Arguably the most important theory in biology is the theory of evolution by natural selection. We studied such Darwinian evolution with computer models, and we focused on adaptive evolution in dynamic environments and the role of mobile genetic elements. If we take fluctuating environmental conditions, we may either enforce such conditions on the population or the individuals may generate changing conditions themselves. We studied two models in which fluctuating conditions are externally imposed on the population: one in which genomes may be structured and a second in which gene regulatory networks are structured. In both models we show that the commonly accepted framework of random mutation and natural selection allows for the at-times-disputed evolution of evolvability. A sequence of repeated short-term events may lead in the long term to the evolution of evolvability, where we define evolvability as the enhanced ability to discover beneficial, heritable adaptations. Next we switch from dictating environmental changes to letting the population shape its own environment. In the setting of resource processing we study the long-term evolutionary outcome of ecosystem evolution. We find that the majority of the simulations can be roughly categorized in two typical evolutionary outcomes. The long term ecosystem dynamics may be dominated by a single, `smart' generalist, or cooperative communities originate that are composed of multiple specialized crossfeeding lineages. The other focal point of this thesis are mobile genetic elements, or transposons. In the model on the evolution of genome structure, transposons played an important, evolutionary beneficial, role. We found that genomes may evolve a specific architecture -- and employ transposons to do so -- to allow for rapid adaptations to changed environments. Finally, we studied the activity of transposons and how hosts control these elements via RNAi. We concentrated on a key protein complex, RNA dependent RNA polymerase (RdRP), that is thought to be essential in the standard pathway, yet is absent in many animals that nevertheless regulate transposon activity. We show that alternative pathways based on antisense transcription are also readily capable of regulating transposon activity. Thus currently known interactions in the nucleus and cytoplasm are sufficient to explain transposon silencing, also if RdRP is not present. This fundamental research has provided new insights in the process of evolution and the role of dynamic environments and mobile genetic elements
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