Lifeboat Foundation

Designer babies are on the horizon after an influential group of scientists concluded that it could be ‘morally permissible’ to genetically engineer human embryos.

In a new report which opens the door to a change in the law, the Nuffield Council on Bioethics, said that DNA editing could become an option for parents wanting to ‘influence the genetic characteristics of their child.’

Although it would be largely used to cure devastating genetic illnesses, or predispositions to cancers and dementia, the experts said they were not ruling out cosmetic uses such as making tweaks to increase height or changing eye or hair colour, if it would make a child more successful.

Continue reading “Designer babies on horizon as ethics council gives green light to genetically edited embryos” »

Australian researchers have made a discovery about telomeres that may have implications for aging, heart disease, cancer, and other age-related diseases.

So, what are telomeres?

Each of the chromosomes that store our genetic information has a telomere at each end. This protective cap consists of a specific DNA sequence that is repeated thousands of times and has two purposes: firstly, it protects the coding regions of the chromosomes and prevents them from being damaged, and secondly, it acts as a clock that controls the number of replications a cell can undergo; this is thought to act as a quality control system to ensure that aged and potentially damaged cells do not remain in circulation.

I’m excited to share I’ll be speaking/debating at the upcoming #Biohack the Planet 2018 conference in Oakland on Aug 31 & Sept 1. Many interesting biohackers will be there. Tickets are still available and very reasonably priced right now, but they will likely sell out. Hope to see you there! Here’s the speaker list: http://biohacktheplanet.com/2018-speakers/ #transhumanism #biohacker & ticket page: https://www.eventbrite.com/e/biohack-the-planet-2018-ticket…

Bryan Johnson is the founder and CEO of Kernel, OS Fund and Braintree.

In 2016, Bryan invested $100M in Kernel to build advanced neural interfaces to treat disease and dysfunction, illuminate the mechanisms of intelligence, and extend cognition. Kernel is on a mission to dramatically increase our quality of life as healthy lifespans extend. He believes that the future of humanity will be defined by the combination of human and artificial intelligence (HI +AI). In 2014, Bryan invested $100M to start OS Fund which invests in entrepreneurs commercializing breakthrough discoveries in genomics, synthetic biology, artificial intelligence, precision automation, and new materials development. Bryan founded Braintree in 2007, later acquiring Venmo, which he sold to Ebay in 2013 for $800M. He is an outdoor-adventure enthusiast, pilot, and author of a children’s book, Code 7.

Continue reading “2018 Speakers” »

BIRMINGHAM, Ala. — Wrinkled skin and hair loss are hallmarks of aging. What if they could be reversed?

Keshav Singh, Ph.D., and colleagues have done just that, in a mouse model developed at the University of Alabama at Birmingham. When a mutation leading to mitochondrial dysfunction is induced, the mouse develops wrinkled skin and extensive, visible hair loss in a matter of weeks. When the mitochondrial function is restored by turning off the gene responsible for mitochondrial dysfunction, the mouse returns to smooth skin and thick fur, indistinguishable from a healthy mouse of the same age.

“To our knowledge, this observation is unprecedented,” said Singh, a professor of genetics in the UAB School of Medicine.

Some viruses sacrifice themselves so that others may multiply.

THAT predators often hunt in packs is a commonplace. Wolves do it. Killer whales do it. Even Velociraptor, a species of dinosaur made famous by “Jurassic Park”, is believed to have done it. These are, or were, all intelligent species, capable of exchanging and interpreting information. But the logic of pack hunting, that many may achieve what one alone cannot, and that individual pack members may perform different roles, does not depend on intelligence. Indeed, evidence has now emerged that this logic applies to viruses, the simplest biological entities of all. It was published this week in Cell, by Edze Westra and Stineke van Houte at the University of Exeter, in England.

The viruses in question are bacteriophages, which “hunt” bacteria. They do not eat their prey. Rather, they take over its genetic apparatus to create replicas of themselves, killing the host as a consequence. To do so they have to penetrate a bacterium’s cell wall and then subvert its internal defences, of which there are several. One of the best known, because it is the basis of an emerging gene-editing technology (see article), is called CRISPR. The CRISPR system detects and cuts up alien DNA. In the wild, such DNA will almost always have come from a virus. To counter this, some bacteriophages have evolved ways of gumming up CRISPR’s cellular machinery. Dr Westra and Dr van Houte have shown that, in essence, such phages collaborate. Some do the gumming. Others hijack the genetic apparatus.

Continue reading “Viruses that attack bacteria have evolved to collaborate” »

When CRISPR-Cas9 is used to edit genomes, off-target DNA damage is more common than previously thought.

A GREAT deal rides on the accuracy of the gene-editing tool known as CRISPR-Cas9. Since its discovery in 2012 it has become popular for tinkering with genomes of all kinds, thanks to its ability to make editing cheap and easy. Firms such as CRISPR Therapeutics, Intellia Therapeutics and Editas Medicine have been built on the idea that it could be used to develop treatments for human diseases. Editas, based in Cambridge, Massachusetts, announced this year that it would work on five new human medicines over the next five years.

In China the technology is already in clinical use. In Hangzhou Cancer Hospital, for example, CRISPR-Cas9 is being employed to engineer immune-system cells removed from patients with cancer of the oesophagus. The hope is that when the engineered cells are returned to a patient’s body, the editing will have improved their ability to attack tumours. More studies involving human beings are expected in other countries for the treatment of beta-thalassaemia, a blood disorder, and Leber’s congenital amaurosis, a form of blindness. Further ahead, there is hope that CRISPR-Cas9 will help treat diseases such as AIDS, cystic fibrosis, Huntington’s chorea and Duchenne muscular dystrophy.

Continue reading “The safety of CRISPR-Cas9 gene editing is being debated” »

Scientists like Dan Carlson are in high demand, thanks to recently discovered tools that enable them to tweak the DNA of all kinds of organisms.

Mitochondrial dysfunction is associated with many mitochondrial diseases, most of which are the result of dysfunctional mitochondrial oxidative phosphorylation (OXPHOS). Mitochondrial OXPHOS accounts for the generation of most of the cellular adenosine triphosphate (ATP) in a cell. The OXPHOS function largely depends on the coordinated expression of the proteins encoded by both nuclear and mitochondrial genomes. The human mitochondrial genome encodes for 13 polypeptides of the OXPHOS, and the nuclear genome encodes the remaining more than 85 polypeptides required for the assembly of OXPHOS system. Mitochondrial DNA (mtDNA) depletion impairs OXPHOS that leads to mtDNA depletion syndromes (MDSs)^{1, 2}. The MDSs are a heterogeneous group of disorders, characterized by low mtDNA levels in specific tissues. In different target organs, mtDNA depletion leads to specific pathological changes. MDS results from the genetic defects in the nuclear-encoded genes that participate in mtDNA replication, and mitochondrial nucleotide metabolism and nucleotide salvage pathway^{1, 4,5,6,7,8,9,10}. mtDNA depletion is also implicated in other human diseases such as mitochondrial diseases, cardiovascular^{11, 12}, diabetes^13,14,15, age-associated neurological disorders^16,17,18, and cancer^{19,20,21,22,23,24,25}.

A general decline in mitochondrial function has been extensively reported during aging^{26,27,28,29,30,31,32,33}. Furthermore, mitochondrial dysfunction is known to be a driving force underlying age-related human diseases^{16,17,18, 34,35,36}. A mouse that carries elevated mtDNA mutation is also shown to present signs of premature aging^{37, 38}. In addition to mutations in mtDNA, studies also suggest a decrease in mtDNA content and mitochondrial number with age^{27, 29, 32, 33, 39}. Notably, there is an age-related mtDNA depletion in a number of tissues^40,41,42. mtDNA depletion is also frequently observed among women with premature ovarian aging⁴³. Low mtDNA copy number is linked to frailty and, for a multiethnic population, is a predictor of all-cause mortality⁴⁴. A recent study revealed that humans on an average lose about four copies of mtDNA every ten years. This study also identified an association of decrease in mtDNA copy number with age-related physiological parameters³⁹.

To help define the role of mtDNA depletion in aging and various diseases, we created an inducible mouse expressing, in the polymerase domain of POLG1, a dominant-negative (DN) mutation that induces depletion of mtDNA in the whole animal. Interestingly, skin wrinkles and visual hair loss were among the earliest and most predominant phenotypic changes observed in these mice. In the present study, we demonstrate that mtDNA depletion-induced phenotypic changes can be reversed by restoration of mitochondrial function upon repletion of mtDNA.

https://paper.li/e-1437691924#/

In a newly released report, an influential UK ethics council concludes that editing human embryos is “morally permissible.”