PubMed Health⌕ Search

Biomedical subjects

Martin Dölling

Publications and source records attributed to Martin Dölling.

2 recordsLinked to original sources

Symmetrically dividing cells of the fission yeast schizosaccharomyces pombe do age.

Theories of the evolution of senescence state that symmetrically dividing organisms do not senesce. However, this view is challenged by experimental evidence. We measured by immunofluorescence the occurrence and intensity of protein carbonylation in single and symmetrically dividing cells of Schizosaccharomyces pombe. Cells of S. pombe show different levels of carbonylated proteins. Most cells have little damage, a few show a lot, an observation consistent with the gradual accumulation of carbonylation over time. At reproduction, oxidized proteins are shared between the two resulting cells. These results indicate that S. pombe does age, but does so in a different way from other studied species. Damaged cells give rise to damaged cells. The fact that cells with no or few carbonylated proteins constitute the main part of the population can explain why, although age is not reset to zero in one of the cells during division, the pool of young cells remains large enough to prevent the rapid extinction of the population.

Cell Division↗

The case for negative senescence.

Negative senescence is characterized by a decline in mortality with age after reproductive maturity, generally accompanied by an increase in fecundity. Hamilton (1966) ruled out negative senescence: we adumbrate the deficiencies of his model. We review empirical studies of various plants and some kinds of animals that may experience negative senescence and conclude that negative senescence may be widespread, especially in indeterminate-growth species for which size and fertility increase with age. We develop optimization models of life-history strategies that demonstrate that negative senescence is theoretically possible. More generally, our models contribute to understanding of the evolutionary and demographic forces that mold the age-trajectories of mortality, fertility and growth.

Aging↗