Adaption, neutrality and life-course diversity.

Heterogeneity among individuals in fitness components is what selection acts upon. Evolutionary theories predict that selection in constant environments acts against such heterogeneity. But observations reveal substantial non-genetic and also non-environmental variability in phenotypes. Here, we examine whether there is a relationship between selection pressure and phenotypic variability by analysing structured population models based on data from a large and diverse set of species. Our findings suggest that non-genetic, non-environmental variation is in general neither truly neutral, selected for, nor selected against. We find much variations among species and populations within species, with mean patterns suggesting nearly neutral evolution of life-course variability. Populations that show greater diversity of life courses do not show, in general, increased or decreased population growth rates. Our analysis suggests we are only at the beginning of understanding the evolution and maintenance of non-genetic non-environmental variation.

Senescence in Bacteria and Its Underlying Mechanisms.

Bacteria have been thought to flee senescence by dividing into two identical daughter cells, but this notion of immortality has changed over the last two decades. Asymmetry between the resulting daughter cells after binary fission is revealed in physiological function, cell growth, and survival probabilities and is expected from theoretical understanding. Since the discovery of senescence in morphologically identical but physiologically asymmetric dividing bacteria, the mechanisms of bacteria aging have been explored across levels of biological organization. Quantitative investigations are heavily biased toward Escherichia coli and on the role of inclusion bodies-clusters of misfolded proteins. Despite intensive efforts to date, it is not evident if and how inclusion bodies, a phenotype linked to the loss of proteostasis and one of the consequences of a chain of reactions triggered by reactive oxygen species, contribute to senescence in bacteria. Recent findings in bacteria question that inclusion bodies are only deleterious, illustrated by fitness advantages of cells holding inclusion bodies under varying environmental conditions. The contributions of other hallmarks of aging, identified for metazoans, remain elusive. For instance, genomic instability appears to be age independent, epigenetic alterations might be little age specific, and other hallmarks do not play a major role in bacteria systems. What is surprising is that, on the one hand, classical senescence patterns, such as an early exponential increase in mortality followed by late age mortality plateaus, are found, but, on the other hand, identifying mechanisms that link to these patterns is challenging. Senescence patterns are sensitive to environmental conditions and to genetic background, even within species, which suggests diverse evolutionary selective forces on senescence that go beyond generalized expectations of classical evolutionary theories of aging. Given the molecular tool kits available in bacteria, the high control of experimental conditions, the high-throughput data collection using microfluidic systems, and the ease of life cell imaging of fluorescently marked transcription, translation, and proteomic dynamics, in combination with the simple demographics of growth, division, and mortality of bacteria, make the challenges surprising. The diversity of mechanisms and patterns revealed and their environmental dependencies not only present challenges but also open exciting opportunities for the discovery and deeper understanding of aging and its mechanisms, maybe beyond bacteria and aging.

Neutral theory for life histories and individual variability in fitness components.

Individuals within populations can differ substantially in their life span and their lifetime reproductive success but such realized individual variation in fitness components need not reflect underlying heritable fitness differences visible to natural selection. Even so, biologists commonly argue that large differences in fitness components are likely adaptive, resulting from and driving evolution by natural selection. To examine this argument we use unique formulas to compute exactly the variance in life span and in lifetime reproductive success among individuals with identical (genotypic) vital rates (assuming a common genotype for all individuals). Such individuals have identical fitness but vary substantially in their realized individual fitness components. We show by example that our computed variances and corresponding simulated distribution of fitness components match those observed in real populations. Of course, (genotypic) vital rates in real populations are expected to differ by small but evolutionarily important amounts among genotypes, but we show that such differences only modestly increase variances in fitness components. We conclude that observed differences in fitness components may likely be evolutionarily neutral, at least to the extent that they are indistinguishable from distributions generated by neutral processes. Important consequences of large neutral variation are the following: Heritabilities for fitness components are likely to be small (which is in fact the case), small selective differences in life histories will be hard to measure, and the effects of random drift will be amplified in natural populations by the large variances among individuals.