Obesity, A Condition That Mimics Premature Aging

2021 ◽  
pp. 551-571
Author(s):  
Raffaele Carraro ◽  
Tania Romacho ◽  
Concepción Peiró ◽  
Emiliano Corpas ◽  
Carlos F. Sánchez-Ferrer
Keyword(s):  
Premature Aging

DNA Repair and Transcription in Human Premature Aging Disorders

1998 ◽  
Vol 3 (1) ◽  
pp. 11-13 ◽  
Author(s):  
Vilhelm A Bohr ◽  
Grigoiy Dianov ◽  
Adayabalam Balajee ◽  
Alfred May ◽  
David K Orren
Keyword(s):  
Dna Repair ◽  
Premature Aging

Understanding premature aging

2009 ◽  
Author(s):  
Mohammed Yahia
Keyword(s):  
Premature Aging

Premature aging of bone is delayed by dietary restriction

2014 ◽  
Author(s):  
der Eerden Bram van ◽  
Sander Botter ◽  
Erwin Reiling ◽  
Jan Hoeijmakers ◽  
Martijn Dolle ◽  
...  
Keyword(s):  
Dietary Restriction ◽  
Premature Aging

The Role of Cellular Senescence in Werner Syndrome: Toward Therapeutic Intervention in Human Premature Aging

2007 ◽  
Vol 1100 (1) ◽  
pp. 455-469 ◽  
Author(s):  
T. DAVIS ◽  
F. S. WYLLIE ◽  
M. J. ROKICKI ◽  
M. C. BAGLEY ◽  
D. KIPLING
Keyword(s):  
Cellular Senescence ◽  
Therapeutic Intervention ◽  
Werner Syndrome ◽  
Premature Aging

scholarly journals The Short Life Span of Saccharomyces cerevisiae sgs1 and srs2 Mutants Is a Composite of Normal Aging Processes and Mitotic Arrest Due to Defective Recombination

Genetics ◽  
2001 ◽  
Vol 157 (4) ◽  
pp. 1531-1542 ◽  
Author(s):  
Mitch McVey ◽  
Matt Kaeberlein ◽  
Heidi A Tissenbaum ◽  
Leonard Guarente
Keyword(s):  
Cell Cycle ◽  
Life Span ◽  
Mitotic Cell ◽  
Dna Helicase ◽  
Premature Aging ◽  
Growth Defect ◽  
Short Life Span ◽  
Single Strand Annealing ◽  
Late Generation ◽  
Strand Annealing

Abstract Evidence from many organisms indicates that the conserved RecQ helicases function in the maintenance of genomic stability. Mutation of SGS1 and WRN, which encode RecQ homologues in budding yeast and humans, respectively, results in phenotypes characteristic of premature aging. Mutation of SRS2, another DNA helicase, causes synthetic slow growth in an sgs1 background. In this work, we demonstrate that srs2 mutants have a shortened life span similar to sgs1 mutants. Further dissection of the sgs1 and srs2 survival curves reveals two distinct phenomena. A majority of sgs1 and srs2 cells stops dividing stochastically as large-budded cells. This mitotic cell cycle arrest is age independent and requires the RAD9-dependent DNA damage checkpoint. Late-generation sgs1 and srs2 cells senesce due to apparent premature aging, most likely involving the accumulation of extrachromosomal rDNA circles. Double sgs1 srs2 mutants are viable but have a high stochastic rate of terminal G2/M arrest. This arrest can be suppressed by mutations in RAD51, RAD52, and RAD57, suggesting that the cell cycle defect in sgs1 srs2 mutants results from inappropriate homologous recombination. Finally, mutation of RAD1 or RAD50 exacerbates the growth defect of sgs1 srs2 cells, indicating that sgs1 srs2 mutants may utilize single-strand annealing as an alternative repair pathway.

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