Juvenile diet restriction and the aging and reproduction of adult Drosophila melanogaster

Abstract

SummaryMutations of the insulin signal pathway in Drosophila melanogaster produce long-lived adults with many correlated phenotypes. Homozygotes of insulin-like receptor ( InR ) and insulin-like receptor substrate ( chico ) delay time to eclosion, reduce body size, decrease reproduction and increase life span. Because these mutations are expressed through all life stages it is unclear when insulin signals must be reduced to increase life span. As a first analysis of this problem in D. melanogaster we have manipulated the larval diet to determine if changes in metabolic regulation at this stage are sufficient to slow aging. We controlled the dietary yeast fed to third instar larvae and studied the size, mortality, fecundity and hormones of the resulting adults, which were fed a normal, yeast-replete diet. Adults from yeast-deprived larvae phenocopied many traits of InR and chico mutants: small body size, delayed eclosion, reduced ovariole number and reduced age-specific fecundity. But unlike constitutive mutants of the insulin/IGF system, adults from yeast-deprived larvae had normal patterns of demographic senescence, and this was accompanied by normal insulin-like peptide and juvenile hormone syntheses. Surprisingly, the normal aging in these adults was also associated with greatly reduced fecundity. Although nutritional conditions of the larvae can affect the subsequent body size and fecundity of adults, these are not sufficient to slow aging.

Curcumin enhances parental reproductive lifespan and progeny viability in Drosophila melanogaster

“…Several studies in the past have successfully enhanced the lifespan of model organisms by dietary supplementation with reactive oxygen species (ROS)-scavenging substances (Howitz et al 2003;Wood et al 2004). However, in most diet manipulation studies (Chippindale et al 1993;Chapman and Partridge 1996;Tu and Tatar 2003) barring that of Chandrashekara and Shakarad (2011), the correlated response to increased longevity has been the reduced fecundity. Any manipulation that reduces fecundity is going to affect the fitness of the organism(s).…”

Cellular senescence in honey bee brain is largely independent of chronological age

“…The vitellogenin protein has an antioxidant function (Seehuus et al, 2006), and in addition vitellogenin activity suppresses the intrinsic JH level of worker bees (Guidugli et al, 2005). In Drosophila melanogaster, JH negatively affects longevity and oxidative stress resistance (Tatar and Yin, 2001;Tu and Tatar, 2003), and accumulated oxidative stress-induced damage is an established biomarker of aging (Sohal et al, 1995;Radak et al, 2002;Sohal, 2002;Soreghan et al, 2003;Nystrom, 2005). It has been proposed that foragers in response to low vitellogenin protein levels and high JH titers age more rapidly than nurse bees and diutinus workers that are characterized by high vitellogenin levels and low intrinsic JH titers (reviewed by ).…”

Reproductive protein protects functionally sterile honey bee workers from oxidative stress

“…S tudies of pathways that regulate longevity have identified endocrine signaling cascades that control fecundity and aging (1)(2)(3)(4). Insulin͞insulin-like growth factor signaling (IIS) is one such conserved pathway (5).…”

“…In the nematode Caenorhabditis elegans, IIS affects fertility and senescence antagonistically by means of separate regulatory events in the larval and adult stages, respectively (6). In Drosophila melanogaster, IIS increases adult reproductive capacity through a positive effect on ovary size during larval development and reduces lifespan in adult female flies (1,7). Life-history regulation by IIS remains to be studied in eusocial organisms (8).…”