Many believe that drug companies should already be updating their vaccines to target mutated versions of the Covid-19 spike protein. But can the patterns of mutations scientists are seeing popping up in Covid-19 around the world offer any clues about how the virus will continue to evolve?
“It is hard to speculate, but it is interesting that all of a sudden there does seem to be a lot of mutations appearing that could be associated with immune escape or immune recognition,” says Brendan Larsen, a PhD student working with Worobey in Arizona. He recently identified a new variant of Covid-19 circulating in Arizona that has the H69/V70 deletion seen in several other versions of the virus. While still only spreading at a relatively low level there and in other states of the US, it suggests that this particular mutation is recurring independently around the world.
Every time the coronavirus passes from person to person it picks up tiny changes to its genetic code, but scientists are starting to notice patterns in how the virus is mutating.
The paper is a preprint available on bioXriv on a study showing the reversal of age in rats through exchange of blood plasma. Blood plasma of older rats was exchanged for that of younger rats which lead to the older rats having a reduced epigenetic age and many improved biomarkers, including reduced inflammation.
The age of the rats’ tissue was assessed by Dr Steve Horvath using 6 separate clocks which covered individual tissue as well as a pan tissue clocks.
An anthropologist dives into the world of genetic engineering to explore whether gene-editing tools such as CRISPR fulfill the hope of redesigning our species for the better.
The Mutant Project: Inside the Global Race to Genetically Modify Humans by Eben Kirksey. St. Martin’s Press, November 2020. Excerpt previously published by Black Inc.
Surreal artwork in the hotel lobby—a gorilla peeking out of a peeled orange, smoking a cigarette; an astronaut riding a cyborg giraffe—was the backdrop for bombshell news rocking the world. In November 2018, Hong Kong’s Le Méridien Cyberport hotel became the epicenter of controversy about Jiankui He, a Chinese researcher who was staying there when a journalist revealed he had created the world’s first “edited” babies. Select experts were gathering in the hotel for the Second International Summit on Human Genome Editing—a meeting that had been called to deliberate about the future of the human species.
Corn hasn’t always been the sweet, juicy delight that we know today. And, without adapting to a rapidly changing climate, it is at risk of losing its place as a food staple. Putting together a plant is a genetic puzzle, with hundreds of genes working together as it grows. Cold Spring Harbor Laboratory (CSHL) Professor David Jackson worked with Associate Professor Jesse Gillis to study genes involved in corn development. Their teams analyzed thousands of individual cells that make up the developing corn ear. They created the first anatomical map that shows where and when important genes turn on and off during key steps in development. This map is an important tool for growing better crops.
Using CRISPR technology, researchers are tracking the lineage of individual cancer cells as they proliferate and metastasize in real-time.
When cancer is confined to one spot in the body, doctors can often treat it with surgery or other therapies. Much of the mortality associated with cancer, however, is due to its tendency to metastasize, sending out seeds of itself that may take root throughout the body. The exact moment of metastasis is fleeting, lost in the millions of divisions that take place in a tumor. “These events are typically impossible to monitor in real time,” says Jonathan Weissman, MIT professor of biology and Whitehead Institute for Biomedical Research member.
Now, researchers led by Weissman, who is also an investigator with the Howard Hughes Medical Institute, have turned a CRISPR tool into a way to do just that. In a paper published on January 212021, in Science, Weissman’s lab, in collaboration with Nir Yosef, a computer scientist at the University of California at Berkeley, and Trever Bivona, a cancer biologist at the University of California at San Francisco, treats cancer cells the way evolutionary biologists might look at species, mapping out an intricately detailed family tree. By examining the branches, they can track the cell’s lineage to find when a single tumor cell went rogue, spreading its progeny to the rest of the body.
Forever we have held a view that AGING, DISEASE & DEATH is an un-alterable eventuality, those who dared question were ostracised for playing God.
If you choose to look deeper you will surely be amazed. Bowhead whales live for over 200 yrs “Turriptosis Dohnri” is a Jellyfish that lives forever. Can these #genetics traits be replicated in humans? Could the removal of #senescence #cells that accelerates aging be the answer Is it even possible to control or reverse aging? Can we grow old healthily? 150000 die every day & over 100000 of them are caused by aging.
Catch Joao Pedro de Magalhaes microbiologist at Centaura & founder at Magellan Science Ltd. share his insights on the science of #humanlongevity #gerontology.
Change Transform INDIA-CHANGE I M POSSIBLE is a podcast & a platform for the brave Disruptors who don’t conform to the convention. subscribe, support & share India’s 1st #futuretech #podcast #agereversal #reverseaging #longevity #immortality #science
Joao Pedro Magalhaes is a Professor at the University of Liverpool in England.
How would the ability to genetically customize children change society? Sci-fi author Eugene Clark explores the future on our horizon in Volume I of the “Genetic Pressure” series.
Fair to say that we all assume that aging is inevitable. In reality however, there is no biological law that says we must age. Over the years we’ve seen a variety of theories proposed to explain why we age including the accumulation of damage to our DNA, the damaging effects of chemicals called “free radicals, changes in the function of our mitochondria, and so many others.
Our guest today, Dr. David Sinclair, believes that aging is related to a breakdown of information. Specifically, he describes how, with time, our epigenome accumulates changes that have powerful downstream effects on the way our DNA functions. Reducing these changes to the epigenome is achievable and in fact, even taking it further, his research now reveals that the epigenome can be reprogrammed back to a youthful state.
David A. Sinclair, PhD, AO is Professor of Genetics at Harvard Medical School, and is the author of Lifespan — Why We Age and Why We Don’t Have To. He is the Founding Director of the Paul F. Glenn Center for the Biological Mechanisms of Aging at Harvard. One of the leading innovators of his generation, he is listed by TIME magazine as one of the “100 most influential people in the world” (2014) and top 50 most important people in healthcare (2018). He is a board member of the American Federation for Aging Research, a Founding Editor of the journal Aging, and has received more than 35 awards for his research on resveratrol, NAD, and reprogramming to reverse aging, which have been widely hailed as major scientific breakthroughs and are topics we discuss in our time together.
In 2018, Dr. Sinclair became an Officer of the Order of Australia, the equivalent of a knighthood, for his work on national security matters and human longevity. Dr. Sinclair and his work have been featured on 60 Minutes, Today, The Wall Street Journal, The New York Times, Fortune, and Newsweek, among others.
In closing, I really need to say that Lifespan (https://amzn.to/3sSoCNS) ranks as one of the most influential books I have ever read. Please enjoy today’s interview.
Whereas cellular senescence is known to promote aging, many of the mechanisms controlling this process remain poorly understood. Using human mesenchymal precursor cells (hMPCs) carrying pathogenic mutations of the premature aging diseases Werner syndrome and Hutchinson-Gilford progeria syndrome, the authors conducted a genome-wide CRISPR-Cas9–based screen to identify genes that could affect cellular senescence. They identified KAT7, a histone acetyltransferase gene, as a driver of senescence. Inactivation of Kat7 in mice aging normally and in prematurely aging progeroid mice extended their life span. Although KAT7 requires further study in other cell types, these experiments highlight the utility of genome-wide CRISPR-Cas9 screens and shed further light on mechanisms controlling senescence.
Understanding the genetic and epigenetic bases of cellular senescence is instrumental in developing interventions to slow aging. We performed genome-wide CRISPR-Cas9–based screens using two types of human mesenchymal precursor cells (hMPCs) exhibiting accelerated senescence. The hMPCs were derived from human embryonic stem cells carrying the pathogenic mutations that cause the accelerated aging diseases Werner syndrome and Hutchinson-Gilford progeria syndrome. Genes whose deficiency alleviated cellular senescence were identified, including KAT7, a histone acetyltransferase, which ranked as a top hit in both progeroid hMPC models. Inactivation of KAT7 decreased histone H3 lysine 14 acetylation, repressed p15INK4b transcription, and alleviated hMPC senescence.
Numerous natural products are awaiting discovery in all kinds of natural habitats. Especially microorganisms such as bacteria or fungi are able to produce diverse natural products with high biomedical application potential in particular as antibiotics and anticancer agents. This includes the so-called red yeast of the species Rhodotorula mucilaginosa, isolated from a deep-sea sediment sample from the Mid-Atlantic Ridge and analyzed for its genome and chemical constituents by researchers from GEOMAR Centre for Marine Biotechnology (GEOMAR-Biotech) of GEOMAR Helmholtz Centre for Ocean Research Kiel and Kiel University (CAU). In a joint effort, the scientists succeeded in demonstrating its anticancer and antibacterial effects. This study, partly-funded by Kiel Marine Science (KMS) of Kiel University, was recently published in the renowned scientific journal Marine Drugs.
A unique opportunity arose for researchers in the Department of Botanical Genetics and Molecular Biology at Kiel University, headed by Professor Frank Kempken. Via the Institute of Geosciences at Kiel University, his group had access to sediment samples from the Mid-Atlantic Ridge in 1600—4000 m depth collected during a research cruise with the German research vessel MARIA S. MERIAN. From one of these sediment cores taken at a depth of 3600 m, Prof. Kempken´s group succeeded in isolating and cultivating living fungi of the species Rhodotorula mucilaginosa. This slowly growing type of yeast, which belongs to the so-called Basidiomycete yeasts should not be confused with the well-known baker’s yeast. The species originally grows at great depth tolerating high hydrostatic pressure and rather cold temperatures.
“With the applied methodology we have succeeded in cultivating yeast colonies that can withstand and grow at room temperatures and under atmospheric pressure. These experiments have shown once more that microorganisms with specific physiological properties thrive in distinct ecological niches. The experiments have shown us further that special ecological niches can produce microorganisms with special characteristics. The assumption about the adaptability of this special genus has therefore encouraged us to further analyze this species,” says Kempken, whose research group has been analyzing genomes of marine fungi for more than ten years.
