How a Mutation that Slows Aging Can Also Disproportionately Extend End-of-Life Decrepitude
| Autor: | Katie Podshivalova, Cynthia Kenyon, Rex Kerr |
|---|---|
| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Aging media_common.quotation_subject Population Colony Count Microbial Physiology Biology medicine.disease_cause General Biochemistry Genetics and Molecular Biology Article Life extension 03 medical and health sciences Bacterial colonization Risk Factors Long period medicine Escherichia coli Animals Colonization education Caenorhabditis elegans Caenorhabditis elegans Proteins lcsh:QH301-705.5 media_common Mutation education.field_of_study Ecology Longevity 030104 developmental biology lcsh:Biology (General) Digestive tract |
| Zdroj: | Cell Reports, Vol 19, Iss 3, Pp 441-450 (2017) |
| ISSN: | 2211-1247 |
| Popis: | Summary: The goal of aging research is to extend healthy, active life. For decades, C. elegans daf-2 insulin/insulin-like growth factor 1 (IGF-1) receptor mutants have served as a model for extended lifespan and youthfulness. However, a recent report suggested that their longevity is associated with an undesirable phenotype: a disproportionately long period of decrepitude at the end of life. In the human population, such an outcome would be a burden to society, bringing into question the relevance of daf-2 mutants as a model for life extension. However, here we report that, following an extended period of movement, daf-2 mutants survive longer in a decrepit state because of a beneficial trait: they are resistant to colonization of the digestive tract by dietary bacteria, a condition that leads to premature death in the wild-type and prevents their manifestation of decrepitude. If bacterial colonization is prevented, then daf-2 mutants lead both chronologically and proportionately healthier lives relative to the wild-type. : Podshivalova et al. show that long-lived C. elegans insulin/IGF-1 receptor mutants remain active longer but then resist bacterially induced mortality, allowing them to survive into a state of end-of-life decrepitude. Thus, changes that slow aging and also prevent an age-associated catastrophe can extend both the youthful and infirm periods of life. Keywords: aging, lifespan, healthspan, daf-2, mortality, IGF-1, pathogenesis |
| Databáze: | OpenAIRE |
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