Unraveling the non-senescence phenomenon in Hydra

Unlike other metazoans, Hydra does not experience the distinctive rise in mortality with age known as senescence, which results from an increasing imbalance between cell damage and cell repair. We propose that the Hydra controls damage accumulation mainly through damage-dependent cell selection and cell sloughing. We examine our hypothesis with a model that combines cellular damage with stem cell renewal, differentiation, and elimination. The Hydra individual can be seen as a large single pool of three types of stem cells with some features of differentiated cells. This large stem cell community prevents “cellular damage drift,” which is inevitable in complex conglomerate (differentiated) metazoans with numerous and generally isolated pools of stem cells. The process of cellular damage drift is based on changes in the distribution of damage among cells due to random events, and is thus similar to Muller׳s ratchet in asexual populations. Events in the model that are sources of randomness include budding, cellular death, and cellular damage and repair. Our results suggest that non-senescence is possible only in simple Hydra-like organisms which have a high proportion and number of stem cells, continuous cell divisions, an effective cell selection mechanism, and stem cells with the ability to undertake some roles of differentiated cells

Age-related changes of physiological performance and survivorship of bank voles selected for high aerobic capacity

Variation in lifespans is an intriguing phenomenon, but how metabolic rate influence this variation remains unclear. High aerobic capacity can result in health benefits, but also in increased oxidative damage and accelerated ageing. We tested these contradictory predictions using bank voles (Myodes=Clethrionomys glareolus) from lines selected for high swim-induced aerobic metabolism (A), which had about 50% higher maximum metabolic rate and a higher basal and routine metabolic rates, than those from unselected control lines (C). We measured sprint speed (VSmax), forced-running maximum metabolic rate (VO_{2}run), maximum long-distance running speed (VLmax), running speed at VO_{2}run (VVO_{2}), and respiratory quotient at VO_{2}run (RQ) at three age classes (I: 3-5, II: 12-14, III: 17-19 months), and analysed survivorship. We asked if ageing, understood as the age-related decline of the performance traits, differs between the A and C lines. At age class I, voles from A lines had 19% higher VO_{2}run, and 12% higher VLmax, but tended to have 19% lower VSmax, than those from C lines. RQ was nearly 1.0 for both A and C lines. The pattern of age-related changes differed between the lines mainly between age classes I and II, but not in older animals. VSmax increased by 27% in A lines and by 10% in C lines between age class I and II, but between classes II and III, it increased by 16% in both selection directions. VO_{2}run decreased by 7% between age class I and II in A lines only, but in C lines it remained constant across all age classes. VLmax decreased by 8% and VVO_{2} by 12% between age classes II and III, but similarly in both selection directions. Mortality was higher in A than in C lines only between the age of 1 and 4 months. The only trait for which the changes in old animals differed between the lines was RQ. In A lines, RQ increased between age classes II and III, whereas in C lines such an increase occurred between age classes I and II. Thus, we did not find obvious effects of selection on the pattern of ageing. However, the physiological performance and mortality of bank voles remained surprisingly robust to ageing, at least until the age of 17-19 months, similar to the maximum lifespan under natural conditions. Therefore, it is possible that the selection could affect the pattern of ageing in even older individuals when symptoms of senility might be more profound

Assessing the quality of data on international migration flows in Europe: the case of undercounting

Undercounting is a critical issue in migration statistics, resulting in bias. It typically arises from insufficient reporting requirements and problems with enforcing such requirements. The main sources of information on undercounting are the metadata accompanying official statistics and expert opinions. However, metadata and arbitrary expert opinions may be limited by overlooking important details in migration data shared by various countries. This includes potential oversight of changes in methodologies, definitions, or retrospective updates to the data following censuses. This work presents a methodological solution with three objectives to address undercounting in international migration data. First, we provide an overview of available metadata and expert opinions on undercounting in European migration flows. Second, we propose a novel data-driven approach that incorporates year-specific and duration-of-stay-adjusted classifications. The proposed methodological solution relies on comparisons of flows in the same direction reported by a given country with high-quality data reported by another set of countries. We use bilateral migration data provided by Eurostat, UN and selected national statistical institutes. Duration-of-stay correction coefficients are derived through an optimization model or borrowed from the literature. Metadata and expert opinion scores can also be integrated to classify undercounting. Finally, we provide a dynamic classification of undercounting for 32 European countries (2002-2019), accessible through an online Shiny application, offering flexibility and adaptability. The findings highlight significant undercounting in new EU member states, particularly Bulgaria, Latvia, and Romania. Interestingly, other European countries, including those presumed to maintain reliable population statistics, also exhibit notable periods of undercounting

Mutation Accumulation May Be a Minor Force in Shaping Life History Traits

Is senescence the adaptive result of tradeoffs between younger and older ages or the nonadaptive burden of deleterious mutations that act at older ages? To shed new light on this unresolved question we combine adaptive and nonadaptive processes in a single model. Our model uses Penna's bit-strings to capture different age-specific mutational patterns. Each pattern represents a genotype and for each genotype we find the life history strategy that maximizes fitness. Genotypes compete with each other and are subject to selection and to new mutations over generations until equilibrium in gene-frequencies is reached. The mutation-selection equilibrium provides information about mutational load and the differential effects of mutations on a life history trait - the optimal age at maturity. We find that mutations accumulate only at ages with negligible impact on fitness and that mutation accumulation has very little effect on the optimal age at maturity. These results suggest that life histories are largely determined by adaptive processes. The non-adaptive process of mutation accumulation seems to be unimportant at evolutionarily relevant ages

Mutation accumulation may only be a minor force in shaping life-history traits, even when reproduction is sexual.

In a previous theoretical study we investigated whether adaptive or non-adaptive processes are more important in the evolution of senescence. We built a model that combined both processes and found that mutation accumulation is important only at those ages where mortality has a negligible impact on fitness. This model, however, was limited to haploid organisms. Here we extend our model by introducing diploidy and sexual reproduction. We assume that only recessive (mutated) homozygotes experience detrimental effects. Our results corroborate our previous conclusions, confirming that life histories are largely determined by adaptive processes. We also found that the equilibrium frequencies of mutated alleles are at higher values than in haploid model, because mutations in heterozygotes are hidden for directional selection. Nevertheless, the equilibrium frequencies of recessive homozygotes that make mutations visible to selection are very similar to the equilibrium frequencies of these alleles in our haploid model. Diploidy and sexual reproduction with recombination slows down approaching selection-mutation balance