced TOR signaling extends chronological and replicative life span in S. cerevisiae /." Thesis, Connect to this title online; UW restricted, 2006. http://hdl.handle.net/1773/5044.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Managbanag, JR. "Application of Shortest-Path Network Analysis to Identify Genes that Modulate Longevity in Saccharomyces cerevisiae." VCU Scholars Compass, 2008. http://scholarscompass.vcu.edu/etd/1613.

Full text

Abstract:

Shortest-path network analysis was employed to identify novel genes that modulate longevity in the baker’s yeast Saccharomyces cerevisiae. Based upon a set of previously reported genes associated with increased life span, a shortest path network algorithm was applied to a pre-existing protein-protein interaction dataset in order to construct a shortest-path longevity network. To validate this network, the replicative aging potential of 88 single gene deletion strains corresponding to predicted components of the shortest path longevity network was determined. The 88 single-gene deletion strains identified by a network approach are significantly enriched for mutation conferring both increased and decreased replicative life span when compared to a randomly selected set of 564 single-gene deletion strains or to the current data set available for the entire haploid deletion collection. In addition, previously unknown longevity genes were identified, several of which function in a longevity pathway believed to mediate life span extension in response to dietary restriction. This study represents the first biologically validated application of a network construct to the study of aging and rigorously demonstrates, also for the first time, that shortest path network analysis is a potentially powerful tool for predicting genes that function as potential modulators of aging.

APA, Harvard, Vancouver, ISO, and other styles

Books on the topic "Replicative longevity"

1

Maskell, Dawn Louise. Influence of stress on replicative longevity in saccharomyces cerevisiae (syn. S. pastorianus). Oxford Brookes University, 2003.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "Replicative longevity"

1

Hayflick, Leonard. "Unlike the Stochastic Events That Determine Ageing, Sex Determines Longevity." In Cellular Ageing and Replicative Senescence. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-26239-0_17.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Lorenzini, Antonello, and Andrea B. Maier. "Influence of Donor Age and Species Longevity on Replicative Cellular Senescence." In Cellular Ageing and Replicative Senescence. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-26239-0_4.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Choi, Kyung-Mi, and Cheol-Koo Lee. "Cellular Longevity of Budding Yeast During Replicative and Chronological Aging." In Aging Mechanisms. Springer Japan, 2015. http://dx.doi.org/10.1007/978-4-431-55763-0_6.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Sudiyani, Yanni, Muhammad Eka Prastya, Roni Maryana, Eka Triwahyuni, and Muryanto. "The Budding Yeast Saccharomyces cerevisiae as a Valuable Model Organism for Investigating Anti-Aging Compounds." In Saccharomyces. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96662.

Full text

Abstract:

Saccharomyces cerevisiae, the budding yeast was long history as industrial baker’s yeast due to its ability to produce numerous product such as ethanol, acetate, industrial bakers etc. Interestingly, this yeast was also important tools for studying biological mechanism in eukaryotic cells including aging, autophagy, mitochondrial response etc. S. cerevisiae has arisen as a powerful chemical and genetic screening platform, due to a rapid workflow with experimental amenability and the availability of a wide range of genetic mutant libraries. Calorie restriction (CR) as the reduction of nutrients intake could promote yeast longevity through some pathways such as inhibition of nutrient sensing target of rapamycin (TOR), serine–threonine kinase (SCH9), protein adenylate cyclase (AC), protein kinase A (PKA) and ras, reduced ethanol, acetic acid and apoptotic process. In addition, CR also induces the expression of antioxidative proteins, sirtuin2 (Sir2), autophagy and induction of mitochondrial yeast adaptive response. Three methods, spotting test; chronological life span (CLS) and replicative life span (RLS) assays, have been developed to study aging in S. cerevisiae. Here, we present strategies for pharmacological anti-aging screens in yeast, discuss common pitfalls and summarize studies that have used yeast for drug discovery.

APA, Harvard, Vancouver, ISO, and other styles

5

"Revised Mitochondrial Hypothesis of Aging Highlights Energy Deciency Caused by Errors of Replication (Mutations) of mtDNA." In Human Longevity. CRC Press, 2014. http://dx.doi.org/10.1201/b17458-13.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Seligmann, Herve. "Mutation Patterns Due to Converging Mitochondrial Replication and Transcription Increase Lifespan, and Cause Growth Rate-Longevity Tradeoffs." In DNA Replication-Current Advances. InTech, 2011. http://dx.doi.org/10.5772/24319.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Davidson, Christopher M. "Advanced Sultanism: A Broader Debate." In From Sheikhs to Sultanism. Oxford University Press, 2021. http://dx.doi.org/10.1093/oso/9780197586488.003.0011.

Full text

Abstract:

The second of two summary discussions, this chapter firstly assesses the likely longevity and stability of MBS and MBZ’s ‘advanced sultanates’. In particular, it notes their apparent strength, while also considering possible dangers they may face alongside some of the more peaceful forms of activity that could also result in regime change. Secondly, it contemplates the possibilities for such advanced sultanism to replicate elsewhere in the world. In particular, it notes that replication may prove difficult (though not impossible) in other contemporary sultanates given their lack of rentier state legacies and poorer access to advanced economies and consultants Nonetheless, it notes that MBS and MBZ may seek to promote—or perhaps diffuse—repressive aspects of their regimes elsewhere in the region, especially if Saudi and UAE diplomatic support and economic aid can be tied to the adoption of MBS and MBZ’s signature policies. Finally, the chapter discusses the relevance of MBS and MBZ’s advanced sultanism to several broader issues, including: the debate on Islam’s supposed incompatibility with capitalism (which their regimes seem to contradict); the prospects for modernization theory (which their regimes also seem to contradict); and--more philosophically--the extent which their regimes may complicate global intellectual support for monarchy.

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!