Lifeboat Foundation

Summary: In mice genetically more susceptible to PTSD following a stressful event, researchers found an increased expression of cortisol receptors on neurons in the CA1 region of the dorsal hippocampus. Those increased receptors enabled an elevated expression of the HCN1 protein and TRIP8b, reducing neural excitability.

Source: medical college of georgia at augusta university.

Social avoidance is a common symptom of PTSD, and scientists working to better understand why have laboratory evidence that while stress hormone levels consistently increase in the immediate aftermath of a traumatic event, there can be polar opposite consequences in parts of the brain down the line.

Chromosome-level engineering is a completely different beast: it’s like rearranging multiple paragraphs or shifting complete sections of an article and simultaneously hoping the changes add capabilities that can be passed onto the next generation.

Reprogramming life isn’t easy. Xiao Zhu’s DNA makeup is built from genetic letters already optimized by eons of evolutionary pressure. It’s no surprise that tinkering with an established genomic book often results in life that’s not viable. So far, only yeast have survived the rejiggering of their chromosomes.

The new study, published in Science, made the technology possible for mice. The team artificially fused together chunks from mice chromosomes. One fused pair made from chromosomes four and five was able to support embryos that developed into healthy—if somewhat strangely behaved—mice. Remarkably, even with this tectonic shift to their normal genetics, the mice could reproduce and pass on their engineered genetic quirks to a second generation of offspring.

Summary: New research in cloned pigs with a mutation of the SORL1 sheds light on Alzheimer’s development. The findings could pave the way for new treatments for the neurodegenerative disorder.

Source: Aarhus University.

For decades, researchers from all over the world have been working hard to understand Alzheimer’s disease. Now, a collaboration between the Department of Biomedicine and the Department of Clinical Medicine at Aarhus University has resulted in a flock of minipigs that could lead to a major step forward in the research and treatment of Alzheimer’s.

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As humanity reaches out to the stars and make new homes on strange new worlds, how will our genetics & DNA change under those alien planets?

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Modern medicine forces bacteria to adapt: in response to antibiotic treatment, they either increase their fitness or die out. Whether a bacterial population survives or not depends on a combination of its genetics and environment—the antibiotic concentration—at a given moment. Now Suman Das of the University of Cologne, Germany, and colleagues simulate the effect on adaptation of an environment that is constantly changing [1]. Using a model that describes how slow-moving disordered systems respond to external forces, the researchers find that microbe evolution in changing drug concentrations exhibits hysteresis and memory formation. They use analytical methods and numerical simulations to connect these statistical physics concepts to bacterial drug resistance.

The team’s model examines changes in a bacterial population’s genetic sequences. By combining data on bacterial growth rates with statistical tools, the researchers describe how the bacterial genome can store information about both present and past drug concentrations. Their simulations start with a genetic sequence optimized for a certain antibiotic concentration. They then track how the sequence mutates when the concentration shifts to another value. When the concentration increases and then reduces to a lower value, the genetic route taken on the downward path depends on the changes on the upward path. How different the mutation routes are depends on the rate of concentration change.

The researchers find that this behavior mimics that of disordered systems driven by external forces, such as ferromagnetic materials subjected to magnetic fields or amorphous materials subjected to a shearing force. They say that while their approach focuses on the evolution of drug resistance, the framework can be adapted to other problems in evolutionary biology that involve changing environmental parameters.

Small but mighty, lysosomes play a surprisingly important role in cells despite their diminutive size. Making up only 1–3% of the cell by volume, these small sacs are the cell’s recycling centers, home to enzymes that break down unneeded molecules into small pieces that can then be reassembled to form new ones. Lysosomal dysfunction can lead to a variety of neurodegenerative or other diseases, but without ways to better study the inner contents of lysosomes, the exact molecules involved in diseases—and therefore new drugs to target them—remain elusive.

A new method, reported in Nature on Sept. 21, allows scientists to determine all the molecules present in the lysosomes of any cell in mice. Studying the contents of these molecular recycling centers could help researchers learn how the improper degradation of cellular materials leads to certain diseases. Led by Stanford University’s Monther Abu-Remaileh, institute scholar at Sarafan ChEM-H, the study’s team also learned more about the cause for a currently untreatable neurodegenerative disease known as Batten disease, information that could lead to new therapies.

“Lysosomes are fascinating both fundamentally and clinically: they supply the rest of the cell with nutrients, but we don’t always know how and when they supply them, and they are the places where many diseases, especially those that affect the brain, start,” said Abu-Remaileh, who is an assistant professor of chemical engineering and of genetics.

The genetic encoding of ncAAs with distinct chemical, biological, and physical properties requires the engineering of bioorthogonal translational machinery, consisting of an evolved aminoacyl-tRNA synthetase/tRNA pair and a “blank” codon. To achieve this, the researchers mimicked the ibis’ ability to synthesize sTyr and incorporate it into proteins.

The Xiao lab employed a mutant amber stop codon to encode the desired sulfotransferase, resulting in a completely autonomous mammalian cell line capable of biosynthesizing sTyr and incorporating it with great precision into proteins.

These engineered cells, the authors wrote, can produce “site-specifically sulfated proteins at a higher yield than cells fed exogenously with the highest level of sTyr reported in the literature.” They used the cells to prepare highly potent thrombin inhibitors with site-specific sulfation.

Summary: Researchers have discovered 69 genetic variants associated with musical beat synchronization, or the ability to move in sync with the beat of music.

Source: Vanderbilt University.

The first large-scale genomic study of musicality — published on the cover of today’s Nature Human Behaviour — identified 69 genetic variants associated with beat synchronization, meaning the ability to move in synchrony with the beat of music.

Don’t think about living forever. Just think about never getting sick, ever again.

At least that’s how Aubrey de Grey would like you to contextualize his work. The notoriously bearded biomedical gerontologist is the scientific spark that lights up so many all-caps “immortality” headlines. De Grey wants to increase human longevity so significantly that death could become a thing of the past, a condition people fell prey to before they developed the medical technology to stop it. It’s been the center of his work for approximately 20 years.

De Grey started as a software guy at the genetics department of Cambridge University in 1992, maintaining a database of genetic information on fruit flies. In 1999 he published a book called “The Mitochondrial Free Radical Theory of Aging,” where he first laid out the key idea we know him for today: preventing damage to mitochondrial DNA ought to make people live much longer. The idea was so well-received that Cambridge awarded him a PhD the following year. De Grey condensed his thesis to a sound byte in a 2007 interview: “[Humans] are machines, and aging is the wearing out of a machine, the accumulation of damage to a machine, and hence potentially fixable.”