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Christoph Adami

Publications and source records attributed to Christoph Adami.

3 recordsLinked to original sources
bioRxiv2016

Evolution of Drift Robustness in Small Populations of Digital Organisms

Most mutations are deleterious and cause a reduction in population fitness known as the mutational load. In small populations, weakened selection against slightly-deleterious mutations results in an additional fitness reduction. Many studies have established that populations can evolve a reduced mutational load by evolving mutational robustness, but it is uncertain whether small populations can evolve a reduced susceptibility to drift-related fitness declines. Here, using mathematical modeling and digital experimental evolution, we show that small populations do evolve a reduced vulnerability to drift, or \"drift robustness\". We find that, compared to genotypes from large populations, genotypes from small populations have a decreased likelihood of small-effect deleterious mutations, thus causing small-population genotypes to be drift-robust. We further show that drift robustness is not adaptive, but instead arises because small populations preferentially adapt to drift-robust fitness peaks. These results have implications for genome evolution in organisms with small population sizes.

Evolutionary Biology↗
bioRxiv2016

Different Evolutionary Paths to Complexity for Small and Large Populations of Digital Organisms

A major aim of evolutionary biology is to explain the respective roles of adaptive versus non-adaptive changes in the evolution of complexity. While selection is certainly responsible for the spread and maintenance of complex phenotypes, this does not automatically imply that strong selection enhances the chance for the emergence of novel traits, that is, the origination of complexity. Population size is one parameter that alters the relative importance of adaptive and non-adaptive processes: as population size decreases, selection weakens and genetic drift grows in importance. Because of this relationship, many theories invoke a role for population size in the evolution of complexity. Such theories are difficult to test empirically because of the time required for the evolution of complexity in biological populations. Here, we used digital experimental evolution to test whether large or small asexual populations tend to evolve greater complexity. We find that both small and large--but not intermediate-sized--populations are favored to evolve larger genomes, which provides the opportunity for subsequent increases in phenotypic complexity. However, small and large populations followed different evolutionary paths towards these novel traits. Small populations evolved larger genomes by fixing slightly deleterious insertions, while large populations fixed rare beneficial insertions that increased genome size. These results demonstrate that genetic drift can lead to the evolution of complexity in small populations and that purifying selection is not powerful enough to prevent the evolution of complexity in large populations.\n\nAuthor SummarySince the early days of theoretical population genetics. scientists have debated the role of population size in shaping evolutionary dynamics. Do large populations possess an evolutionary advantage towards complexity due to the strength of natural selection in these populations? Or do small populations have the advantage, as genetic drift allows for the exploration of fitness landscapes inaccessible to large populations? There are many theories that predict whether large or small populations-those with strong selection or those with strong drift-should evolve the greatest complexity. Here, we use digital experimental evolution to examine the interplay between population size and the evolution of complexity. We found that genetic drift could lead to increased genome size and phenotypic complexity in very small populations. However, large populations also evolved similar large genomes and complexity. Small populations evolved larger genomes through the fixation of slightly deleterious insertions, while large populations utilized rare beneficial insertions. Our results suggest that both strong drift and strong selection can allow populations to evolve similar complexity, but through different evolutionary trajectories.

Evolutionary Biology↗
bioRxiv2013

A genome wide dosage suppressor network reveals genetic robustness and a novel mechanism for Huntington’s disease

Mutational robustness is the extent to which an organism has evolved to withstand the effects of deleterious mutations. We explored the extent of mutational robustness in the budding yeast by genome wide dosage suppressor analysis of 53 conditional lethal mutations in cell division cycle and RNA synthesis related genes, revealing 660 suppressor interactions of which 642 are novel. This collection has several distinctive features, including high co-occurrence of mutant-suppressor pairs within protein modules, highly correlated functions between the pairs, and higher diversity of functions among the co-suppressors than previously observed. Dosage suppression of essential genes encoding RNA polymerase subunits and chromosome cohesion complex suggest a surprising degree of functional plasticity of macromolecular complexes and the existence of degenerate pathways for circumventing potentially lethal mutations. The utility of dosage-suppressor networks is illustrated by the discovery of a novel connection between chromosome cohesion-condensation pathways involving homologous recombination, and Huntingtons disease.

Genomics↗