Lifeboat Foundation

New research from the RIKEN Center for Brain Science (CBS) in Japan shows that a deficit in histone methylation could lead to the development of autism spectrum disorders (ASD). A human variant of the SUV39H2 gene led researchers to examine its absence in mice. Published in Molecular Psychiatry, the study found that when absent, adult mice exhibited cognitive inflexibility similar to what occurs in autism, and embryonic mice showed misregulated expression of genes related to brain development. These findings represent the first direct link between the SUV39H2 gene and ASD.

Genes are turned on and off throughout our development. But genetic variation means that what is turned off in some people remains turned on in others. This is why, for example, some adults can digest dairy products and others are lactose intolerant; the gene for making the enzyme lactase is turned off when some people become adults, but not others. One way that genes can be turned on and off is through a process called histone methylation in which special enzymes transfer methyl groups to histone proteins that are wrapped around DNA.

Variations in genes related to methylation during brain development can lead to serious problems. One such variation occurs in a rare disorder called Kleefstra Syndrome, in which a mutation prevents methylation of H3K9—a specific location on histone H3. Because Kleefstra Syndrome resembles autism in some ways, RIKEN CBS researchers led by Takeo Yoshikawa looked for autism-specific variations in genes that can modify H3K9. Among nine such genes, they found one variant in an H3K9 methyltransferase gene— SUV39H2 —that was present in autism, and the mutated SUV39H2 prevented methylation when tested in the lab. Similar loss-of-function results were found for the mouse version of the variant.

Nick Saraev is 25 years old, far too young, it would seem, to be thinking about death. And yet, since he turned 21, he has taken steps to prevent the infirmities of old age. Every day, he takes 2000 mg of fish oil and 4000 IU of vitamin D to help prevent heart disease and other ailments. He steams or pressure-cooks most of his meals because, he says, charring meats creates chemicals that may increase the risk of cancer. And in the winter, he keeps the humidity of his home at 35 percent, because dry air chaps his skin and makes him cough, both of which he considers manifestations of chronic inflammation, which may be bad for longevity.

Based on the life expectancies of young men in North America, Saraev, a freelance software engineer based near Vancouver, believes he has about 55 years before he really has to think about aging. Given the exponential advances in microprocessors and smartphones in his lifetime, he insists the biotech industry will figure out a solution by then. For this reason, Saraev, like any number of young, optimistic, tech-associated men, believes that if he takes the correct preventative steps now, he might well live forever. Saraev’s plan is to keep his body in good enough shape to hit “Longevity Escape Velocity,” a term coined by English gerontologist Aubrey de Grey to denote slowing down your aging enough to reach each new medical advance as it arrives. If you delay your death by 10 years, for example, that’s 10 more years scientists have to come up with a drug, computer program, or robot assist that can make you live even longer. Keep up this game of reverse leapfrog, and eventually death can’t catch you. The term is reminiscent of “planetary escape velocity,” the speed an object needs to move in order to break free of gravity.

The science required to break free of death, unfortunately, is still at ground level. According to Nir Barzilai, M.D., director of the Institute for Aging Research at Albert Einstein College of Medicine in New York City, scientists currently understand aging as a function of seven to nine biological hallmarks, factors that change as we grow older and seem to have an anti-aging effect when reversed. You can imagine these as knobs you can turn up or down to increase or decrease the likelihood of illness and frailty. Some of these you may have heard of, including how well cells remove waste, called proteostasis; how well cells create energy, or mitochondrial function; how well cells implement their genetic instructions, or epigenetics; and how well cells maintain their DNA’s integrity, called DNA repair or telomere erosion.

“Prime Editing is a wonderful example of the revolution in genetic medicine that we are living through,” said Robert Nelsen, co-founder and Managing Director of ARCH Venture Partners, one of several companies to fund Prime Medicine. “Gene editing technologies like this, when mature, could totally change our conception of what’s possible in treating disease.”

“This is an opportunity to take a giant step toward cures for a much wider range of diseases than previously possible,” said Stephen Knight, President and Managing Partner of F-Prime Capital, another backer of the new company.

The funds raised will be used to continue building the company, expand the capabilities of its technology platform and rapidly advance towards clinical indications. By the end of 2021, Prime Medicine expects to employ more than 100 people full-time.

To date, there are no effective antidotes against most virus infections. An interdisciplinary research team at the Technical University of Munich (TUM) has now developed a new approach: they engulf and neutralize viruses with nano-capsules tailored from genetic material using the DNA origami method. The strategy has already been tested against hepatitis and adeno-associated viruses in cell cultures. It may also prove successful against coronaviruses.

There are antibiotics against dangerous bacteria, but few antidotes to treat acute viral infections. Some infections can be prevented by vaccination but developing new vaccines is a long and laborious process.

Now an interdisciplinary research team from the Technical University of Munich, the Helmholtz Zentrum München, and the Brandeis University (USA) is proposing a novel strategy for the treatment of acute viral infections: The team has developed nanostructures made of DNA, the substance that makes up our genetic material, that can trap viruses and render them harmless.

Viruses that infect bacteria may drive the evolution of drug-resistant superbugs by inserting their genes into the bacterial DNA, a new study suggests.

The bacteria-attacking viruses, called phages, act as parasites in that they depend on their hosts for survival. The viral parasites often kill off their microbial hosts after infiltrating their DNA, said senior study author Vaughn Cooper, director of the Center for Evolutionary Biology and Medicine at the University of Pittsburgh School of Medicine. But sometimes, the phages slip into the bacterial genome and then lay low, making sneaky changes to the bacterium’s behavior, Cooper said.

For the first time ever, researchers from the University of Pittsburgh School of Medicine discovered that phages — tiny viruses that attack bacteria — are key to initiating rapid bacterial evolution leading to the emergence of treatment-resistant “superbugs.” The findings were published today in Science Advances.

The researchers showed that, contrary to a dominant theory in the field of evolutionary microbiology, the process of adaptation and diversification in bacterial colonies doesn’t start from a homogenous clonal population. They were shocked to discover that the cause of much of the early adaptation wasn’t random point mutations. Instead, they found that phages, which we normally think of as bacterial parasites, are what gave the winning strains the evolutionary advantage early on.

“Essentially, a parasite became a weapon,” said senior author Vaughn Cooper, Ph.D., professor of microbiology and molecular genetics at Pitt. “Phages endowed the victors with the means of winning. What killed off more sensitive bugs gave the advantage to others.”

NIH will award nearly $80 million to support the establishment of the Mendelian Genomics Research Consortium and the development of novel methods and approaches that help researchers identify the genetic causes of single-gene diseases.

Newfound genetic material may rev up methane cycling by soil microbes.

That said, the Borgs do clearly contain metabolic genes, which might be able to boost the energy metabolisms of Methanoperedens that host them. If so, these unique genetic elements could provide new insights into reducing methane emissions, which is a major aim for climate change mitigation plans.

These ‘Borg’ elements assimilated genes from other organisms, and could be used to help fight climate change.