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Shorter Lifespans (shorter + lifespan)

Distribution by Scientific Domains

Life Sciences	85%

Selected Abstracts

Sexual selection did not contribute to the evolution of male lifespan under curtailed age at reproduction in a seed beetle

ECOLOGICAL ENTOMOLOGY, Issue 5 2009
ALEXEI A. MAKLAKOV
Abstract. 1. Sexual selection is a powerful evolutionary force that is hypothesised to play an important role in the evolution of lifespan. Here we test for the potential contribution of sexual selection to the rapid evolution of male lifespan in replicated laboratory populations of the seed beetle, Callosobruchus maculatus. 2. For 35 generations, newly hatched virgin male beetles from eight different populations were allowed to mate for 24 h and then discarded. Sexual selection was removed in half of these populations by enforcing random monogamy. 3. Classic theory predicts that because of sexual competition, males from sexually selected lines would have higher age-specific mortality rates and shorter lifespan than males from monogamous lines. 4. Alternatively, condition-dependent sexual selection may also favour genes that have positive pleiotropic effects on lifespan and ageing. 5. Males from all eight populations evolved shorter lifespans compared with the source population. However, there was no difference in lifespan between males from populations with or without sexual selection. Thus, sexual selection did not contribute to the evolution of male lifespan despite the fact that such evolution did occur in our study populations. [source]

Dicer ablation in oligodendrocytes provokes neuronal impairment in mice,

ANNALS OF NEUROLOGY, Issue 6 2009
Daesung Shin PhD
Objective MicroRNAs (miRNAs) regulate gene expression and have many roles in the brain, but a role in oligodendrocyte (OL) function has not been demonstrated. Methods A Dicer floxed conditional allele was crossed with the proteolipid protein promoter-driven inducible Cre allele to generate inducible, OL-specific Dicer -floxed mice. Results OL-specific Dicer mutants show demyelination, oxidative damage, inflammatory astrocytosis and microgliosis in the brain, and eventually neuronal degeneration and shorter lifespan. miR-219 and its target ELOVL7 (elongation of very long chain fatty acids protein 7) were identified as the main molecular components that are involved in the development of the phenotype in these mice. Overexpressing ELOVL7 results in lipid accumulation, which is suppressed by miR-219 co-overexpression. In Dicer mutant brain, excess lipids accumulate in myelin-rich brain regions, and the peroxisomal ,-oxidation activity is dramatically reduced. Interpretation Postnatal Dicer ablation in mature OLs results in inflammatory neuronal degeneration through increased demyelination, lipid accumulation, and peroxisomal and oxidative damage, and therefore indicates that miRNAs play an essential role in the maintenance of lipids and redox homeostasis in mature OLs that are necessary for supporting axonal integrity as well as the formation of compact myelin. Ann Neurol 2009;66:843,857 [source]

Sexual selection did not contribute to the evolution of male lifespan under curtailed age at reproduction in a seed beetle

Contrasting frequencies of parasitism and host mortality among phorid and conopid parasitoids of bumble-bees

ECOLOGICAL ENTOMOLOGY, Issue 2 2002
Michael C. Otterstatter
Abstract 1. Phorid (Diptera, Phoridae) and conopid (Diptera, Conopidae) parasitism among four North American bumble-bee (Hymenoptera, Apidae) species was investigated. Male bumble-bees experienced a significantly higher incidence of parasitism by the phorid, Apocephalus borealis Brues, and a significantly lower incidence of parasitism by the conopid, Physocephala texana Williston, than did workers. 2. The incidence of parasitism by A. borealis and P. texana varied between bumble-bee sexes and species in patterns that did not reflect differences in relative host abundance. Differences in foraging behaviour between bumble-bee workers and males, as well as between species, may explain these results. 3. Bumble-bee workers and males parasitised by A. borealis had significantly shorter lifespans than unparasitised bees. Based on previous estimates of bumble-bee mortality, A. borealis parasitism may reduce worker lifespans by up to 70%. In contrast, the mortality rate of bees parasitised by P. texana was not significantly different from that of unparasitised bees. 4. These results contrast with previous work highlighting the importance of conopid parasitism to bumble-bee populations, and suggest that phorid parasitism may impose greater costs to bumble-bees than does conopid parasitism in local populations. [source]

Reproduction and lifespan: Trade-offs, overall energy budgets, intergenerational costs, and costs neglected by research,

AMERICAN JOURNAL OF HUMAN BIOLOGY, Issue 4 2009
Grazyna Jasienska
In human females allocation of resources to support reproduction may cause their insufficient supply to other metabolic functions, resulting in compromised physiology, increased risks of diseases and, consequently, reduced lifespan. While many studies on both historical and contemporary populations show that women with high fertility indeed have shorter lifespans. This relationship is far from universal: a lack of correlation between fertility and lifespan, or even an increased lifespan of women with high fertility have also been documented. Reduced lifespan in women with high fertility may be undetectable due to methodological weaknesses of research or it may be truly absent, and its absence may be explained from biological principles. I will discuss the following reasons for a lack of the negative relationship, described in some demographic studies, between the number of children and lifespan in women: (1) Number of children is only a proxy of the total costs of reproduction and the cost of breastfeeding is often higher than the pregnancy cost but is often not taken into account. (2) Costs of reproduction can be interpreted in a meaningful way only when they are analyzed in relation to the overall energy budget of the woman. (3) Trade-offs between risks of different diseases due to reproduction yield different mortality predictions depending on the socio-economic status of the studied populations. (4) Costs of reproduction are related not only to having children but also to having grandchildren. Such intergenerational costs should be included in analysis of trade-offs between costs of reproduction and longevity. Am. J. Hum. Biol., 2009. © 2009 Wiley-Liss, Inc. [source]

Effects of leaf emergence on leaf lifespan are independent of life form and successional status

AUSTRAL ECOLOGY, Issue 7 2008
ROGER J. DUNGAN
Abstract The longevity of a leaf is related to the benefit that the plant is able to derive from it. This benefit varies among seasons and as more leaves emerge, such that leaf lifespan can be limited by canopy position rather than physiological age. Using interval-censored failure time analysis, we investigate leaf lifespan for 34 Mediterranean species in a previously published dataset involving species with different life forms and functional strategies. Failure time regression models were used to determine leaf lifespan, and to investigate how these effects varied among species. Median lifespan estimated for each species with two methods differed by less than 10% on average, but varied from 0.02,19.5% depending on the shape of the underlying failure time distribution. Within shoots, later-emerging leaves had shorter lifespans for species with longer periods of leaf emergence, and the reverse was true for species with short emergence. Having accounted for the within-shoot effect, leaves emerging in spring had shorter lifespans, particularly herbaceous species, whereas the reverse was true woody species. These effects were consistent among life forms and successional stages, and consistent with theories of within-shoot translocation of resources following self-shading. [source]

p53 and ageing: too much of a good thing?

BIOESSAYS, Issue 7 2002
Thomas B.L. Kirkwood
A recent report by Tyner et al.1 suggests that p53 is bad for longevity. Heterozygotic mice carrying a p53 mutation that apparently enhances the stability of the wild-type protein showed shorter lifespans and faster ageing while also developing fewer tumours. This fits with the idea that cellular ageing is the price paid for better protection against unlimited proliferation of cancer cells. But other work shows that there is a strong positive association between DNA repair-mediated protection against cancer and ageing. So what are we to make of the new data with regard to overall understanding of the mechanisms of ageing? BioEssays 24:577,579, 2002. © 2002 Wiley Periodicals, Inc. [source]