One mouse is hunched over, graying, and barely moves at 7 months old. Others, at 11 months, have sleek black coats and run around. The videos and other results from a new study have inspired hope for treating children born with progeria, a rare, fatal, genetic disease that causes symptoms much like early aging. In mice with a progeria-causing mutation, a cousin of the celebrated genome editor known as CRISPR corrected the DNA mistake, preventing the heart damage typical of the disease, a research team reports today in. Treated mice lived about 500 days, more than twice as long as untreated animals.
“The outcome is incredible,” says gene-therapy researcher Guangping Gao of the University of Massachusetts, who was not involved with the study.
Although the developers of the progeria therapy aim to improve it, they are also taking steps toward testing the current version in affected children, and some other scientists endorse a rush. The mouse results are “beyond anyone’s wildest expectations,” says Fyodor Urnov, a gene-editing researcher at the University of California, Berkeley. “The new data are an imperative to treat a child with progeria … and do so in the next 3 years.”
Biochemists use protein engineering to transfer photocaging groups to DNA.
DNA (deoxyribonucleic acid) is the basis of life on earth. The function of DNA is to store all the genetic information, which an organism needs to develop, function and reproduce. It is essentially a biological instruction manual found in every cell.
Biochemists at the University of Münster have now developed a strategy for controlling the biological functions of DNA with the aid of light. This enables researchers to better understand and control the different processes which take place in the cell – for example epigenetics, the key chemical change and regulatory lever in DNA.
Ralph Baric, PhD, is the William R. Kenan, Jr. Distinguished Professor in the Department of Epidemiology and Professor in the Department of Microbiology and Immunology. He is a Harvey Weaver Scholar from the National Multiple Sclerosis Society and an Established Investigator Awardee from the American Heart Association. In addition, he is a World Technology Award Finalist and a fellow of the American Association for Microbiology. He has spent the past three decades as a world leader in the study of coronaviruses and is responsible for UNC-Chapel Hill’s world leadership in coronavirus research. For these past three decades, Dr. Baric has warned that the emerging coronaviruses represent a significant and ongoing global health threat, particularly because they can jump, without warning, from animals into the human population, and they tend to spread rapidly.
The Baric Lab uses coronaviruses as models to study the genetics of RNA virus transcription, replication, persistence, pathogenesis, genetics and cross-species transmission. He has used alphavirus vaccine vectors to develop novel candidate vaccines. Dr. Baric has led the world in recognizing the importance of zoonotic viruses as a potentially rich source of new emerging pathogens in humans, with detailed studies of the molecular, genetic and evolutionary mechanisms that regulate the establishment and dissemination of such a virus within a newly adopted host. Specifically, he works to decipher the complex interactions between the virion and cell surface molecules that function in the entry and cross-species transmission of positive-strand RNA viruses.
In 20172018 and 2019, Dr. Baric was named to Clarivate Analytics’ Highly Cited Researchers list, which recognizes researchers from around the world who published the most widely-cited papers in their field. Also in 2017, he was awarded a grant for more than $6 million from the National Institute of Allergy and Infectious Diseases (NIAID) to accelerate the development of a promising new drug in the fight against deadly coronaviruses, which is currently in clinical trials to reverse COVID-19 disease in humans. In this collaboration, he continued his partnership between the Gillings School and Gilead Sciences Inc. to focus on an experimental antiviral treatment that he had previously shown to prevent the development of severe acute respiratory syndrome coronavirus (SARS-CoV) in mice. The drug also was shown to inhibit MERS-CoV and multiple other coronaviruses (CoV), suggesting that it may actually inhibit all CoV. He continues to work with this drug.
Lots of good telomere info but one small problem with Mr Andrews here. He states that he agrees with the FDA that you can’t target aging as a disease since it is not measurable. Well i think this has been shown to be false as a result of epigenetic clocks.
I posted a question under the comments on the matter,(Lord Mon) we’ll see if we get a response.
A piece of high school genetics, relied on for many sorts of genetic testing, has been found to have exceptions. Although mitochondrial DNA (mtDNA) is normally received from the mother, three families have been identified where people received some of their mtDNA, three-quarters in the most extreme case, from their father. The finding may change the way we treat mitochondrial diseases and brings genetic testing for maternal ancestry into question.
MtDNA exists separately from the rest of our DNA, inside the thousands of mitochondria within each cell, rather than the cell nucleus. It is so widely accepted as being from the mother’s side it is sometimes known as the Eve Gene, the idea being that it can be traced back to some primeval mother of all living humans. Testing of mtDNA is used to identify maternal ancestry.
I have to admit, they really sound “alien-like” if you ask me. 😃
Just when we thought octopuses couldn’t be any weirder, it turns out that they and their cephalopod brethren evolve differently from nearly every other organism on the planet.
In a surprising twist, in April 2017 scientists discovered that octopuses, along with some squid and cuttlefish species, routinely edit their RNA (ribonucleic acid) sequences to adapt to their environment.
This is weird because that’s really not how adaptations usually happen in multicellular animals. When an organism changes in some fundamental way, it typically starts with a genetic mutation — a change to the DNA.
Digital data storage is a growing need for our society and finding alternative solutions than those based on silicon or magnetic tapes is a challenge in the era of “big data.” The recent development of polymers that can store information at the molecular level has opened up new opportunities for ultrahigh density data storage, long-term archival, anticounterfeiting systems, and molecular cryptography. However, synthetic informational polymers are so far only deciphered by tandem mass spectrometry. In comparison, nanopore technology can be faster, cheaper, nondestructive and provide detection at the single-molecule level; moreover, it can be massively parallelized and miniaturized in portable devices. Here, we demonstrate the ability of engineered aerolysin nanopores to accurately read, with single-bit resolution, the digital information encoded in tailored informational polymers alone and in mixed samples, without compromising information density. These findings open promising possibilities to develop writing-reading technologies to process digital data using a biological-inspired platform.
DNA has evolved to store genetic information in living systems; therefore, it was naturally proposed to be similarly used as a support for data storage (1–3), given its high-information density and long-term storage with respect to existing technologies based on silicon and magnetic tapes. Alternatively, synthetic informational polymers have also been described (5–9) as a promising approach allowing digital storage. In these polymers, information is stored in a controlled monomer sequence, a strategy that is also used by nature in genetic material. In both cases, single-molecule data writing is achieved mainly by stepwise chemical synthesis (3, 10, 11), although enzymatic approaches have also been reported (12). While most of the progress in this area has been made with DNA, which was an obvious starting choice, the molecular structure of DNA is set by biological function, and therefore, there is little space for optimization and innovation.
You are an apogee of Earthly Nature encompassing numerous generations of humans as well as preceded non-human terrestrial life, sitting atop the tree of life… and so is everyone else who lives today. We all can be regarded as archetypes for future generations as well, or perhaps a “developing pattern,” if you intend to live indefinitely long. At any rate, genetically and anthropologically speaking, we all are one humongous extended family. #Timescape #HomoSapiens #ExponentialPedigree
This demographic research provides a host of quantifiable properties of the human species as a whole for further visualizing the data via certain graphs and diagrams. 5 trillion subjective years would constitute the ‘Timescape’ of Homo sapiens up to the p.
Follow the links in the story for sources, the text is in red. A new strain of COVID-19 is causing a wave of new lockdowns in London and travel restrictions for those coming from the U.K. because some are worried that this may be an even more contagious version of the coronavirus. Experts say it’s definitely something to watch out for, but it’s not clear whether or not this variant is actually more transmissible—and there’s no reason to think the current COVID-19 vaccines won’t be effective against it. So what exactly is different about this new strain of COVID-19? Well, this variant (also called B. 1. 1. 7.) has a few mutations, 17 to be exact. Not all of them are concerning, but a few are. The mutations that have experts a little on edge have to do with genes that encode the virus’s spike protein, which is located on the surface of the virus and is the piece of the virus that helps it actually bind to human cells. (That’s the first step in becoming infected.) One of these mutations (called N501Y) may make it easier for the spike protein to bind to the receptors on our cells, Science explains. Another mutation (called 69-70del) affects the number of amino acids (the building blocks that make up a protein) in the spike protein, and variants with this mutation have been previously identified in some immunocompromised people whose bodies were unable to muster the necessary immune response to protect them from the virus.
It’s causing new lockdowns and travel restrictions.
A team of Johns Hopkins University researchers has developed a new software that could revolutionize how DNA is sequenced, making it far faster and less expensive to map anything from yeast genomes to cancer genes.
The software, detailed in a paper published in Nature Biotechnology, can be used with portable sequencing devices to accelerate the ability to conduct genetic tests and deliver diagnoses outside of labs. The new technology targets, collects and sequences specific genes without sample preparation and without having to map surrounding genetic material like standard methods require.
“I think this will forever change how DNA sequencing is done,” said Michael C. Schatz, a Bloomberg Distinguished Associate Professor of Computer Science and Biology and senior author of the paper.
