Lifeboat Foundation

Scientists have discovered a form of natural selection that doesn’t rely on DNA.

Am Nat. 2017 Nov;190:694–706. doi: 10.1086÷693854. Epub 2017 Sep 5.

Biological invasions offer interesting situations for observing how novel interactions between closely related, formerly allopatric species may trigger phenotypic evolution in situ. Assuming that successful invaders are usually filtered to be competitively dominant, invasive and native species may follow different trajectories. Natives may evolve traits that minimize the negative impact of competition, while trait shifts in invasives should mostly reflect expansion dynamics, through selection for colonization ability and transiently enhanced mutation load at the colonization front. These ideas were tested through a large-scale common-garden experiment measuring life-history traits in two closely related snail species, one invasive and one native, co-occurring in a network of freshwater ponds in Guadeloupe. We looked for evidence of recent evolution by comparing uninvaded or recently invaded sites with long-invaded ones.

Astronomers have discovered a mysterious new class of objects at the heart of the Milky Way, unlike anything else found previously in our galaxy. The objects “look like gas but behave like stars,” according to senior researcher Andrea Ghez, as they start off small and compact but are stretched to a larger size when they approach the supermassive black hole in the center of the galaxy.

The researchers believe these objects could teach us about the evolution of stars and what happens to celestial bodies in environments of extreme gravity.

Continue reading “Astronomers Discover Stretchy Objects Unlike Anything Else in Our Galaxy” »

“Tim Crow must be proud to see his theory being tested at a complex level.” That’s how I tweeted the news on a recent Brain article by van den Heuvel et al (2019). Tim Crow’s theory on schizophrenia as a possible by-product of human brain evolution was quite inspiring and led to many fruitful discussions in our evolutionary psychiatry group when I was a junior trainee (which I wrote about a while ago: EPSIG Newsletter, June 2018). And here it was, the theory was tested by using novel methodology. Now I am pleased to say that the article did not disappoint, so I can enjoy the initial thrill and share my take with the Mental Elf World.

Tim Crow’s original question was intriguing: “Is schizophrenia the price that Homo sapiens pay for language?” (Crow, 1997). He argued that schizophrenia may be considered an extreme variation of brain systems which are relatively new in evolutionary timescale. Brain structures that are mostly implicated in schizophrenia were also unique to humans as mediators of language and higher cognitive functions. Those relatively new (in evolutionary timescale) brain systems may be more vulnerable to insults (e.g. stress, trauma, neurodevelopmental conditions) and manifest as dysfunctional brain circuits in schizophrenia.

The prevalence of schizophrenia is fairly constant across human populations (Jablensky et al. 1992), and the prevalence does not change despite low fecundity rates of people with schizophrenia. This can only be possible in the case of overall genetic predisposition across the population.

The size of the human brain increased profoundly during evolution. A certain gene that is only found in humans triggers brain stem cells to form a larger pool of stem cells. As a consequence, more neurons can arise, which paves the way to a bigger brain. This brain size gene is called ARHGAP11B and so far, how it works was completely unknown. Researchers at the Max Planck Institute of Molecular Cell Biology and Genetics in Dresden now uncovered its mode of action. They show that the ARHGAP11B protein is located in the powerhouse of the cell—the mitochondria—and induces a metabolic pathway in the brain stem cells that is characteristic of cancer cells.

The research group of Wieland Huttner, a founding director of the Max Planck Institute of Molecular Cell Biology and Genetics, has been investigating the molecular mechanisms underlying the expansion of the brain during mammalian evolution for many years. In 2015, the group reported a key role for a gene that is only present in humans and in our closest extinct relatives, the Neanderthals and Denisovans. This gene, named ARHGAP11B, causes the so-called basal brain stem cells to expand in number and to eventually increase the production of neurons, leading to a bigger and more folded brain in the end. How the gene functions within the basal brain stem cells has been unknown so far.

Takashi Namba, a postdoctoral scientist in the research group of Wieland Huttner, wanted to find the answer to this question, together with colleagues from the Max Planck Institute, the University Hospital Carl Gustav Carus Dresden, and the Department of Medical Biochemistry at the Semmelweis University, Budapest. He found that the ARHGAP11B protein is located in mitochondria, the organelles that generate most of the cell’s source of chemical energy and hence are often referred to as the powerhouse of the cell. Takashi Namba explains the results: We found that ARHGAP11B interacts with a protein in the membrane of mitochondria that regulates a membrane pore. As a consequence of this interaction, the pores in the membrane are closing up, preventing calcium leakage from the mitochondria. The resulting higher calcium concentration causes the mitochondria to generate chemical energy by a metabolic pathway called glutaminolysis.

Let’s be clear.

What can we trust? Why is the ‘information ecology’ so damaged, and what would it take to make it healthy?

Continue reading “The War on Sensemaking, Daniel Schmachtenberger” »

Holochain is a next generation protocol and an evolution of blockchain for web 3.0 leading to a more distributed world.

https://holo.host/
We are en route to build a more healthier, more empowered internet!

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The discovery of an exceptionally strong “forbidden” beta-decay involving fluorine and neon could change our understanding of the fate of intermediate-mass stars.

Every year roughly 100 billion stars are born and just as many die. To understand the life cycle of a star, nuclear physicists and astrophysicists collaborate to unravel the physical processes that take place in the star’s interior. Their aim is to determine how the star responds to these processes and from that response predict the star’s final fate. Intermediate-mass stars, whose masses lie somewhere between 7 and 11 times that of our Sun, are thought to die via one of two very different routes: thermonuclear explosion or gravitational collapse. Which one happens depends on the conditions within the star when oxygen nuclei begin to fuse, triggering the star’s demise. Researchers have now, for the first time, measured a rare nuclear decay of fluorine to neon that is key to understanding the fate of these “in between” stars [1, 2]. Their calculations indicate that thermonuclear explosion and not gravitational collapse is the more likely expiration route.

The evolution and fate of a star strongly depend on its mass at birth. Low-mass stars—such as the Sun—transition first into red giants and then into white dwarfs made of carbon and oxygen as they shed their outer layers. Massive stars—those whose mass is at least 11 times greater than the Sun’s—also transition to red giants, but in the cores of these giants, nuclear fusion continues until the core has turned completely to iron. Once that happens, the star stops generating energy and starts collapsing under the force of gravity. The star’s core then compresses into a neutron star, while its outer layers are ejected in a supernova explosion. The evolution of intermediate-mass stars is less clear. Predictions indicate that they can explode both via the gravitational collapse mechanism of massive stars and by a thermonuclear process [3– 6]. The key to finding out which happens lies in the properties of an isotope of neon and its ability to capture electrons.

Neurochemicals such as serotonin and dopamine play crucial roles in cognitive and emotional functions of our brain. Vesicular monoamine transporter 1 (VMAT1) is one of the genes responsible for transporting neurotransmitters and regulating neuronal signaling. A research team led by Tohoku University has reconstructed ancestral VMAT1 proteins, revealing the functional changes in neurotransmitter uptake of VMAT1 throughout the course of human evolution.

Human bodies are made up of millions of cells. Each individual contains a specific set of instruction of codes that make up all of a living thing’s genetic material. These instructions are known as genomes. PhD candidate Daiki Sato and Professor Masakado Kawata of the Graduate School of Life Sciences at Tohoku University, and two of the authors involved in the current study, previously discovered VMAT1 to be one of the genes that had evolved throughout human lineage.

VMAT 1 contains two human-specific mutations, or where the genomes changed, with the change being represented as 130Glu to 130Gly and from 136Asn to 136Thr. Previous studies have shown that having the new 130Gly/136Thr variant decreases the uptake of neurotransmitters and is associated with higher depression and/or anxiety. In this study, Sato, Kawata and their colleagues revealed the evolutionary changes in neurotransmitter uptake of VMAT1 by reconstructing ancestral VMAT1 proteins. First they applied a fluorescent substrate to visualize and quantify the neurotransmitter uptake of each genotype. The ancestral (130Glu/136Asn) VMAT1 protein exhibited an increased uptake of neurotransmitters compared to a derived (130Gly/136Thr) genotype. Given that the derived (130Gly/136Thr) genotype is shown to be associated with depression and/or anxiety in modern human populations. “This results of our study reveal that our ancestors may have been able to withstand higher levels of anxiety or depression,” noted the authors.

Continue reading “Evolutionary Changes in Brain Potentially Make us More Prone to Anxiety” »