There was once a time when the view that model organisms would actually lead us to informative views regarding human aging was but a pious hope. That time has passed. Much of what we now know or suspect about human aging is based on studies originally done in model organisms. It turns out that the major gene systems regulating aging are highly conserved public mechanisms; the characterization of the genetic and metabolic pathways involved in longevity regulation, and the environmental conditions necessary for their expression, required the integration of data from the four most commonly used species: yeast, worm, fly, and mouse. A good review of the various genetic attributes and tools that make Drosophila melanogaster such an excellent experimental tool for investigation of the aging phenomenon is found in chapter 22 by Miwa and Cohen. This chapter will be concerned with the three different longevity phenotypes known in this organism and the nature of the gene expression patterns characteristic of each, with special emphasis on the extended longevity phenotype brought about by a delayed onset of senescence.
The laboratory experiments done over the past few decades have allowed the robust identification of four different—but intertwined—genetic and physiological pathways which seem to regulate longevity in all four of our model systems. These four major public longevity processes may be summarily listed as follows: (1) Metabolic Control, (2) Stress Resistance, (3) Genetic Stability, and (4) Reproductive Effects. Information regarding different patterns of senescence is still sketchy but we will deal with it under the fifth heading of Patterns of Senescence. [A more extensive discussion of these topics in all four model systems is given by Arking (2005a)]. Each of these categories should be regarded, not as an autonomous set of metabolic reactions, but rather as sets of regulatory reactions that are more closely linked to one another than to any of the other categories. Such a view obviously permits the existence of crosstalk between these several network hubs. Much of the variation inherent in aging may stem from such cross-reactions. Table 25.1 contains an outline summary of these major processes which play an important role in bringing about differential longevity and senescence in Drosophila melanogaster. These processes may be induced or repressed by a variety of stimuli, including pharmecutical interventions.
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