Max Planck Institute for Evolutionary Biology

A model weighs individual costs and social benefits of interventions during the Covid-19 pandemic

The presence of multiple rRNA/tRNA gene copies may be advantageous under conditions that promote increasingly rapid translation and growth

The evolution of humans and artificial intelligence could one day be intertwined

Rapid switching between different antibiotics could prevent the evolution of resistance

Rewards only promote cooperation if the other person also learns about them

This fall, millions of birds in the northern hemisphere once again heading south towards their non-breeding grounds. Miriam Liedvogel will be keeping her fingers crossed that some of them in particular will return safely next spring. The scientist at the Max Planck Institute for Evolutionary Biology in Plön has provided them with a bit of extra luggage to carry: specialized sensors known as light-level geolocators. Upon safe return next spring, these tiny light-sensors should reveal the birds whereabouts throughout the winter.

Cheaters can leave. In the case of the bacteria in Paul Rainey’s lab, that’s exactly what is wanted. In his laboratory at the Max Planck Institute for Evolutionary Biology in Ploen, the evolutionary biologist studies how multicellular life emerges from individual cells. Their findings show that too much cohesion can be counterproductive.

Everything has its price – especially health, of course. At the Max Planck Institute for Evolutionary Biology in Ploen, Tobias Lenz and his team are researching what the evolutionary costs of perfect immunity might be and why we are not immune to all pathogens.

Around 40 percent of all species on Earth are parasitic – apparently a highly successful way of life. Even a fish such as the three-spined stickleback is plagued by up to 25 different parasites. One of them particularly appealed to Martin Kalbe, Tina Henrich and Nina Hafer from the Max Planck Institute for Evolutionary Biology in Plön: the tapeworm Schistocephalus solidus. The scientists are researching the numerous tricks that host and parasite use to outdo each other.

Wherever people live, there are mice. It would be difficult to find another animal that has adapted to the habitats created by humans as well as the house mouse has. It thus seemed obvious to Diethard Tautz at the Max Planck Institute for Evolutionary Biology in Plön that the species would make an ideal model system for investigating how evolution works.

Plants are colonized by diverse microbial communities. Some of the microbial species produce antifungal compounds that inhibit the growth of fungal and other pathogens. Likewise, fungal pathogens can produce antibacterial compounds to manipulate the plant microbiota.

Self-replicating sequences are not unusual in genomes, they make up more than 50% of the human genome. Usually, such sequences are molecular parasites that do not benefit the host. However, we have identified populations of self-replicating sequences that provide a benefit to their bacterial hosts. The evolution of these sequences is fascinating, not only because one generation in these populations lasts thousands of years, but also because evolutionary conflicts, reminiscent of those between organisms and cells, can be observed between the sequence populations and their bacterial hosts.

How do bacteria become resistant to antibiotics? Often, extra-DNA, so-called plasmids, that bacteria carry in addition to their chromosomes plays an important role. At cell division, the plasmids are passed on to the daughter cells, however not neatly, but with some randomness. Stochastic models can elegantly describe this process over many generations, contributing to a clear picture of the dynamics of plasmid-encoded genes, for example resistance genes. This knowledge is the basis for influencing the evolution of bacterial populations and preventing the emergence of resistance.

Even among simply structured organisms a fascinating variety of cellular communities from chain-forming bacteria to the formation and coordinated dissolution of large colonies can be found. Where does this diversity come from? And are there any fundamental rules for this diversity? General statements actually can be made applying mathematical models: Even without detailed knowledge about the biology of living organisms, one can understand which life cycles are theoretically feasible, and thus identify the conditions for the emergence of simple life cycles.

Molecular biology can be repeated in the laboratory and in wild populations. This could mean that evolution might follow rules. Work with experimental bacterial populations suggests the genotype-to-phenotype map to be an important central contributor. Recent work using mathematical models and experimental evolution shows that short-term mechanistic-level predictions of mutational pathways to new adaptive phenotypes can be made. Future challenges stem from the current inability to a priori predict locus-specific mutational biases and environment-specific fitness effects.