The RAS genes: a homeostatic device in Saccharomyces cerevisiae longevity☆

Jazwinski, S. Michal

doi:10.1016/s0197-4580(99)00095-0

Cited by 40 publications

(20 citation statements)

References 45 publications

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“…Considering that ruption of MIG2 has on replicative life span. Strikingly, PKA activity inhibits the APC and reduces life span MIG2 disruption extends life span in both APC5 and (Kotani et al 1998;Jazwinski 1999;Lin et al 2002), apc5 CA cells to the same extent ( Figure 8B). This indian antagonistic interaction between Snf1p and PKA cates that Mig2p normally reduces life span and that (Hubbard et al 1992) would suggest that Snf1p may reduced apc5 CA life span requires Mig2p.…”

mentioning

confidence: 85%

A Functional Analysis Reveals Dependence on the Anaphase-Promoting Complex for Prolonged Life Span in Yeast

et al. 2004

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Defects in anaphase-promoting complex (APC) activity, which regulates mitotic progression and chromatin assembly, results in genomic instability, a hallmark of premature aging and cancer. We investigated whether APC-dependent genomic stability affects aging and life span in yeast. Utilizing replicative and chronological aging assays, the APC was shown to promote longevity. Multicopy expression of genes encoding Snf1p (MIG1) and PKA (PDE2) aging-pathway components suppressed apc5 CA phenotypes, suggesting their involvement in APC-dependent longevity. While it is known that PKA inhibits APC activity and reduces life span, a link between the Snf1p-inhibited Mig1p transcriptional modulator and the APC is novel. Our mutant analysis supports a model in which Snf1p promotes extended life span by inhibiting the negative influence of Mig1p on the APC. Consistent with this, we found that increased MIG1 expression reduced replicative life span, whereas mig1⌬ mutations suppressed the apc5 CA chronological aging defect. Furthermore, Mig1p and Mig2p activate APC gene transcription, particularly on glycerol, and mig2⌬, but not mig1⌬, confers a prolonged replicative life span in both APC5 and acp5 CA cells. However, glucose repression of APC genes was Mig1p and Mig2p independent, indicating the presence of an uncharacterized factor. Therefore, we propose that APC-dependent genomic stability is linked to prolonged longevity by the antagonistic regulation of the PKA and Snf1p pathways.

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confidence: 85%

A Functional Analysis Reveals Dependence on the Anaphase-Promoting Complex for Prolonged Life Span in Yeast

et al. 2004

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“…Aging is controlled by both environmental factors and the genetic constitution of the individual [1] and has been described as a progressive decline of the ability to withdraw stress, damage and disease. Furthermore, it is characterized by an increase of degenerative and neoplastic disorders [2]. …”

Section: Endogenous Skin Agingmentioning

confidence: 99%

“…Recent studies on models such as the yeast Saccharomyces cerevisiae [2], the nematode Caenorhabditis elegans [58], the fly Drosophila melanogaster [59,60,61], the mouse Mus musculus [62] and humans [63] show that single gene mutations can contribute to the initiation of aging and induce premature aging syndromes. However, there are no special genes that can cause aging-associated damages.…”

Section: Genes and Mutationsmentioning

confidence: 99%

Characteristics and Pathomechanisms of Endogenously Aged Skin

2007

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The skin, being in direct contact with several environmental factors (e.g. UV irradiation), does not only undergo endogenous aging, which has to do with the ‘biological clock’ of the skin cells per se, but also exogenous aging. While exogenous skin aging has been extensively studied, the pathomechanisms of endogenous skin aging remain far less clear. Endogenous skin aging reflects reduction processes, which are common in internal organs. These processes include cellular senescence and decreased proliferative capacity, decrease in cellular DNA repair capacity and chromosomal abnormalities, loss of telomeres, point mutations of extranuclear mtDNA, oxidative stress and gene mutations. As a consequence, aged skin in nonexposed areas shows typical characteristics including fine wrinkles, dryness, sallowness and loss of elasticity. Recent data have illustrated that lack of hormones occurring with age may also contribute to the aging phenotype. Improvement of epidermal skin moisture, elasticity and skin thickness, enhanced production of surface lipids, reduction of wrinkle depth, restoration of collagen fibers and increase of the collagen III/I ratio have been reported after hormone replacement therapy or local estrogen treatment in postmenopausal women. Furthermore, an in vitro model of endogenous skin aging consisting of human SZ95 sebocytes which were incubated under a hormone-substituted environment illustrated that hormones at age- and sex-specific levels were able to alter the development of cells by regulating their transcriptome. In conclusion, among other factors the hormone environment plays a distinct role in the generation of aged skin.

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“…Recent studies on models such as the yeast Saccharomyces cerevisiae [32], the nematode Caenorhabditis elegans [33], the fly Drosophila melanogaster . Figure 9.1 A schematic overview of major biochemical changes and signaling pathways involved in the generation of endogenously aged skin.…”

Section: Genes and Mutationsmentioning

confidence: 99%