Proteostatic stress as a nodal hallmark of replicative aging

2020 ◽  
Vol 394 (2) ◽  
pp. 112163
Author(s):  
David F. Moreno ◽  
Martí Aldea
Keyword(s):  
Replicative Aging

scholarly journals Telomeres and replicative cellular aging of the human placenta and chorioamniotic membranes

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Tsung-Po Lai ◽  
Mark Simpson ◽  
Krunal Patel ◽  
Simon Verhulst ◽  
Jungsik Noh ◽  
...  
Keyword(s):  
Dna Damage ◽  
Preterm Birth ◽  
Telomere Length ◽  
Human Placenta ◽  
Replicative Senescence ◽  
Preterm Births ◽  
Full Term ◽  
Cellular Aging ◽  
Telomere Dysfunction ◽  
Replicative Aging

AbstractRecent hypotheses propose that the human placenta and chorioamniotic membranes (CAMs) experience telomere length (TL)-mediated senescence. These hypotheses are based on mean TL (mTL) measurements, but replicative senescence is triggered by short and dysfunctional telomeres, not mTL. We measured short telomeres by a vanguard method, the Telomere shortest length assay, and telomere-dysfunction-induced DNA damage foci (TIF) in placentas and CAMs between 18-week gestation and at full-term. Both the placenta and CAMs showed a buildup of short telomeres and TIFs, but not shortening of mTL from 18-weeks to full-term. In the placenta, TIFs correlated with short telomeres but not mTL. CAMs of preterm birth pregnancies with intra-amniotic infection showed shorter mTL and increased proportions of short telomeres. We conclude that the placenta and probably the CAMs undergo TL-mediated replicative aging. Further research is warranted whether TL-mediated replicative aging plays a role in all preterm births.

scholarly journals Replicative Aging in Pathogenic Fungi

2020 ◽  
Vol 7 (1) ◽  
pp. 6
Author(s):  
Somanon Bhattacharya ◽  
Tejas Bouklas ◽  
Bettina C. Fries
Keyword(s):  
Cell Division ◽  
Candida Glabrata ◽  
Asymmetric Cell Division ◽  
Pathogenic Fungi ◽  
Yeast Cells ◽  
Candida Auris ◽  
Replicative Aging ◽  
Yeast Saccharomyces Cerevisiae ◽  
Phenotypic Variations ◽  
Systemic Infections

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.

scholarly journals Replicative Aging in Candida auris Has an Effect on Antifungal Resistance

2017 ◽  
Vol 4 (suppl_1) ◽  
pp. S115-S115 ◽  
Author(s):  
Bettina C Fries ◽  
Somanon Bhattacharya ◽  
Erika Orner ◽  
Tejas Bouklas
Keyword(s):  
Antifungal Resistance ◽  
Candida Auris ◽  
Replicative Aging

scholarly journals Advances in quantitative biology methods for studying replicative aging in Saccharomyces cerevisiae

2020 ◽  
Vol 4 ◽  
pp. 151-160 ◽  
Author(s):  
Richard O'Laughlin ◽  
Meng Jin ◽  
Yang Li ◽  
Lorraine Pillus ◽  
Lev S. Tsimring ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Quantitative Biology ◽  
Replicative Aging

scholarly journals Altered States of Telomere Deprotection and the Two-Stage Mechanism of Replicative Aging

2009 ◽  
Vol 29 (9) ◽  
pp. 2390-2397 ◽  
Author(s):  
Ying Zou ◽  
Sandeep Misri ◽  
Jerry W. Shay ◽  
Tej K. Pandita ◽  
Woodring E. Wright
Keyword(s):  
Chromosomal Rearrangements ◽  
Qualitative Difference ◽  
Nonhomologous End Joining ◽  
End Joining ◽  
Replicative Aging ◽  
Dicentric Chromosomes ◽  
Dna Damage Signaling ◽  
Radiation Induced ◽  
Chromosome Formation ◽  
Quantitative Changes

ABSTRACT The molecular distinctions between mortality stages 1 (M1; senescence) and 2 (M2; crisis) of human replicative aging are ill defined. We demonstrate a qualitative difference between telomeric end associations at M1 and the end fusions that produce dicentric chromosomes and breakage-fusion cycles. Knockdown of ligase IV sufficient to completely inhibit radiation-induced dicentric chromosome formation had no effect on the frequency of telomere associations (TAs), establishing that TAs are not covalent conventional nonhomologous end-joining (NHEJ) products. TAs preceded and were more numerous than dicentric chromosomes. Cells initially tolerated dicentric chromosomes without dying, but eventually, a combination of too many TAs and dicentrics/complex chromosomal rearrangements resulted in apoptosis. We propose a working model in which end associations represent abortive DNA repair intermediates when the number of telomeric repeats is too small to completely inhibit DNA damage signaling but is sufficient to prevent the final covalent ligation step of NHEJ and induces the M1 checkpoint arrest in normal human cells. Rather than being all-or-none, telomere deprotection would thus proceed first through TAs before additional shortening leads to dicentric chromosomes. M2/crisis involves both qualitative changes (a shift from TAs to TAs plus dicentric chromosomes) and quantitative changes (an increase in the number of dysfunctional telomeres).

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