Think of DNA and chances are the double helix structure comes to mind, but that’s only one piece of the puzzle. Another major part is mitochondrial DNA, and in plants that’s even more important – and so complex that scientists haven’t yet been able to edit the genes in there. Now a team of Japanese researchers has managed to do just that, which could help improve the genetic diversity of crops.
Renowned longevity researcher David Sinclair believes aging is not inevitable but a treatable condition. In his talk at Science Unlimited 2019, he explained why we age – and how we can reverse aging to extend human healthspan and lifespan.
David Sinclair is Professor in the Department of Genetics, Blavatnik Institute and co-Director of the Paul F. Glenn Center for the Biological Mechanisms of Aging at Harvard Medical School. Science Unlimited is held in Montreux, Switzerland, as part of the annual Frontiers Forum. See all speakers: https://forum.frontiersin.org
A new method enables researchers to test algorithms for spotting genes that contribute to a complex trait or condition, such as autism.
Researchers often study the genetics of complex traits using genome-wide association studies (GWAS). In these studies, scientists compare the genomes of people who have a condition with those of people without the condition, looking for genetic variants likely to contribute to the condition. These studies often require tens of thousands of people to yield statistically significant results.
GWAS have identified more than 100 genomic regions associated with schizophrenia, for example, and 12 linked to autism. Results are often difficult to interpret, however. Causal variants for a condition may be inherited with nearby sections of DNA that do not play a role.
David Sinclair PhD is a biologist and Professor of Genetics at Harvard Medical School, co-director of the Paul F. Glenn Center for the Biological Mechanisms of Aging and author of the forthcoming book “Lifespan: The Revolutionary Science of Why We Age — and Why We Don’t Have To”.
This conversation is about the science behind aging and David’s research on the biology of lifespan extension, treating diseases of aging and extending human lifespan.
When I was kid I used to watch the Incredible Hulk on TV and wait for Bruce Banner to fly into a rage, his muscles inflating like balloons, pants torn to shreds while his entire body turns green as he transforms into the Hulk. As I grew up, and learned more about the advances in genetics, it never occurred to me that cutting-edge genome-editing techniques could explain the scientific principles behind the Hulk’s metamorphosis or his fellow Marvel Comics star-spangled hero Captain America. In a recent Stanford Report story, Sebastian Alvarado Opens in a new window, a postdoctoral research fellow in biology, creatively applies the concepts of epigenetics to illuminate the process by which average Joes become superheroes.
As Alvarado notes in the piece Opens in a new window and above video, over the past 70 years scientists have developed tools for selectively activating and deactivating individual genes through chemical reactions, a process termed epigenetics. Similar to flipping on a light, switch gene expression can be “turned on” or “turned off. ”We have a lot of genome-editing tools – like zinc finger nucleases, or CRISPR/Cas9 systems – that could theoretically allow you to epigenetically seek out and turn on genes that make your muscles physically large, make you strategically minded, incredibly fast, or increase your stamina,” he said.
Different African killifish species vary extensively in their lifespans—from just a few months to several years. Scientists from the Max Planck Institute for Biology of Ageing in Cologne investigated how different lifespans have evolved in nature and discovered a fundamental mechanism by which detrimental mutations accumulate in the genome causing fish to age fast and become short-lived. In humans, mutations accumulate mainly in the genes that are active in old age.
The emerging field of synthetic biology—designing new biological components and systems—is revolutionizing medicine. Through the genetic programming of living cells, researchers are creating engineered systems that intelligently sense and respond to diverse environments, leading to more specific and effective solutions in comparison to current molecular-based therapeutics.
At the same time, cancer immunotherapy—using the body’s immune defenses to fight cancer—has transformed cancer treatment over the past decade, but only a handful of solid tumors have responded, and systemic therapy often results in significant side effects. Designing therapies that can induce a potent, anti–tumor immune response within a solid tumor without triggering systemic toxicity has posed a significant challenge.
Researchers at Columbia Engineering and Columbia University Irving Medical Center (CUIMC) announced today that they are addressing this challenge by engineering a strain of non–pathogenic bacteria that can colonize solid tumors in mice and safely deliver potent immunotherapies, acting as a Trojan Horse that treats tumors from within. The therapy led not only to complete tumor regression in a mouse model of lymphoma, but also significant control of distant, uninjected tumor lesions. Their findings are published today in Nature Medicine.
