Transcriptional (dys)regulation and aging in Caenorhabditis elegans

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Abstract

New work could link laboratory-defined longevity pathways to the process of normal aging.

Abstract

A circuit of transcription factors has been discovered in Caenorhabditis elegans that could provide a link between laboratory-defined intracellular 'longevity pathways', gene dysregulation and the process of normal aging.

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Most cited references 21

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Stochastic and genetic factors influence tissue-specific decline in ageing C. elegans.

Laura Herndon, Peter Schmeissner, Justyna M Dudaronek … (2002)

The nematode Caenorhabditis elegans is an important model for studying the genetics of ageing, with over 50 life-extension mutations known so far. However, little is known about the pathobiology of ageing in this species, limiting attempts to connect genotype with senescent phenotype. Using ultrastructural analysis and visualization of specific cell types with green fluorescent protein, we examined cell integrity in different tissues as the animal ages. We report remarkable preservation of the nervous system, even in advanced old age, in contrast to a gradual, progressive deterioration of muscle, resembling human sarcopenia. The age-1(hx546) mutation, which extends lifespan by 60-100%, delayed some, but not all, cellular biomarkers of ageing. Strikingly, we found strong evidence that stochastic as well as genetic factors are significant in C. elegans ageing, with extensive variability both among same-age animals and between cells of the same type within individuals.

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The genetics of caloric restriction in Caenorhabditis elegans.

B Lakowski, S Hekimi (1998)

Low caloric intake (caloric restriction) can lengthen the life span of a wide range of animals and possibly even of humans. To understand better how caloric restriction lengthens life span, we used genetic methods and criteria to investigate its mechanism of action in the nematode Caenorhabditis elegans. Mutations in many genes (eat genes) result in partial starvation of the worm by disrupting the function of the pharynx, the feeding organ. We found that most eat mutations significantly lengthen life span (by up to 50%). In C. elegans, mutations in a number of other genes that can extend life span have been found. Two genetically distinct mechanisms of life span extension are known: a mechanism involving genes that regulate dauer formation (age-1, daf-2, daf-16, and daf-28) and a mechanism involving genes that affect the rate of development and behavior (clk-1, clk-2, clk-3, and gro-1). We find that the long life of eat-2 mutants does not require the activity of DAF-16 and that eat-2; daf-2 double mutants live even longer than extremely long-lived daf-2 mutants. These findings demonstrate that food restriction lengthens life span by a mechanism distinct from that of dauer-formation mutants. In contrast, we find that food restriction does not further increase the life span of long-lived clk-1 mutants, suggesting that clk-1 and caloric restriction affect similar processes.

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A stress-sensitive reporter predicts longevity in isogenic populations of Caenorhabditis elegans.

James Vaupel, Shane Rea, J Cypser … (2005)

When both genotype and environment are held constant, 'chance' variation in the lifespan of individuals in a population is still quite large. Using isogenic populations of the nematode Caenorhabditis elegans, we show that, on the first day of adult life, chance variation in the level of induction of a green fluorescent protein (GFP) reporter coupled to a promoter from the gene hsp-16.2 predicts as much as a fourfold variation in subsequent survival. The same reporter is also a predictor of ability to withstand a subsequent lethal thermal stress. The level of induction of GFP is not heritable, and GFP expression levels in other reporter constructs are not associated with differences in longevity. HSP-16.2 itself is probably not responsible for the observed differences in survival but instead probably reflects a hidden, heterogeneous, but now quantifiable, physiological state that dictates the ability of an organism to deal with the rigors of living.

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Author and article information

Journal

Journal ID (nlm-ta): Genome Biol

Title: Genome Biology

Publisher: BioMed Central

ISSN (Print): 1465-6906

ISSN (Electronic): 1465-6914

Publication date (Print): 2008

Publication date (Electronic): 16 September 2008

Volume: 9

Issue: 9

Page: 233

Affiliations

[1 ]Department of Molecular, Cellular and Developmental Biology, Yale University, New Haven, CT 06520, USA

Article

Publisher ID: gb-2008-9-9-233

DOI: 10.1186/gb-2008-9-9-233

PMC ID: 2592707

PubMed ID: 18828877

SO-VID: eed8cbd8-7949-4072-95ce-9dcbecdf1521

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Transcriptional (dys)regulation and aging in Caenorhabditis elegans

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Aging Pathobiology and Therapeutics

Most cited references 21

Stochastic and genetic factors influence tissue-specific decline in ageing C. elegans.

The genetics of caloric restriction in Caenorhabditis elegans.

A stress-sensitive reporter predicts longevity in isogenic populations of Caenorhabditis elegans.

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