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Category: genetics

This amino acid may help the body fight tumors and viral infections

The amino acid arginine helps keep the human body humming, most notably by synthesizing proteins that carry out a range of cellular processes. It’s produced by our bodies and found in common high-protein foods. Low levels of arginine are associated with a number of diseases, including colon cancer.

Sohail Tavazoie, head of Rockefeller University’s Elizabeth and Vincent Meyer Laboratory of Systems Cancer Biology, has been investigating that connection for years. In 2023, Tavazoie’s team found that starving colon cancer cells of arginine increases the number of mutations they accumulate. Now they’ve discovered that an arginine-deficient diet also affects the immune system by stalling the production of the MHC-I protein, which alerts the immune system to dangers such as a mutating cell or an invading virus.

Intriguingly, they also found that a moderate dose of arginine—about as much as is found in a couple of over-the-counter tablets—could potentially restore expression of the genes responsible for MHC-I production. They published the results in the journal Cell.

How the heart’s ‘little brain’ helps it function and protects it against stress

For years, scientists have known that the heart has its own network of nerves, the intrinsic cardiac nervous system (ICNS), sometimes called its “little brain.” Exactly how it functions has remained something of a mystery, but a new paper published in the journal Cell sheds light on how these heart nerves work to keep the heart beating steadily.

The heart’s nerve cells fine-tune signals coming from the brain to control heart function, including heart rate. But because they are so few, doctors have struggled to determine exactly what they do. To solve this, researchers from Yale University School of Medicine genetically engineered adult mice so their heart nerves would glow, making them much easier to study.

After locating the nerves, the team analyzed which genes were active in them. They discovered that the nerves fell into two categories, which they called Npy neurons and Ddah1 neurons.

Unzipping the Code of Life: Scientists Pinpoint Where DNA First Opens

Researchers mapped where DNA first opens and how a helicase gate may release one strand as genome copying begins.

Before a cell can divide, it must open its tightly wound DNA and begin copying the entire genome. Researchers at the MRC Laboratory of Medical Sciences (LMS) and collaborating institutions have now traced this process to one of its earliest moments, revealing where DNA first separates inside living cells and identifying a molecular gate that helps launch replication.

Published in Nature Communications, the findings provide a closer view of how cells begin duplicating their genetic material. Because copying errors can damage the genome, the start of DNA replication must be controlled with exceptional precision.

Gene editing tool reduces Huntington’s toxic protein fragments and symptoms in mice

A gene-editing tool designed to precisely rewrite the gene that causes Huntington’s disease reduced toxic protein fragments and symptoms associated with the disease in mice, researchers at the University of Illinois Urbana-Champaign report.

While other gene-based treatments have focused on turning the gene off, the Illinois team took a different approach. The researchers designed a base-editing tool to alter a specific point in the huntingtin gene so the cell’s machinery would skip over a small section prone to generating toxic fragments while preserving enough huntingtin protein to support its normal functions.

Led by Pablo Perez-Pinera and Thomas Gaj, professors of bioengineering at the U. of I., the researchers published their findings in the journal Nature Biomedical Engineering.

Genetic deletions may help explain differences in schizophrenia severity

Schizophrenia affects approximately 23 million people worldwide, with onset usually occurring during a person’s late adolescence or 20s. Impairments associated with schizophrenia include hallucinations, delusions, and disorganized thinking and behavior.

Now, researchers at the University of Washington are investigating how genetic changes affect the severity of schizophrenia symptoms. A new study, published in the American Journal of Psychiatry, supports the idea that deletions in genes that regulate early brain and neuron development are associated with more severe features of schizophrenia spectrum disorders, particularly lower cognitive abilities.

Bloodstream-delivered cell therapy slows muscle decline in young people with Duchenne muscular dystrophy, trial finds

A cell therapy called deramiocel could slow muscle weakening in boys and young men with advanced Duchenne muscular dystrophy (DMD) and may also slow heart damage in those who already have heart muscle disease, a Phase III clinical trial published in The Lancet has found.

It is the first Phase III trial of a cell therapy made from donor cells and administered through the bloodstream to treat a genetic disease, and the first such trial in boys and young men whose DMD is already advanced. The therapy is grown from heart cells that were donated for transplant but could not be used.

There is no cure for DMD, a serious genetic condition that causes the muscles, including the heart, to gradually weaken and waste away. It almost exclusively affects boys and young men because the gene involved sits on the X chromosome. As the disease progresses, most patients lose the ability to walk and come to depend on their arms and hands for everyday tasks and independence.

Hesperidin and Hesperetin: EpigeneticStemness Crosstalk, Antitumor Mechanisms, Preclinical Data and Translation Barriers

Hesperidin is a natural flavonoid derived from citrus plants, which can be hydrolyzed into hesperetin in vivo. Both compounds have anti-inflammatory, antioxidant and antitumor activities. At present, there is a lack of reviews focusing on the epigenetic regulation of cancer stem cells (CSCs) mediated by hesperidin and hesperetin. This review summarizes the molecular crosstalk between hesperidin/hesperetin and CSCs mediated via three major epigenetic pathways, including direct regulatory effects, indirect modulatory actions, and mechanistic relationships proposed based on scientific hypotheses. We elaborate their effects on inhibiting the self-renewal, invasion and metastasis of CSCs as well as reversing chemoresistance, and analyze the crosstalk between epigenetic networks and classical signaling pathways of CSCs.

Blocking a mitochondrial transporter may curb inflammation from ‘zombie’ cells without killing them

Researchers have uncovered a previously unknown mechanism that helps aging cells drive the chronic inflammation linked to many age-related diseases. The findings reveal how dysfunctional mitochondria—the cell’s energy-producing structures—work with the cell’s epigenetic machinery to switch on inflammatory genes, opening the door to a new therapeutic approach for promoting healthier aging.

The study, published in Nature, builds on years of research showing that senescent, or “zombie,” cells accumulate with age. While these cells no longer divide, they remain metabolically active and release a cocktail of inflammatory molecules known as the senescence-associated secretory phenotype, or SASP.

This persistent inflammation is thought to contribute to frailty, cardiovascular disease, cancer, neurodegeneration and other disorders of aging.

Scientists identify new mitochondrial pathway linked to harmful inflammation in aging

ROCHESTER, Minn. — Researchers have uncovered a previously unknown mechanism that helps aging cells drive the chronic inflammation linked to many age-related diseases. The findings reveal how dysfunctional mitochondria — the cell’s energy-producing structures — work with the cell’s epigenetic machinery to switch on inflammatory genes, opening the door to a new therapeutic approach for

Inflammation may drive Dravet syndrome, offering a potential new treatment target

An overactive immune response in the brain may play a role in Dravet syndrome, a rare and severe genetic epilepsy that typically begins in infancy, according to Weill Cornell Medicine researchers. Children with the condition experience frequent seizures that are often difficult to control with medication and may also face developmental, cognitive and behavioral challenges. Until now, most research has focused on how a mutation in the SCN1A gene disrupts electrical signaling in the brain.

“Rather than being a disorder only involving abnormal electrical signaling, the disease may also involve a self-sustaining immune response triggered by DNA released from stressed neurons,” said study senior author Dr. Li Gan, the Burton P. and Judith B. Resnick Distinguished Professor in Neurodegenerative Diseases and director of the Helen and Robert Appel Alzheimer’s Disease Research Institute at Weill Cornell. “As a result, inflammation may help drive and sustain the disease. This finding links seizures to the brain’s immune system in a way that had not been fully appreciated before.”

The new preclinical study, published July 29 in Nature Neuroscience, identified an inflammatory pathway called cGAS-STING-interferon (IFN-I) signaling as a major contributor to disease progression. Blocking this molecular pathway could lead to new therapeutic strategies for epilepsy disorders.

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