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You won’t be able to blame it on your genetics anymore: with CRISPR, it’s so easy to hacn into your DNA. CRISPR technology is our future, and experiments with DNA hacking are booming. CRISPR biotechnology is not science fiction anymore, it is our very near future. Would you hack and reprogram your own DNA with CRISPR? Breaking the code of life, hacking DNA at home.

Welcome to the world of a new nature. We can now literally cut and paste DNA with the new CRISPR technology. There is a revolutionary development going on that will have major consequences for humans, plants and animals. The new biotechnology is here.

Continue reading “Hack your DNA with CRISPR — VPRO documentary” »

U.S. regulators have approved a new purple tomato, genetically engineered to be packed with antioxidants and anthocyanins. The fruit will go on sale in 2023.

(Medical Xpress)—A team of researchers at the Max Planck Institute has found what they believe is the DNA mutation that led to a change in function of a gene in humans that sparked the growth of a larger neocortex. In their paper published in the journal Science Advances, the team describes how they engineered a gene found only in humans, Denisovans and Neanderthals to look like a precursor to reveal its neuroproliferative effect.

A year ago, another team of researchers found the human gene that most in the field believe was a major factor in allowing the human brain to grow bigger, allowing for more complex processing. In this new effort, the researchers have found what they believe was the DNA change that arose in that gene.

To pinpoint that change, the researchers engineered the unique ARHGAP11B gene to make it more similar to the ARHGAP11A gene, which researchers believe was a predecessor gene—they swapped a single nucleotide (out of 55 possibilities) for another and in so doing, found the ARHGAP11B gene lost its neuroproliferative abilities. This, the team claims, shows that it was a single mutation that allowed humans to grow bigger brains. Such a mutation, they note, was not likely due to natural selection, but was more likely a simple mistake that occurred as a brain cell was splitting. Because it conferred an advantage (the ability to grow higher than normal amounts of brain cells) the mutation was retained through subsequent generations. They also point out that such a mutation would have resulted specifically in a larger neocortex—a portion of the cortex that has been associated with hearing and sight.

When the right gene is expressed in the right manner in the right population of stem cells, the developing mouse brain can exhibit primate-like features. In a paper publishing August 7th in the Open Access journal PLOS Biology, researchers at the Max Planck Institute of Molecular Cell Biology and Genetics (MPI-CBG) succeeded in mimicking the sustained expression of the transcription factor Pax6 as seen in the developing human brain, in mouse cortical progenitor cells. This altered the behavior of these cells to one that is akin to that of progenitors in the developing primate neocortex. Consequently, the mouse progenitors generated more neurons — a prerequisite for a bigger brain.

The neocortex consists of different types of progenitors, but one particular class, the basal progenitors, behave differently in small-brained animals such as mice than in large-brained animals such as humans. In humans, basal progenitors can undergo multiple rounds of cell division, thereby substantially increasing neuron number and ultimately the size of the neocortex. In mice, these progenitors typically undergo only one round of cell division, thus limiting the number of neurons produced. A potential cause underlying this difference in the proliferative capacity of basal progenitors could be the differential expression of Pax6 between species. Mouse basal progenitors, in contrast to human, do not express Pax6. “We were very curious to see what would happen if we were to change the expression pattern of Pax6 in developing mouse brain to mimic that observed in large-brained animals”, says Fong Kuan Wong, a PhD student in the lab of Wieland Huttner and first author of the study.

To this end, another PhD student in the lab, Ji-Feng Fei, generated a novel transgenic mouse line. This line provided the basis for altering the expression of Pax6 in the cortical stem cell lineage such that it would be sustained in basal progenitors. The researchers then introduced the Pax6 gene into the stem cells of these mice. Strikingly, sustaining Pax6 expression in mouse basal progenitors increased their capacity to undergo multiple rounds of cell division, as typically observed in primates. This not only expanded the size of the basal progenitor population in a way somewhat reminiscent to what is seen in large-brained animals. It also resulted in an increase in cortical neurons, notably those in the top layer, another characteristic feature of an expanded neocortex.

About 99 percent of human genes are shared with chimpanzees. Only the small remainder sets us apart. However, we have one important difference: The brain of humans is three times as big as the chimpanzee brain.

During evolution our genome must have changed in order to trigger such brain growth. Wieland Huttner, Director and Research Group Leader a the Max Planck Institute of Molecular Cell Biology and Genetics (MPI-CBG), and his team identified for the first time a gene that is only present in humans and contributes to the reproduction of basal brain stem cells, triggering a folding of the neocortex. The researchers isolated different subpopulations of human brain stem cells and precisely identified, which genes are active in which cell type. In doing so, they noticed the gene ARHGAP11B: it is only found in humans and in our closest relatives, the Neanderthals and Denisova-Humans, but not in chimpanzees. This gene manages to trigger brain stem cells to form a bigger pool of stem cells. In that way, during brain development more neurons can arise and the cerebrum can expand. The cerebrum is responsible for cognitive functions like speaking and thinking.

Wieland Huttner’s researchers developed a method that isolates and identifies special subpopulations of brain stem cells from the developing human cerebrum. No one has managed to do this so far. The scientists first isolated different stem and progenitor cell types from fetal mice and human cerebrum tissue. In contrast to the big and folded human brain, the brain of mice is small and smooth. After the isolation, the researchers compared the genes that are active in the various cell types and were able to identify 56 genes that are only present in humans and which play a role in brain development. “We noticed that the gene ARHGAP11B is especially active in basal brain stem cells. These cells are really important for the expansion of the neocortex during evolution,” says Marta Florio, PhD student in Wieland Huttner’s lab, who carried out the main part of the study.

The neocortex is the part of the brain that enables us to speak, dream, or think. The underlying mechanism that led to the expansion of this brain region during evolution, however, is not yet understood. A research team headed by Wieland Huttner, director at the Max Planck Institute of Molecular Cell Biology and Genetics, now reports an important finding that paves the way for further research on brain evolution: The researchers analyzed the gyrencephaly index, indicating the degree of cortical folding, of 100 mammalian brains and identified a threshold value that separates mammalian species into two distinct groups: Those above the threshold have highly folded brains, whereas those below it have only slightly folded or unfolded brains. The research team also found that differences in cortical folding did not evolve linearly across species.

The Dresden researchers examined brain sections from more than 100 different mammalian species with regard to the gyrencephaly index, which indicates the degree of folding of the neocortex. The data indicate that a highly folded neocortex is ancestral – the first mammals that appeared more than 200 million years ago had folded brains. Like brain size, the folding of the brain, too, has increased and decreased along the various mammalian lineages. Life-history traits seem to influence this: For instance, mammals with slightly folded or unfolded brains live in rather small social groups in narrow habitats, whereas those with highly folded brains form rather large social groups spreading across wide habitats.

A threshold value of the folding index at 1.5 separates mammalian species into two distinct groups: Dolphins and foxes, for example, are above this threshold value – their brains are highly folded and consist of several billion neurons. This is so because basal progenitors capable of symmetric proliferative divisions are present in the neurogenic program of these animals. In contrast, basal progenitors in mice and manatees lack this proliferative capacity and thus produce less neurons and less folded or unfolded brains.

To an untrained observer, the electrical storm that takes place over the brain’s neural network seems a chaotic flurry of activity. But as neuroscientists understand it, the millions of neurons are actually engaged in a sort of tightly choreographed dance, a tango of excitatory and inhibitory neurons. How is this precise balance that makes normal function possible achieved during development? And how does it go wrong in diseases like epilepsy when brain activity goes out of control?

Focusing on the cerebral cortex, the part of the brain controlling thought, sensory awareness, and motor function, a group of Harvard Stem Cell Institute (HSCI) researchers in the Department of Stem Cell and Regenerative Biology (SCRB), led by Assistant Professor Paola Arlotta, has discovered that excitatory neurons control the positioning of inhibitory neurons in a process that is critically important for generating balanced circuitry and proper cortical response.

Professor Takao Hensch, a collaborator on the study in the Harvard Center for Brain Science, Department of Molecular & Cellular Biology (MCB), had previously shown that the maturation of this circuit balance triggers critical periods of brain development. Certain inhibitory cells appear particularly vulnerable to genetic or environmental factors in early life, contributing to mental illness, such as schizophrenia or autism spectrum disorders.

According to a new meta-analysis, gene variants associated with a person’s blood type may be linked to their risk of early stroke.

“Non-O blood types have previously been linked to a risk of early stroke, but the findings of our meta-analysis showed a stronger link between these blood types with early stroke compared to late stroke, and in linking risk mostly to blood type A,” said study author Braxton D. Mitchell, PhD, MPH, of University of Maryland School of Medicine in Baltimore. “Specifically, our meta-analysis suggests that gene variants tied to blood types A and O represent nearly all of those genetically linked with early stroke. People with these gene variants may be more likely to develop blood clots, which can lead to stroke.”

48 studies on genetics and ischemic stroke from North America, Europe, and Asia were reviewed in the meta-analysis. 16,927 people with stroke and 576,353 people who did not have a stroke were included in the studies. Of those with stroke, 5,825 people had early onset stroke and 9,269 people had late onset stroke. Early onset stroke was defined as an ischemic stroke occurring before age 60 and late-onset stroke was older than 60 years old.

An alzheimer’s-proof brain: a groundbreaking case.

In a groundbreaking case researchers from the Massachusetts General Hospital have discovered a gene variant that seems to have disrupted the pathology of Tau Protein. The case of Aliria Rosa Piedrahita de Villegas.

Continue reading “Groundbreaking Alzheimer’s Case: Gene APOE3” »