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Populations of indigenous people in southern Africa carry a gene that causes lighter skin, and scientists have now identified the rapid evolution of this gene in recent human history.

The gene that causes lighter pigmentation, SLC24A5, was introduced from eastern African to southern African populations just 2,000 years ago. Strong positive selection caused this gene to rise in frequency among some KhoeSan populations.

UC Davis anthropologist Brenna Henn and colleagues have shown that a gene for lighter skin spread rapidly among people in southern Africa in the last 2,000 years.

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Neoliberalism slows down evolution! Just kidding…or am I? 🧐😁🤣🙈.


Like other organisms, bacteria constantly have to fight to survive in hostile living conditions. Together with colleagues in Finland, researchers at the Max Planck Institute for Evolutionary Biology in Plön have discovered that bacteria adapt to their environment more slowly and less efficiently as soon as they are exposed to two stress factors rather than one. This is due to mutations in different genes. The slower rate of evolution led to smaller population sizes. This means that evolution can take divergent paths if an organism is exposed to several stress factors.

Bacteria rarely live alone; they are usually part of a community of species that is exposed to various stress factors. They can often react to these factors by adapting to new environmental conditions with astonishing speed. Antibiotics that enter soil and water via and accumulate there in low concentrations can trigger the evolution of resistance in – even though these concentrations are so low that they inhibit only slightly or not at all. However, bacteria do not only have to fight ; they also have to deal with predators. This is why they often grow in large colonies that cannot be consumed by predatory organisms.

Typically, scientists investigate the effects that a single stress factor has on an organism. Researchers at the Max Planck Institute for Evolutionary Biology in Plön and the Universities of Helsinki and Jyväskylä, Finland, have now investigated the question of how microorganisms behave when they are confronted with more than one stress factor. “We simulated natural environmental conditions in the lab and exposed bacteria to both predators and antibiotics. This allows us to estimate how likely it is to find evolution of resistance to antibiotics outdoors,” explains study leader Lutz Becks.

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What would it be like to live through our own species’ evolution? The biological process of natural selection that gave rise to every species on Earth takes hundreds of generations to turn one species into another, but what if that process could be skipped entirely?


A look at the future of transhumanist technologies and what their evolution will mean for our society.

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I just love it when the reductionists are wrong…again. I can not help myself. bigsmile


University of Nebraska-Lincoln researchers have found revolutionary evidence that an evolutionary phenomenon at work in complex organisms is at play in their single-celled counterparts, too.

Species most often evolve through DNA mutations inherited by successive generations. A few decades ago, researchers began discovering that multicellular species can also evolve through epigenetics: traits originating from the inheritance of cellular proteins that control access to an organism’s DNA, rather than genetic changes.

Because those proteins can respond to shifts in an organism’s environment, epigenetics resides on the ever-thin line between nature and nurture. Evidence for it had emerged only in eukaryotes, the multicellular domain of life that comprises animals, plants and several other kingdoms.

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Over the past 90 years, scientists have discovered hundreds of antibiotics—microbe-killing drugs that have brought many pernicious diseases to heel. But every time researchers identify a new drug, bacteria inevitably evolve to resist it within a matter of years. We thrust; they parry. Now, with the flow of new antibiotics having dried up for decades, our stalemated duel with infectious bacteria threatens to end in outright defeat. Superbugs are ascendant around the world, including those that resist all commonly used drugs.


Scientists have pinpointed a molecule that accelerates the evolution of drug-resistant microbes. Now they’re trying to find a way to block it.

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We found that the evolution of anti-predatory defense in the prey species stabilized predator population size but that this was delayed in the presence of the abiotic stressor. This corresponded with a lack or delay in the evolution of resistance to the abiotic stressor. Therefore, the abiotic stressor had a big effect on the eco-evolutionary dynamics, weakening the evo-to-eco link. One might expect that this is caused by competition between (asexual) bacterial lineages possessing different adaptations, decreasing the rate and directionality of evolution under multiple selection pressures. Instead, the genomic investigation showed that different targets (genes or duplicated sites) were repeatedly mutated in the individual and combined treatments. The population genetics thus revealed complex mechanistic underpinnings for a seemingly sensible difference in dynamics. Perhaps a specific type of bacterial cell clumping or another adaptation is favored in the dual-stressor environment because of conferring a degree of resistance to both types of stressors? This could then direct the mutational path away from the optimal adaptations to the individual stressors.


It took us five years to disentangle the complex interplay between ecology and evolution in an experimental system consisting of bacteria, ciliates and antibiotics.

Go to the profile of Johannes Cairns

Johannes Cairns

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