Abstract
Aging/senescence includes not just decline in lifespan but also etiologies of age associated morbidities which are inadequately understood. Extensive research has been undertaken to delineate the pathways and generate mutants with extended lifespan. However, little is known about the health status of these long lived mutants in the background of important genetic perturbations. Caenorhabditis elegans is one of the leading in vivo model organisms to study aging. Deletion of SIN-3, a transcription coregulator in C. elegans has been shown to reduce the lifespan of the mutant worms by half as compared to the wild-type and isogenic controls. The current study focuses on the effect of SIN-3 deletion on the healthspan of the worms. We find that not only are sin-3 mutants more susceptible to stress, but the overall stress intolerance and physiological decline is sex dependent. The severity of the phenotype is more pronounced in hermaphrodites as compared to the males carrying the same mutation with respect to the controls. The results further suggest that genetic perturbation along with the gender play an important role in determining the lifespan, healthspan and overall fitness of an organism.
Highlights
Lifespan analysis as a measure of aging has been a conventional parameter explored by bio-gerontologists
The results further suggest that genetic perturbation along with the gender play an important role in determining the lifespan, healthspan and overall fitness of an organism
Diminished muscle function and decreased lifespan is an outcome of sin-3 deletion in C. elegans
Summary
Lifespan analysis as a measure of aging has been a conventional parameter explored by bio-gerontologists. Mere enhancement in lifespan or longevity does not translate into a healthy aging as the quality of life declines and organism becomes more susceptible to late-life illness [2,3]. Further studies done in long-lived mutants of reduced insulin/IGF signaling showed delayed onset of diseases in both worms and mouse model system [8]. Caenorhabditis elegans is one of the most extensively used model organism for studying aging. Behavioral parameters such as pharyngeal pumping, swimming, movement assays and reproductive phase etc. Chronological correlation between the healthspan to lifespan extension in various long-lived mutants of C. elegans such as daf-2, eat-2, ife-2 and clk-1 suggested that the mutations merely prolonged aging without any benefits in the healthspan [9]
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