Bits of DNA known as gene drives that force themselves through a population could be use maliciously, but thankfully there is a way to detect them before they spread.
Biologists often speak of switching genes on and off to give microbes new abilities–like producing biofuels or drugs, or gobbling up environmental toxins. For the most part, though, it’s nearly impossible to turn off a gene without deleting it (which means you can’t turn it on again). This limits biologists’ ability to control how much of a particular protein a microbe produces. It also restricts bioengineers’ ability to design new microbes.
Now researchers at Boston University, led by biomedical engineering professor James Collins, have developed a highly tunable genetic “switch” that offers a greater degree of control over microbes. It makes it possible to stop the production of a protein and restart it again. The switch, which could be used to control any gene, can also act as a “dimmer switch” to finely tune how much protein a microbe would produce over time.
The researchers made a highly effective microbe “kill switch” to demonstrate the precision of the approach. For years, researchers have been trying to develop these self-destruction mechanisms to allay concerns that genetically engineered microbes might prove impossible to eradicate once they’ve outlived their usefulness. But previous kill switches haven’t offered tight enough control to pass governmental regulatory muster because it was difficult to make it turn on in all the cells in a population at the same time.
The plastic tips attached to the ends of shoelaces keep them from fraying. Telomeres are repetitive DNA (deoxyribonucleic acid) sequences that serve a similar function at the end of chromosomes, protecting its accompanying genetic material against genome instability, preventing cancers and regulating the aging process.
Each time a cell divides in our body, the telomeres shorten, thus functioning like a molecular “clock” of the cell as the shortening increases progressively with aging. An accurate measure of the quantity and length of these telomeres, or “clocks,” can provide vital information if a cell is aging normally, or abnormally, as in the case of cancer.
To come up with an innovative way to diagnose telomere abnormalities, a research team led by Assistant Professor Cheow Lih Feng from the NUS Institute for Health Innovation & Technology (iHealthtech) has developed a novel method to measure the absolute telomere length of individual telomeres in less than three hours. This unique telomere profiling method can process up to 48 samples from low amounts (1 ng) of DNA.
Genetic variants may contribute to increased levels of antibodies against proteins of the Epstein-Barr virus — a known environmental risk factor for multiple sclerosis (MS) — in MS patients and their siblings, a study suggests.
The study, “EBNA-1 titer gradient in families with multiple sclerosis indicates a genetic contribution,” was published in the journal Neurology, Neuroimmunology and Neuroinflammation.
After a decade of heated debate, free-flying swarms aimed at shrinking dengue-carrying mosquito populations gets a nod for 2021 in the Florida Keys.
How we adapt to aging late in life may be genetically influenced, according to a study led by a psychologist at the University of California, Riverside.
The research, published in Aging Cell, has implications for how epigenetic factors relate to aging. Epigenesis is a process in which chemicals attached to DNA control its activity. Epigenetic changes, which can be passed on to offspring, may be critical to accelerated aging as well as declines in cognitive and physical functioning that often accompany aging. Epigenetic modifications resulting in altered gene expression may occur due to a number of biological processes, including one the researchers focused on: DNA methylation.
In DNA methylation, methyl groups are added to the DNA molecule. DNA has four different types of nucleotides: A, T, G, and C. DNA methylation occurs at the C bases of eukaryotic DNA. Changes in DNA methylation correlate strongly with aging.
Summary: Researchers identified a group of closely related genes that capture molecular links between Alzheimer’s and LATE, a common brain disorder that mimics Alzheimer’s symptoms.
Source: Brigham and Women’s Hospital
Alzheimer’s disease is one of the most common causes of dementia, and while most people might know someone who is affected by it, the genetic factors behind the disease are less known. A new study by investigators from Brigham and Women’s Hospital uncovered a group of closely related genes that may capture molecular links between Alzheimer’s disease and Limbic-predominant Age-related TDP-43 Encephalopathy, or LATE, a recently recognized common brain disorder that can mimic Alzheimer’s symptoms. LATE is often combined with Alzheimer’s disease to cause a more rapid cognitive decline. The study’s results are published in Neuron.
“I HOPE THIS STUDY CHANGES THE DIALOG AROUND HERPES RESEARCH AND OPENS UP THE IDEA THAT WE CAN START THINKING ABOUT CURE, RATHER THAN JUST CONTROL OF THE VIRUS.”
In a landmark study, researchers have successfully used gene editing to remove the oral herpes virus (HSV-1) in mice.
While previous research has mostly focused on treating and suppressing the sometimes painful symptoms of herpes, this study took a more radical approach by attempting to eliminate the virus altogether.
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For decades, greater than 60% of the human genome was believed to be “junk DNA” that served little or no purpose in the course of human development. Recent research by Colorado State University is challenging this notion to show that junk DNA might be important after all.
A new study, published on June 5 in Aging Cell, found that a portion of noncoding genetic material, called repetitive element transcripts, might be an important biomarker of the aging process.
Tom LaRocca, an assistant professor in the Department of Health and Exercise Science and faculty member in the Columbine Heath Systems Center for Healthy Aging at CSU, led the study to investigate a growing body of evidence that repetitive elements—transposons and other sequences that occur in multiple copies in the human genome —may become active over time as we age.
Newswise — Most of modern medicine has physical tests or objective techniques to define much of what ails us. Yet, there is currently no blood or genetic test, or impartial procedure that can definitively diagnose a mental illness, and certainly none to distinguish between different psychiatric disorders with similar symptoms. Experts at the University of Tokyo are combining machine learning with brain imaging tools to redefine the standard for diagnosing mental illnesses.
“Psychiatrists, including me, often talk about symptoms and behaviors with patients and their teachers, friends and parents. We only meet patients in the hospital or clinic, not out in their daily lives. We have to make medical conclusions using subjective, secondhand information,” explained Dr. Shinsuke Koike, M.D., Ph.D., an associate professor at the University of Tokyo and a senior author of the study recently published in Translational Psychiatry.
“Frankly, we need objective measures,” said Koike.
