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Category: genetics

For the first time, researchers appear to have effectively treated a genetic disorder by directly injecting a CRISPR therapy into patients’ bloodstreams — overcoming one of the biggest hurdles to curing diseases with the gene editing technology.

The therapy appears to be astonishingly effective, editing nearly every cell in the liver to stop a disease-causing mutation.

The challenge: CRISPR gives us the ability to correct genetic mutations, and given that such mutations are responsible for more than 6,000 human diseases, the tech has the potential to dramatically improve human health.

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There are synergies between the two kinds of intelligence. The brain serves the genes by improving the organism’s capability to survive and reproduce. In exchange, evolution favors genetic mutations that improve the brain’s innate and learning capacities for each species (this is why some animals are born with the ability to walk while others learn it weeks or months later).

At the same time, the brain comes with tradeoffs. Genes lose some of their control over the behavior of the organism when they relegate their duties to the brain. Sometimes, the brain can go chasing rewards that do not serve the self-replication of the genes (e.g., addiction, suicide). Also, the behavior learned by the brain does not pass on through genes (this is why you didn’t inherit your parents’ knowledge and had to learn language, math, and sports from scratch).

As Lee writes in Birth of Intelligence, “The fact that brain functions can be modified by experience implies that genes do not fully control the brain. However, this does not mean that the brain is completely free from genes, either. If the behaviors selected by the brain prevent the self-replication of its own genes, such brains would be eliminated during evolution. Thus, the brain interacts with the genes bidirectionally.”

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Scientists have discovered a way to stop the COVID-19 virus from replicating in infected human cells, marking major progress towards a definitive treatment for the deadly illness and accentuating the potential of genetic engineering to cure viral diseases.

The study explores the use of CRISPR, a genome editing tool, and builds on research that started at Australia’s Peter MacCallum Cancer Center in 2019, when Dr. Mohamed Fareh and Prof. Joe Trapani showed that CRISPR could be used to eliminate abnormal RNAs that drive children’s cancers.

At the beginning of the pandemic, and in collaboration with Director Prof. Sharon Lewin and Dr. Wei Zhao from the Doherty Institute, the scientists reprogrammed the same CRISPR tool to suppress replication of the RNA virus SARS-CoV-2 — and importantly, its “variants of concern” — in a test tube model. SARS-CoV-2, which is short for Severe Acute Respiratory Syndrome Coronavirus 2, is the virus that causes COVID-19.

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Researchers have imaged a major component in conjugation—the process bacteria use to share DNA with each other.

During conjugation, bacteria can exchange genetic information in the form of special pieces of DNA. These include genes that help them resist attacks from common antimicrobial drugs, making many illnesses caused by these bacteria resistant to treatment.

Better understanding conjugation could therefore allow scientists to find ways to stop the process and reduce the spread of antimicrobial resistance.

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ROME, July 2 (Reuters) — A United Nations-backed scientific research centre has teamed up with an Italian tech firm to explore whether laser light can be used to kill coronavirus particles suspended in the air and help keep indoor spaces safe.

The joint effort between the International Centre for Genetic Engineering and Biotechnology (ICGEB) of Trieste, a city in the north of Italy, and the nearby Eltech K-Laser company, was launched last year as COVID-19 was battering the country.

They created a device that forces air through a sterilization chamber which contains a laser beam filter that pulverizes viruses and bacteria.

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A cell stores all of its genetic material in its nucleus, in the form of chromosomes, but that’s not all that’s tucked away in there. The nucleus is also home to small bodies called nucleoli — clusters of proteins and RNA that help build ribosomes.

Using computer simulations, MIT chemists have now discovered how these bodies interact with chromosomes in the nucleus, and how those interactions help the nucleoli exist as stable droplets within the nucleus.

Their findings also suggest that chromatin-nuclear body interactions lead the genome to take on a gel-like structure, which helps to promote stable interactions between the genome and transcription machineries. These interactions help control gene expression.

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The SARS-CoV-2 gene set remains unresolved, hindering dissection of COVID-19 biology. Comparing 44 Sarbecovirus genomes provides a high-confidence protein-coding gene set. The study characterizes protein-level and nucleotide-level evolutionary constraints, and prioritizes functional mutations from the ongoing COVID-19 pandemic.

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Over the past several decades, researchers have moved from using electric currents to manipulating light waves in the near-infrared range for telecommunications applications such as high-speed 5G networks, biosensors on a chip, and driverless cars. This research area, known as integrated photonics, is fast evolving and investigators are now exploring the shorter—visible—wavelength range to develop a broad variety of emerging applications. These include chip-scale LIDAR (light detection and ranging), AR/VR/MR (augmented/virtual/mixed reality) goggles, holographic displays, quantum information processing chips, and implantable optogenetic probes in the brain.

The one device critical to all these applications in the is an optical phase modulator, which controls the phase of a light wave, similar to how the phase of radio waves is modulated in wireless computer networks. With a phase modulator, researchers can build an on-chip that channels light into different waveguide ports. With a large network of these optical switches, researchers could create sophisticated integrated optical systems that could control light propagating on a tiny chip or light emission from the chip.

But phase modulators in the visible range are very hard to make: there are no materials that are transparent enough in the visible spectrum while also providing large tunability, either through thermo-optical or electro-optical effects. Currently, the two most suitable materials are silicon nitride and lithium niobate. While both are highly transparent in the visible range, neither one provides very much tunability. Visible-spectrum phase modulators based on these materials are thus not only large but also power-hungry: the length of individual waveguide-based modulators ranges from hundreds of microns to several mm and a single modulator consumes tens of mW for phase tuning. Researchers trying to achieve large-scale integration—embedding thousands of devices on a single microchip—have, up to now, been stymied by these bulky, energy-consuming devices.

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Two new methods make it possible to delete long sections of the genome, expanding the capabilities of the gene editor CRISPR. The techniques could lead to therapies that excise large insertions or duplications tied to autism, such as the DNA repeats that underlie fragile X syndrome.

To remove a segment of DNA, CRISPR systems typically use an enzyme called Cas9 to snip double-stranded DNA at two target sites. The cell’s own repair machinery can then join the cut ends, omitting the intervening sequence. But this process is error prone and can insert or delete unintended segments of DNA, called ‘indels,’ or rearrange large sections of the genome. Snipping double-stranded DNA can also cause cell death.

A different CRISPR-based system called ‘prime editing’ can make DNA repair more precise. In one version of the technique, a protein complex called a prime editor cuts only one strand of DNA at one of the two sites and the opposite strand at the other site. The prime editor adds a sequence to one of the cut strands to guide the repair.

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Eliminating old, dysfunctional cells in human fat also alleviates signs of diabetes, researchers from UConn Health report. The discovery could lead to new treatments for Type 2 diabetes and other metabolic diseases.

The cells in your body are constantly renewing themselves, with older cells aging and dying as new ones are being born. But sometimes that process goes awry. Occasionally damaged cells linger. Called senescent cells, they hang around, acting as a bad influence on other cells nearby. Their bad influence changes how the neighboring cells handle sugars or proteins and so causes metabolic problems.

Type 2 diabetes is the most common metabolic disease in the US. About 34 million people, or one out of every 10 inhabitants of the US, suffers from it, according to the Centers for Disease Control and Prevention (CDC). Most people with diabetes have insulin resistance, which is associated with obesity, lack of exercise and poor diet. But it also has a lot to do with senescent cells in people’s body fat, according to new findings by UConn Health School of Medicine’s Ming Xu and colleagues. And clearing away those senescent cells seems to stop diabetic behavior in obese mice, they report in the 22 November issue of Cell Metabolism. Ming Xu, assistant professor in the UConn Center on Aging and the department of Genetics and Genome Sciences at UConn Health, led the research, along with UConn Health researchers Lichao Wang and Binsheng Wang as major contributors. Alleviating the negative effects of fat on metabolism was a dramatic result, the researchers said.

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