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      Healthy Aging – Insights from Drosophila

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          Abstract

          Human life expectancy has nearly doubled in the past century due, in part, to social and economic development, and a wide range of new medical technologies and treatments. As the number of elderly increase it becomes of vital importance to understand what factors contribute to healthy aging. Human longevity is a complex process that is affected by both environmental and genetic factors and interactions between them. Unfortunately, it is currently difficult to identify the role of genetic components in human longevity. In contrast, model organisms such as C. elegans, Drosophila, and rodents have facilitated the search for specific genes that affect lifespan. Experimental evidence obtained from studies in model organisms suggests that mutations in a single gene may increase longevity and delay the onset of age-related symptoms including motor impairments, sexual and reproductive and immune dysfunction, cardiovascular disease, and cognitive decline. Furthermore, the high degree of conservation between diverse species in the genes and pathways that regulate longevity suggests that work in model organisms can both expand our theoretical knowledge of aging and perhaps provide new therapeutic targets for the treatment of age-related disorders.

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          Most cited references171

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          Pleiotropy, Natural Selection, and the Evolution of Senescence

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            Extension of life-span by loss of CHICO, a Drosophila insulin receptor substrate protein.

            The Drosophila melanogaster gene chico encodes an insulin receptor substrate that functions in an insulin/insulin-like growth factor (IGF) signaling pathway. In the nematode Caenorhabditis elegans, insulin/IGF signaling regulates adult longevity. We found that mutation of chico extends fruit fly median life-span by up to 48% in homozygotes and 36% in heterozygotes. Extension of life-span was not a result of impaired oogenesis in chico females, nor was it consistently correlated with increased stress resistance. The dwarf phenotype of chico homozygotes was also unnecessary for extension of life-span. The role of insulin/IGF signaling in regulating animal aging is therefore evolutionarily conserved.
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              Cost of mating in Drosophila melanogaster females is mediated by male accessory gland products.

              Female Drosophila melanogaster with environmentally or genetically elevated rates of mating die younger than controls. This cost of mating is not attributable to receipt of sperm. We demonstrate here that seminal fluid products from the main cells of the male accessory gland are responsible for the cost of mating in females, and that increasing exposure to these products increases female death rate. Main-cell products are also involved in elevating the rate of female egg-laying, in reducing female receptivity to further matings and in removing or destroying sperm of previous mates. The cost of mating to females may therefore represent a side-effect of evolutionary conflict between males.
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                Author and article information

                Journal
                Front Physiol
                Front Physiol
                Front. Physio.
                Frontiers in Physiology
                Frontiers Research Foundation
                1664-042X
                01 April 2012
                18 April 2012
                2012
                : 3
                : 106
                Affiliations
                [1] 1simpleProgram in Developmental and Stem Cell Biology, The Hospital for Sick Children Toronto, ON, Canada
                [2] 2simpleDepartment of Molecular Genetics, University of Toronto Toronto, ON, Canada
                Author notes

                Edited by: Vladimir Titorenko, Concordia University, Canada

                Reviewed by: Mildred Audrey Pointer, North Carolina Central University, USA; William Donald Phillips, The University of Sydney, Australia

                *Correspondence: Konstantin G. Iliadi and Gabrielle L. Boulianne, Program in Developmental and Stem Cell Biology, The Hospital for Sick Children, TMDT, 101 College Street, Room 12-305, Toronto, ON, Canada M5G 1L7. e-mail: iliadi@ 123456sickkids.com ; gboul@ 123456sickkids.ca

                This article was submitted to Frontiers in Integrative Physiology, a specialty of Frontiers in Physiology.

                Article
                10.3389/fphys.2012.00106
                3328947
                22529821
                0ae3fe7b-bd75-4da7-9bcc-7d67af7927cf
                Copyright © 2012 Iliadi, Knight and Boulianne.

                This is an open-access article distributed under the terms of the Creative Commons Attribution Non Commercial License, which permits non-commercial use, distribution, and reproduction in other forums, provided the original authors and source are credited.

                History
                : 05 March 2012
                : 03 April 2012
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 198, Pages: 11, Words: 12504
                Categories
                Physiology
                Review Article

                Anatomy & Physiology
                environment,genetics,lifespan,drosophila,aging
                Anatomy & Physiology
                environment, genetics, lifespan, drosophila, aging

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