Genetics, Aging, and Longevity in Model Organisms

This study shows that artificially stimulating retrotransposon activity in Drosophila reduces lifespan and accelerates some aging phenotypes, with dFOXO partially rescuing these effects.

The paper confirms that set-2 mutants in C. elegans extend lifespan when fed HT115 E. coli, but not OP50-1, suggesting diet-dependent regulation of COMPASS complex effects on aging.

The paper shows that aging and lifestyle factors cause genotoxic damage, leading to reduced transcription of long genes across multiple species and tissues.

The paper shows ASI sensory neurons control the CEP-1/p53 DNA damage response in PGCs via TGF-beta signaling, reducing inherited mutations.

This study shows that chromosome XII fragments, not ERCs, drive senescence in yeast, despite rDNA copy number increases with age.

The paper develops a multi-scale model of yeast replicative ageing, identifying metabolic phases and interventions that influence lifespan by linking protein damage and ATP demand.

The paper shows that reducing Cth2 activity in yeast increases lifespan by improving mitochondrial function through reduced repression of iron-related genes.

The paper uses supervised machine learning with feature selection to prioritize aging-related genes in C. elegans, identifying known and novel genes associated with cellular dysfunction markers.

This study examines pharyngeal pumping defects in C. elegans feeding mutants using high-speed video microscopy to identify specific timing and contraction issues affecting particle transport.

The paper identifies natural variation in the irld gene family affecting starvation resistance in C. elegans using MIP-seq and genome-wide association.

This study identifies age-related disruptions in excitatory/inhibitory balance in C. elegans neurons, showing that inhibitory signaling loss and calcium channel mutations contribute to functional decline.

The paper identifies CCF-1/CNOT7 as a CCR4-NOT subunit required for C. elegans stress response, interacting with PAL-1 to regulate elt-2 and elt-3 expression.

This study develops an ex vivo mouse brain slice model that mimics brain aging and shows prions accelerate aging-related molecular changes.

The paper links growth and aging through a mathematical model showing both processes are tied to the reduction in the fraction of cells dividing, providing insights into aging mechanisms and potential applications in improving vaccine effectiveness in the elderly.

The paper shows that ETS-5 in C. elegans BAG neurons regulates INS-1 expression, linking neuronal activity to systemic metabolism through diet-induced changes.

The paper shows that resveratrol and copper reduce multiple ageing and neurodegeneration markers by deactivating cell-free chromatin particles in mice.

The paper investigates the role of XRN-2 endoribonuclease activity in dauer state maintenance and post-dauer life cycle continuity in C. elegans, finding that its disruption leads to metabolic and developmental defects.

The paper measures developmental stage durations in C. elegans under varied conditions and finds that stages respond differently to environmental factors, supporting a linear progression model.

This study identifies Spt4 as a factor that accelerates cellular senescence by promoting non-coding RNA transcription in rDNA clusters, leading to genomic instability and reduced lifespan in yeast.

The paper compares protein aggregation propensity and mutation tolerance between naked mole-rat and mouse orthologous proteins, finding significant differences in specific protein subsets related to aging processes.

The paper identifies ALDH4A1 genetic variation as a biomarker for age-related muscle health across species using C. elegans and human data.

This study finds that somatic mutation rates per year decrease with species lifespan across mammals, suggesting evolutionary constraints on mutagenesis and its role in ageing.

The paper shows that a steroid hormone pathway regulates both entry into and exit from dauer diapause in C. elegans, with similar spatiotemporal dynamics for both processes.

This study shows neuronal HLH-30/TFEB improves thermoresistance in C. elegans by inducing mitochondrial fragmentation in muscles, independent of DAF-16/FOXO.

The paper identifies a heat shock factor, hsalHSF2, that contributes to extended lifespan in reproductive ants and shows its transferable role in enhancing survival in fruit flies.

This study identifies HPK-1 as a neuronal regulator of proteostasis that delays aging through distinct serotonergic and GABAergic pathways.

The paper investigates how intrinsic and extrinsic factors disrupt the gut visceral musculature in Drosophila and zebrafish, identifying four phenotypes as indicators of musculature deterioration.

This study develops a high-dimensional phenotyping platform to evaluate physiological aging and resilience in mice, finding that aging begins early and resilience declines with age.

This study investigates how curcumin's anti-aging effects are mediated through AhR-dependent and -independent pathways in different contexts.

The paper analyzes transcriptome and proteome data from aged mouse hearts to identify molecular changes associated with aging, revealing distinct biological processes and genetic loci influencing age-related changes.