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Chronological and replicative aging have been studied in yeast as alternative paradigms for post-mitotic and mitotic aging, respectively. It has been known for more than a decade that cells of the S288C background aged chronologically in rich medium have reduced replicative lifespan relative to chronologically young cells. Here we report replication of this observation in the diploid BY4743 strain background. We further show that the reduction in replicative lifespan from chronological aging is accelerated when cells are chronologically aged under standard conditions in synthetic complete medium rather than rich medium. The loss of replicative potential with chronological age is attenuated by buffering the pH of the chronological aging medium to 6.0, an intervention that we have previously shown can extend chronological lifespan. These data demonstrate that extracellular acidification of the culture medium can cause intracellular damage in the chronologically aging population that is asymmetrically segregated by the mother cell to limit subsequent replicative lifespan.
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http://dx.doi.org/10.4161/cc.21465 | DOI Listing |
PLoS One
September 2025
Mechanical and Nuclear Engineering Department, Khalifa University of Science and Technology, Abu Dhabi, United Arab Emirates.
Sectionally nonlinearly functionally graded (SNFG) structures with triply periodic minimal surface (TPMS) are considered ideal for bone implants because they closely replicate the hierarchical, anisotropic, and porous architecture of natural bone. The smooth gradient in material distribution allows for optimal load transfer, reduced stress shielding, and enhanced bone ingrowth, while TPMS provides high mechanical strength-to-weight ratio and interconnected porosity for vascularization and tissue integration. Wherein, The SNFG structure contains sections with thickness that varies nonlinearly along their length in different patterns.
View Article and Find Full Text PDFAging Cell
September 2025
CREEC/CANECEV, MIVEGEC (CREES) Department, University of Montpellier, CNRS, IRD, Montpellier, France.
Aging, and by extension age-related diseases, has traditionally been understood through classical evolutionary genetic models, such as the mutation accumulation and antagonistic pleiotropy theories. However, these frameworks primarily focus on the declining efficacy of organismal-level selection against mutations with deleterious effects in late life. Here, we propose a novel hypothesis: many chronic diseases associated with aging may emerge, at least in part, as a result of selection acting at lower organizational levels, including non-replicative biological entities, enabled by the relaxation of selective pressures that constrained within-organism evolutionary processes in early life.
View Article and Find Full Text PDFCell Host Microbe
August 2025
Division of Molecular Microbiology, School of Life Sciences, University of Dundee, Dundee DD1 5EH, UK. Electronic address:
Streptococcus pneumoniae colonizes human airways, where it acquires sugars from glycosylated mucins using glycoside hydrolases and sugar transport systems. This study identifies widespread nucleotide sequence variation in the promoter of a pneumococcal operon encoding a glycan scavenging system. We identify 78 promoter sequence patterns across 21,155 genomes, with variation clustered within a stretch of adenines, where mutations accumulate via strand slippage during DNA replication.
View Article and Find Full Text PDFElife
September 2025
Department of Health Management and Institute of Health Management, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, China.
The regulation of cellular metabolism and growth in response to nutrient availability is crucial for cell survival and can significantly impact on lifespan. Central to this regulation is a class of transporters that sense and transport specific nutrients and transduce the signal downstream to control genes responsible for growth and survival. In this study, we identified SUL1, a plasma membrane transporter responsible for regulating the entry of extracellular sulfate in , as a key gene for regulating lifespan.
View Article and Find Full Text PDFJ Virol
September 2025
Department of Molecular Microbiology, School of Medicine, Washington University in St. Louis, St. Louis, Missouri, USA.
Viruses depend on their hosts for completing their life cycle, and a better understanding of virus replication can inform therapeutic strategies. Using the Orsay virus- experimental platform, we identified by a forward genetic screen the host gene (renamed ) as a novel host factor critical for Orsay virus replication. Three distinct mutations of each resulted in a >1,000-fold reduction in Orsay viral load, demonstrating a pro-viral function of had no previously described function in , but in the absence of viral infection, deletion of the locus by CRISPR/Cas9 led to a reduction in brood size and a shortened lifespan.
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