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Category: genetics – Page 438

The complicated ethics of genetic engineering

With new technology to edit genes, scientists are now working on things that once seemed impossible. But what are the boundaries? See the full 60 Minutes interview with Church, here: https://cbsn.ws/34ZhuTs

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Evolutionary Changes in Brain Potentially Make us More Prone to Anxiety

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.

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.

The researcher’s next step is to identify the neurological and behavioral consequences of the mutations in mice to clarify how the variants contributed to our brain evolution. “This would be the striking evidence that links evolution of our genome and brain,” said the authors. The researchers hope that this finding provides insights into our diverse psychological traits including psychiatric disorders.

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Researchers develop new method that could facilitate cancer diagnosis

Researchers led by the European Molecular Biology Laboratory (EMBL) in Heidelberg and the Center for Bioinformatics at Saarland University in Saarbrücken, Germany, have developed a cheaper and faster method to check for genetic differences in individual cells. It outperforms existing techniques with respect to the information received. This new method could become a new standard in single-cell research, and potentially for clinical diagnosis in disease genetics, including cancer. The results have been published in Nature Biotechnology.

“Our new method to study genetic variations in could transform the field of mutation detection,” says Ashley Sanders, one of the lead authors of the study, working at EMBL Heidelberg, Germany. The method she and her colleagues developed, termed tri-channel processing (scTRIP), allows them to study genetic variations within the DNA of a single cell and measure genetic variations directly as they form in new . In contrast to existing methods that were able to detect only large-scale changes in the genome, scTRIP can detect small-scale changes along with many types of genetic variations that were invisible using other single-cell methods.

The researchers tested their method in patient-derived leukemia cells. In their sample, the team found four times more variants in the patient than were detected by standard clinical diagnostics. These included a missed clinically relevant translocation that drove the overexpression of a cancer-causing gene. They also observed a catastrophic chromosome rearrangement that was missed in the initial leukemia diagnosis. It probably occurred when a single chromosome shattered and was then glued back together in a rearranged order.

New Aging Clock based on Proteins in the Blood

Methylation clocks are far and away the most accurate markers of a person’s age, and so are a promising tool for evaluating anti-aging interventions, but they are a bit of a black box. We know from statistics that certain places on chromosomes become steadily methylated ( or demethylated ) with age, but we often don’t know what effect that has on expression of particular genes.

For the first time, a clock has been devised based on proteins in the blood that is comparable in accuracy to the best methylation clocks. This has the advantage of being downstream of epigenetics, so it is less of a black box. What can we learn from the proteins that are increased ( and decreased ) with age?

I’ve written often and enthusiastically about the utility of methylation clocks for evaluation of anti-aging interventions [ blog, blog, blog, journal article ]. This technology offers a way to promptly identify small age-reversal successes (perhaps not in individuals, but averaged over a cohort of ~50 to 100 subjects). Before these tests were available, we had no choice but to wait — usually 10 years or more — for enough experimental subjects to die that we could be sure the intervention we were evaluating affected life expectancy. (This is the plan of the worthy but ridiculously expensive TAME trial promoted by Nir Barzilai.)

This Year’s 4 Most Mind-Boggling Stories About the Brain

2019 was nuts for neuroscience. I said this last year too, but that’s the nature of accelerating technologies: the advances just keep coming.

There’re the theoretical showdowns: a mano a mano battle of where consciousness arises in the brain, wildly creative theories of why our brains are so powerful, and the first complete brain wiring diagram of any species. This year also saw the birth of “hybrid” brain atlases that seek to interrogate brain function from multiple levels—genetic, molecular, and wiring, synthesizing individual maps into multiple comprehensive layers.

Brain organoids also had a wild year. These lab-grown nuggets of brain tissue, not much larger than a lentil, sparked with activity similar to preterm babies, made isolated muscles twitch, and can now be cloned into armies of near-identical “siblings” for experimentation—prompting a new round of debate on whether they’ll ever gain consciousness.

Zinaida Good | Reversing Epigenetic Aging and Immunosenescent Trends in Humans | VISION WEEKEND 2019

You heard about reversing the epigenetic clock 2.5 years? Living drugs? CAR T cells? Fight cancer? Here ya go.

Vision Weekend is the annual member gathering of Foresight Institute, a non-profit for advancing beneficial technologies for the long-term flourishing of life.

More info on speakers and program: https://foresight.org/vision-weekend-2019/.
Join Foresight Institute’s community: www.bit.ly/foresightnews

Scientists Gene-Edited Tomatoes to Make Them Grow Like Grapes

It’s 2050, and you’ve just arrived on Mars. Your first meal awaits: a plate of spaghetti marinara made from fresh vine-ripened tomatoes. Tough to imagine, right?

The idea that astronauts might enjoy the fresh, cherry-red fruits has seemed borderline absurd. Tomato plants, with their sprawling vines and bulbous fruits, take up space—valuable space. And they’re extremely finicky.

But now, scientists have developed a way to genetically modify cherry tomatoes so they grow in tighter bunches and take up less space. This could be a game changer as the push to grow vertical, rooftop gardens increases and as humanity stretches out past low-Earth orbit toward the moon, and eventually, Mars.

Polina Mamoshina — The Beginning of an AI Healthcare Revolution

From insilico meddicine — the beginning of an AI healthcare revolution.

Poly Mamoshina on Machine Learning for small molecule drug discovery and the beginning of an AI healthcare revolution — interviewed at the Undoing Aging conference in Berlin 2019!

Polina Mamoshina is a senior research scientist at Insilico Medicine, Inc (www.insilico.com), a Baltimore-based bioinformatics and deep learning company focused on reinventing drug discovery and biomarker development and a part of the computational biology team of Oxford University Computer Science Department. Polina graduated from the Department of Genetics of the Moscow State University. She was one of the winners of GeneHack a Russian nationwide 48-hour hackathon on bioinformatics at the Moscow Institute of Physics and Technology attended by hundreds of young bioinformaticians. Polina is involved in multiple deep learning projects at the Pharmaceutical Artificial Intelligence division of Insilico Medicine working on the drug discovery engine and developing biochemistry, transcriptome, and cell-free nucleic acid-based biomarkers of aging and disease. She recently co-authored seven academic papers in peer-reviewed journals.

https://scholar.google.com/citations?user=YrLgl8gAAAAJ&hl=en

https://uk.linkedin.com/in/polymamoshina

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Targeted screening could prevent one in six prostate cancer deaths

Nearly one in six deaths from prostate cancer could be prevented if targeted screening was introduced for men at a higher genetic risk of the disease, according to a new UCL-led computer modelling study.

Prostate cancer is the most common form of cancer in men with around 130 new cases diagnosed in the UK every day and more than 10,000 men a year dying as a result of the disease. However, unlike breast and there is currently no national programme for this disease in the UK.

A blood test that detects raised levels of the prostate-specific antigen (PSA) can be used to screen for . However, this test is not a reliable indicator as it does not accurately distinguish between dangerous cancers from harmless ones—leading to both unnecessary operations and missed cancers that are harmful.

Finding familiar pathways in kidney cancer

P53 is the most famous cancer gene, not least because it’s involved in causing over 50% of all cancers. When a cell loses its p53 gene—when the gene becomes mutated—it unleashes many processes that lead to the uncontrolled cell growth and refusal to die, which are hallmarks of cancer growth. But there are some cancers, like kidney cancer, that that had few p53 mutations. In order to understand whether the inactivation of the p53 pathway might contribute to kidney cancer development, Haifang Yang, Ph.D., a researcher with the Sidney Kimmel Cancer Center—Jefferson Health probed kidney cancer’s genes for interactions with p53.

Earlier work found that PBRM1—the second most mutated gene in —could interact with p53. However, other researchers were unable to definitively show that it was truly an important mechanism in kidney cancer.

Rather than looking at the p53 protein itself, first author Weijia Cai a postdoc in Dr. Yang’s lab and other collaborators looked at an activated version of p53, one that is studded with an additional chemical marker—an —at many specific spots.

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