Two-dimensional protein electrophoretic analysis of postponed aging in Drosophila

Abstract

Five populations of Drosophila melanogaster that had been selected for postponed aging were compared with five control populations using two-dimensional protein gel electrophoresis. The goals of the study were to identify specific proteins associated with postponed aging and to survey the population genetics of the response to selection. A total of 321 proteins were resolvable per population; these proteins were scored according to their intensity. The resulting data were analyzed using resampling, combinatoric, and maximum parsimony methods. The analysis indicated that the populations with postponed aging were different from their controls with respect to specific proteins and with respect to the variation between populations. The populations selected for postponed aging were more heterogeneous between populations than were the control populations. Maximum parsimony trees separate the selected populations, as a group, from their controls, thereby exhibiting a homoplastic pattern.

Ageing: The Many-Headed Monster

“…From such theory it follows that many loci, and many biochemical pathways, are expected to produce the deleterious effects of ageing, because it is a secondary side-effect of normal evolution. Earlier, less definitive work using selected stocks [9] indicated that many loci contribute to ageing in Drosophila [10,11]. So Pletcher et al [1] are probably correct to implicate hundreds of loci in the control of Drosophila ageing.…”

Senescence: In search of causality

“…For instance, it has been estimated that >lo0 loci may be involved in aging in Drosophila based on comparisons of polypeptides found in long-lived strains (selected on the basis of late reproduction) and nonselected "short-lived" strains [Fleming et al, 1993; Rose, 19841. Nevertheless, it has been possible by analysis of hybrids formed between long-lived and short-lived strains to show the presence of both additive and nonadditive genetic determinants and to show that most of the additive effects seem t o reside on the third chromosome [Luckinbill et al, 1988;Buck et al, 19931. In C. elegans, where hybrid vigor does not complicate genetic analysis [Johnson and Wood, 19821, progress in localizing longevity determinants has been more rapid.…”

Rules for the use of model organisms in antiaging pharmacology

“…Many of these pathways are already considered candidates for pharmaceutical modulation (Melov et al ., 2000(Melov et al ., , 2001Lonn et al ., 2002;Evason et al ., 2005). However, the treatment of aging is highly likely to involve secondary and nonadditive effects, given the multifold pathways that affect aging (Fleming et al ., 1993;Pletcher et al ., 2002;Rose & Long, 2002). Therefore, the most reasonable expectation is that particular pharmaceuticals that affect aging may do so through multiple pathways, not just the pathway that is of a priori interest.…”