Introduction

Aging is a universal process conserved in evolution, which cripples the organism at the end stages of life, ultimately resulting in death (Hamet and Tremblay, 2003). Since the dawn of time, man wanted to be eternal and always wished to conquer aging and death. While ecologically conquering aging may not be compatible for normal evolution, improving the quality of life and extending the lifespan remain the major goals of aging research. For example, in classical studies on dietary restriction, it has been shown that a caloric restriction extends the lifespan (Masoro, 2005). In addition, reduction of oxidative stress by antioxidants has been shown to extend the lifespan in several organisms (Droge, 2003). Since all biological pathways are controlled by genes and their products, one would anticipate that there will be genes whose function, if they are modulated, may result in the extension of lifespan, including those involved in the processes mentioned above such as dietary restriction and oxidative stress (Johnson and Wood, 1982). In fact, recently such information on genes conferring longevity has been gathered using different model organisms and using both classical genetic methods as well as surrogate genetic approaches (Kenyon, 2005). In model organisms such as Drosophila and C. elegans, long-lived mutants have been selected by genetic approaches (Helfand and Rogina, 2003; Luo, 2004). In mice, the extension of the lifespan has been noted by modulating the gene dosage, utilizing transgenic methods and by using knockout methods (Liang et al., 2003). In these two approaches, the identification of mutant phenotypes by classical genetic methods is a powerful genetic approach that allows the identification of genes in an ''unbiased'' manner in a given pathway, as opposed to the gene-by-gene approach employed by knockout studies as well as by transgenic methods. Furthermore, even if one has to overexpress genes or knock out the genes to identify the players involved in aging, large-scale mutagenesis methods by retroviral insertion and expression methods would be suitable in a global search for genes conferring longevity. At present, neither classical genetic approaches nor large-scale insertion mutagenesis methods and overexpression studies have been applied to study aging in vertebrates, largely because of the difficulties of applying these approaches in the classical vertebrate model organism, the mouse.

Recently, fish have become genetic models for studying vertebrate development and disease (Kimmel, 1989; Patton and Zon, 2001). We and others have conceived the utility of fish as a model organism for studying genetics of aging (Gerhard et al., 2002; Herrera and Jagadeeswaran, 2002). In this chapter, arguments are put forth that fish are excellent genetic models for studying aging, and opinions are provided for why annual fish are better models for studying the genetics of aging as compared to other species of fish (Herrera and Jagadeeswaran, 2004). Furthermore, the applications of annual fish to study aging and the detailed approaches and their advantages are described.

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