Age-dependent decline in stress response capacity revealed by proteins dynamics analysis

Chen, Kaiyue; Wang, Shen; Zhang, Zhiwen; Xiong, Fangzheng; Ouyang, Qi; Luo, Chunxiong

doi:10.1038/s41598-020-72167-4

Cited by 27 publications

(21 citation statements)

References 44 publications

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“…Aging and attenuated stress responses are commonly observed in different organisms ranging from yeast to man [1][2][3]. Understanding the molecular mechanism involved in sensing stress and activating the stress response axis is essential for studying the aging process.…”

Section: Introductionmentioning

confidence: 99%

Augmentation of the heat shock axis during exceptional longevity in Ames dwarf mice

et al. 2021

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How the heat shock axis, repair pathways, and proteostasis impact the rate of aging is not fully understood. Recent reports indicate that normal aging leads to a 50% change in several regulatory elements of the heat shock axis. Most notably is the age-dependent enhancement of inhibitory signals associated with accumulated heat shock proteins and hyper-acetylation associated with marked attenuation of heat shock factor 1 (HSF1)–DNA binding activity. Because exceptional longevity is associated with increased resistance to stress, this study evaluated regulatory check points of the heat shock axis in liver extracts from 12 months and 24 months long-lived Ames dwarf mice and compared these findings with aging wild-type mice. This analysis showed that 12M dwarf and wild-type mice have comparable stress responses, whereas old dwarf mice, unlike old wild-type mice, preserve and enhance activating elements of the heat shock axis. Old dwarf mice thwart negative regulation of the heat shock axis typically observed in usual aging such as noted in HSF1 phosphorylation at Ser307 residue, acetylation within its DNA binding domain, and reduction in proteins that attenuate HSF1–DNA binding. Unlike usual aging, dwarf HSF1 protein and mRNA levels increase with age and further enhance by stress. Together these observations suggest that exceptional longevity is associated with compensatory and enhanced HSF1 regulation as an adaptation to age-dependent forces that otherwise downregulate the heat shock axis.

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Section: Introductionmentioning

confidence: 99%

Augmentation of the heat shock axis during exceptional longevity in Ames dwarf mice

et al. 2021

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“…Stress resistance is a key feature for the maintenance of healthspan and declines with age in C. elegans as well as in humans [17][18][19]. Therefore, heat stress resistance was selected to assess the health status of the nematodes.…”

Section: Resultsmentioning

confidence: 99%

Genes implicated in Caenorhabditis elegans and human health regulate stress resistance and physical abilities in aged Caenorhabditis elegans

et al. 2021

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Recently, nine Caenorhabditis elegans genes, grouped into two pathways/clusters, were found to be implicated in healthspan in C. elegans and their homologues in humans, based on literature curation, WormBase data mining and bioinformatics analyses. Here, we further validated these genes experimentally in C. elegans . We downregulated the nine genes via RNA interference (RNAi), and their effects on physical function (locomotion in a swim assay) and on physiological function (survival after heat stress) were analysed in aged nematodes. Swim performance was negatively affected by the downregulation of acox-1.1 , pept-1 , pak-2 , gsk-3 and C25G6.3 in worms with advanced age (twelfth day of adulthood) and heat stress resistance was decreased by RNAi targeting of acox-1.1 , daf-22 , cat-4 , pig-1 , pak-2 , gsk-3 and C25G6.3 in moderately (seventh day of adulthood) or advanced aged nematodes. Only one gene, sad-1 , could not be linked to a health-related function in C. elegans with the bioassays we selected. Thus, most of the healthspan genes could be re-confirmed by health measurements in old worms.

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“…This highly innovative technique uses an inducible genetic system in which mother cells maintain a normal replicative life span, while the daughter cells are eliminated [ 23 ]. This technique was first developed and applied to study age-related phenotypes of S. cerevisiae [ 24 , 25 , 26 ] and does not require any micromanipulations. The mother enrichment program (MEP) uses a Cre-lox recombinase system to knockout two essential genes— UBC9 (encoding SUMO-conjugating enzyme) and CDC20 (encoding activator of the anaphase-promoting complex)—in the daughter cells.…”

Section: Methods To Analyze Replicative Life Span (Rls)mentioning

confidence: 99%

Replicative Aging in Pathogenic Fungi

Bhattacharya

Bouklas

Fries

2020

JoF

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Candida albicans, Candida auris, Candida glabrata, and Cryptococcus neoformans are pathogenic yeasts which can cause systemic infections in immune-compromised as well as immune-competent individuals. These yeasts undergo replicative aging analogous to a process first described in the nonpathogenic yeast Saccharomyces cerevisiae. The hallmark of replicative aging is the asymmetric cell division of mother yeast cells that leads to the production of a phenotypically distinct daughter cell. Several techniques to study aging that have been pioneered in S. cerevisiae have been adapted to study aging in other pathogenic yeasts. The studies indicate that aging is relevant for virulence in pathogenic fungi. As the mother yeast cell progressively ages, every ensuing asymmetric cell division leads to striking phenotypic changes, which results in increased antifungal and antiphagocytic resistance. This review summarizes the various techniques that are used to study replicative aging in pathogenic fungi along with their limitations. Additionally, the review summarizes some key phenotypic variations that have been identified and are associated with changes in virulence or resistance and thus promote persistence of older cells.

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Age-dependent decline in stress response capacity revealed by proteins dynamics analysis

Cited by 27 publications

References 44 publications

Augmentation of the heat shock axis during exceptional longevity in Ames dwarf mice

Augmentation of the heat shock axis during exceptional longevity in Ames dwarf mice

Genes implicated in Caenorhabditis elegans and human health regulate stress resistance and physical abilities in aged Caenorhabditis elegans

Replicative Aging in Pathogenic Fungi

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