Genetics, Aging, and Longevity in Model Organisms

This study shows that C. elegans mothers transfer yolk to offspring via lactation, a process promoted by insulin/IGF-1 signalling, leading to reproductive death.

This study shows that AMPK enhances associative learning in C. elegans by promoting neuronal mitochondrial fusion, which is critical for maintaining neuronal function with age and in neurodegenerative conditions.

This paper develops an aging clock using human and microbial gene expression data, showing associations between biological age and lifestyle factors.

This study shows that NHR-49 promotes longevity and innate immunity in C. elegans through distinct tissue-specific mechanisms and transcriptional programs.

This study uses scRNA-seq to analyze yeast ageing, finding increased transcriptional variability and identifying FIT3 as a marker of early heterogeneity.

This study identifies age-vulnerable motor circuit functions in Drosophila under oxidative and temperature stress, showing distinct aging patterns and highlighting potential neurophysiological markers.

The paper identifies SOD-2 as the only active SOD enzyme in C. elegans through in-gel activity analysis and mutant studies.

This study identifies nhx-2 as a modulator that extends reproductive longevity and ameliorates alpha-synuclein aggregation effects in C. elegans by mimicking dietary restriction.

This study identifies age-dependent changes in rDNA copy number, methylation, and sequence variations in mice, linking these alterations to reduced pre-rRNA levels and shortened yeast lifespan.

The paper identifies an amino acid substitution in the Drosophila insulin receptor that extends lifespan without affecting growth or reproduction.

This study identifies genes contributing to beaver longevity and cancer resistance through genomic analysis of gene copy number, expression, and evolutionary changes.

This study examines the effects of phenolic acids on aging and metabolism in C. elegans, finding they improve lifespan and stress resistance but do not enhance mitochondrial function.

This study identifies a conserved metallophosphodiesterase in Drosophila that influences lifespan, with neuronal expression capable of rescuing lifespan defects.

The paper investigates amino acid variations in p53 across species and finds correlations between specific substitutions and extended lifespan.

The paper analyzes longevity interventions across species and identifies a structured 'landscape of longevity' with soft bounds on achievable lifespan, including a human upper limit of ~138 years.

The paper identifies ELT-3 as a GATA transcription factor that regulates cuticle collagen expression in C. elegans in response to environmental stimuli.

The paper maps oxidative DNA damage in C. elegans across age periods, showing age-specific patterns and a negative association between oxidative modification and pro-longevity gene expression.

This study shows that Hedgehog signaling in Drosophila glial cells protects proteostasis and extends lifespan, with potential therapeutic implications for degenerative diseases.

The paper identifies translational control of methionine and serine metabolic pathways as the mechanism underlying paralog-specific phenotypes in Rpl22 ribosomal protein mutants, linking these changes to cell division and replicative longevity.

The paper shows that early developmental ROS increases stress resistance and lifespan by reducing histone H3K4me3 levels in C. elegans and mammalian cells.

The paper argues that biological ageing involves a decrease in cellular sensitivity and information transmission due to accumulated damage, leading to increased noise in biological networks.

The paper shows age-related decline in heavy isotope content in mouse tissues, suggesting a potential link to aging and healthspan extension.

This study shows astaxanthin extends C. elegans lifespan by altering mitochondrial complex III biogenesis, with cross-species effects on oxidative phosphorylation.

The paper analyzes aging dynamics across 17 organs and plasma proteomics in mice, revealing consistent gene expression trajectories with organ-specific timing and amplitude.

The paper develops a dynamic model of damage accumulation in yeast cells to understand how damage retention and asymmetric division affect replicative ageing.

This study shows that inhibiting GMP synthesis extends yeast replicative lifespan through a mechanism independent of known nutrient-sensing and sirtuin pathways.

This study examines the effects of sugars and lipids on C. elegans growth, finding that excessive intake reduces lifespan, reproductive capacity, and body length while altering gene expression.

The paper combines theory and experiments in mice to show that senescent cells have a rapid turnover that saturates with age, leading to persistent differences in cell accumulation and explaining demographic mortality laws.

This study shows that ferrous-glutathione coupling promotes ferroptosis and frailty in C. elegans, and blocking ferroptosis extends lifespan and healthspan.

This study uses multi-parametric phenotyping to analyze ageing trajectories in C. elegans, revealing divergent ageing patterns in disease models and quantifying health states through phenotypic flexibility.