Different age-specific demographic profiles are generated in the same normal-lived Drosophila strain by different longevity stimuli.
We review the empirical data obtained with our normal-lived Ra control strain of Drosophila and show that this one genome is capable of invoking at least three different responses to external stimuli that induce the animal to express one of three different extended longevity phenotypes, each of which arises from one of three different antagonistic molecular mechanisms of stress resistance. The phenotypes are distinguished by different age-specific mortality patterns. Depending on the selected mechanism, the genome may respond by expressing a delayed onset of senescence (type 1), an increased early survival (type 2), or an increased late survival (type 3) phenotype, suggesting their different demographic effects. We suggest that the different demographic effects stem in part from the differential ability of each selection regime to reallocate the organism's energy from reproduction to somatic maintenance. These data document the complexity of the aging process and argue for a relationship between molecular mechanisms and longevity phenotypes.
Arking
Robert
R
Department of Biological Sciences, Wayne State University, Detroit, Michigan 48202, USA. rarking@biology.biosi.wayne.edu
Novoseltseva
Janna
J
Hwangbo
Dae-Sung
DS
Novoseltsev
Vassily
V
Lane
Mark
M
D000375:Aging / Q000235:genetics; D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D004330:Drosophila / Q000235:genetics*; D004351:Drug Resistance / Q000235:genetics; D005298:Fertility / Q000235:genetics; D006358:Hot Temperature; D008136:Longevity / Q000235:genetics*; D010269:Paraquat / Q000633:toxicity; D010641:Phenotype
D000975:Antioxidants; D010269:Paraquat