A University of Wisconsin-Madison researcher and his collaborators at the University of California, San Francisco have repurposed the gene-editing tool CRISPR to study which genes are targeted by particular antibiotics, providing clues on how to improve existing antibiotics or develop new ones.
Tobacco and alcohol use, both genetically inheritable behaviors, influence risk for many complex diseases and disorders and are leading causes of mortality.
The University of Minnesota was part of a research collaboration that conducted the first study, recently published in Nature Genetics, to identify hundreds of genomic locations associated with addictive behaviors. Researchers found more than 500 genetic variants that affect the use of and addiction to tobacco and alcohol. Until now, only a few of such variants had been identified.
Researchers studied 1.2 million people and looked five characteristics including the age when a participant began smoking; the number of cigarettes per day the participant smoked; whether the participant has ever been a regular smoker; whether the participant ever quit smoking; and the number of alcoholic drinks the participant had per week.
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A new, very good article on aging, modern aging research and its history, RAAD feest and other initiatives, on model organisms, genetics and future lifespans. “… In early December 2018, just a few months after RAADfest, I visited the Buck Institute for a daylong symposium titled “Live Better Longer: A Celebration of 30 Years of Research on Aging.” That wasn’t an arbitrary demarcation: Aging is one of the rare areas of modern science with a specific launch date. In this case, it was January 1988, when Tom Johnson, a behavioral geneticist at the University of California, Irvine, published a paper that linked a genetic mutation he named “age-1” to longer lifespans in a transparent, microscopic, mostly hermaphroditic roundworm known in scientific circles as C. elegans. Prior to Johnson’s discovery, aging had not received a lot of attention from researchers. In the 1820s, Benjamin Gompertz, a self-trained mathematician, concluded that humans don’t start to break down at some magic age but are constantly declining and losing the ability to repair themselves, a concept now referred to as the Gompertz law of mortality. The first hint that there might be a cellular mechanism underlying the aging process came more than a century later, in the 1930s, when two Cornell scientists discovered that rats kept on calorically restricted diets lived significantly longer than their more satiated brethren. But overall, the field was mostly known as being a haven for charlatans and quacks peddling immortality elixirs and other magical cures — a reputation that continued even after Johnson’s work was published…In 1993, Cynthia Kenyon, an assistant professor at the University of California, San Francisco, discovered that mutations on a different gene, called daf-2, caused C. elegans to live twice as long as expected. Several years later, Gary Ruvkun, a researcher at Harvard Medical School, showed that these so-called worm-aging genes were closely related to genes in the insulin-signaling system of humans. Around the same time, MIT’s Guarente and some of his colleagues discovered the first of several genes in yeast — which are also present in humans — linked to dramatically extended lifespan…” https://medium.com/s/2069/how-long-will-we-live-in-2069-f03e698f6de2
With this promising research on the horizon, how long might humans live in the future? Fantastical claims to longevity have existed since the dawn of recorded time, but reliable data about maximum human lifespan only dates to the mid-1950s, when the Guinness Book of World Records began independently verifying claims. Even then, initially corroborated ages can end up disproven: On December 27, Russian researchers published a paper arguing that the current world record holder, a Frenchwoman named Jeanne Calment, who said she was 122 when she died in 1997, had stolen her mother’s identity and was actually 99 at the time.
Assuming Calment wasn’t a fraud, since 1955, 46 people have made it to age 115. Nine of them have made it to 117 — and only two, Calment and an American woman named Sarah Knauss, have made it past 117. (Knauss died in 1999 at age 119). Over that same time frame, just under 11 billion people have been alive. That means roughly .0000004204133 percent of people have made it to 115. You’re 79,333 times more likely to get hit by lightning than you are to live to 115; 22,455 times more likely to end up in the emergency room from a golf cart accident; and 11,817 times more likely to get murdered.
CRISPR/Cas9 is a form of genetic editing that holds a lot of promise, such as the killing of cancer cells, but also comes with some hefty warnings, such as that it may cause DNA damage. So far, scientists have been using CRISPR/Cas9 in a variety of plants and animals to edit genetic information, including attempts to practice what is called ‘active genetics’.
This last approach is an attempt to edit the genome that controls which of the two copies of a gene is passed to the next generation. But the technique is complicated and rife with obstacles so thus far been used only on insects. Not anymore!
A team of biologists has now achieved the world’s first CRISPR/Cas9-based approach to control genetic inheritance in a mammal.
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Parts of human DNA are of viral origin: many of them were inserted into the primordial genetic material of our ancestors many millions of years ago and have been inherited by successive generations ever since. Thus, they are not thought to vary much in the genomes of modern humans. Human endogenous retroviruses (HERV) are by far the most common virus-derived sequences in our genome. New research published in Mobile DNA shows a mechanism that has introduced more inter-individual variation in HERV content between humans than previously appreciated.
Jainy Thomas & Cédric Feschotte 25 Jan 2019.
The adult brain has learned to calculate an image of its environment from sensory information. If the input signals change, however, even the adult brain is able to adapt − and, ideally, to return to its original activity patterns once the perturbation has ceased. Scientists at the Max Planck Institute of Neurobiology in Martinsried have now shown in mice that this ability is due to the properties of individual neurons. Their findings demonstrate that individual cells adjust strongly to changes in the environment but after the environment returns to its original state it is again the individual neurons which reassume their initial response properties. This could explain why despite substantial plasticity the perception in the adult brain is rather stable and why the brain does not have to continuously relearn everything.
Everything we know about our environment is based on calculations in our brain. Whereas a child’s brain first has to learn the rules that govern the environment, the adult brain knows what to expect and, for the most part, processes environmental stimuli in a stable manner. Yet even the adult brain is able to respond to changes, to form new memories and to learn. Research in recent years has shown that changes to the connections between neurons form the basis of this plasticity. But, how can the brain continually change its connections and learn new things without jeopardizing its stable representation of the environment? Neurobiologists in the Department of Tobias Bonhoeffer in Martinsried have now addressed this fundamental question and looked at the interplay between plasticity and stability.
The scientists studied the stability of the processing of sensations in the visual cortex of the mouse. It has been known for about 50 years that when one eye is temporarily closed, the region of the brain responsive to that eye increasingly becomes responsive to signals from the other eye that is still open. This insight has been important to optimize the use of eye patches in children with a squint. “Thanks to new genetically encoded indicators, it has recently become possible to observe reliably the activity of individual neurons over long periods of time,” says Tobias Rose, the lead author of the study. “With a few additional improvements, we were able to show for the first time what happens in the brain on the single-cell level when such environmental changes occur.”
Buried deep within the DNA of Asian individuals is a genetic clue pointing to the existence of an unknown human ancestor. Remarkably, it wasn’t a human who reached this startling conjecture, but rather an artificially intelligent algorithm. Welcome to archaeology in the 21st century.
New research published last week in Nature Communications suggests a yet-to-be discovered hominid interbred with modern humans tens of thousands of years ago. This mystery species eventually went extinct, but an AI developed by researchers from the Institute of Evolutionary Biology (IBE) and several other European institutions found traces of its existence in the DNA of present-day people with Asian ancestry. A press release issued by the Centre for Genomic Regulation said it’s the first time deep learning has been used to explain human history, “paving the way for this technology to be applied in other questions in biology, genomics and evolution.”
