Origin of Information —“Something Very Old, Very Powerful and Very Special has Been Unleashed on Earth” | The Daily Galaxy.
“Humans are strange…We are the aliens,” observes Columbia University astrophysicist, Caleb Scharf, noting that humans are a striking anomaly in the natural world. “We also have a truly outsize impact on the planetary environment without much in the way of natural attrition to trim our influence (at least not yet).
Like a Sudden Invasion by Extraterrestrials
But the strangest thing of all, notes Scharf for Scientific American, is how we generate, exploit, and propagate information that is not encoded in our heritable genetic material, yet travels with us through time and space. Not only is much of that information represented in purely symbolic forms—alphabets, languages, binary codes—it is also represented in each brick, alloy, machine, and structure we build from the materials around us. Even the symbolic stuff is housed in some material form or the other, whether as ink on pages or electrical charges in nanoscale pieces of silicon.
Wines and table grapes exist thanks to a genetic exchange so rare that it’s only happened twice in nature in the last 6 million years. And since the domestication of the grapevine 8000 years ago, breeding has continued to be a gamble.
When today’s growers cultivate new varieties – trying to produce better-tasting and more disease-resistant grapes – it takes two to four years for breeders to learn whether they have the genetic ingredients for the perfect flower.
Females set fruit, but produce sterile pollen. Males have stamens for pollen, but lack fruit. The perfect flower, however, carries both sex genes and can self-pollinate. These hermaphroditic varieties generally yield bigger and better-tasting berry clusters, and they’re the ones researchers use for additional cross-breeding.
DNA was personified in Jurassic Park, where the animated double helix that called himself Mr. DNA took you and a group of skeptical scientists through the oversimplified (and obviously fictional) steps to creating dino DNA — but there is some reality in this.
For all you dinosaur enthusiasts out there, synthesizing DNA can’t bring T.Rex and Brachiosaurus back from extinction. Though creating genes in a lab sounds like the original eureka moment of Jurassic Park, synthesizing human DNA has done everything from genetic sequencing and editing to detecting diseases like the current plague we are living through. There is just one step that has always been problematic.
To answer this question, an internal team of scientists, consisting of researchers affiliated with the Buck Institute for Research on Ageing, and researchers from Nanjing University decided to modify both the Insulin and the rapamycin pathways of a group of C.elegans worms, expecting to see a cumulative result of a 130% increase in lifespan. However, instead of seeing a cumulative effect in lifespan, the worms lived five times longer than they normally would.
“The synergistic extension is really wild. The effect isn’t one plus one equals two, it’s one plus one equals five. Our findings demonstrate that nothing in nature exists in a vacuum; in order to develop the most effective anti-aging treatments we have to look at longevity networks rather than individual pathways.” – Jarad Rollins of Nanjing University.
What could this mean for human regenerative medicine? Humans are not worms, however on a cellular level they do possess very similar biology. Both the insulin pathway and the rapamycin pathway are what is known as ‘conserved’ between humans and C.elegans, meaning that these pathways have been maintained in both organisms. In the distant past, both humans and C.elegans had a common ancestor, in exactly the same way as humans and Chimpanzees have a common ancestor. Evolution has changed our bodies significantly over the millions of years that humans and C.elegans have diverged from one another, but a lot of our fundamental biological functions remain largely unchanged.
The secret to longevity is already in the animals around us.
Some species live unexpectedly long lives. By studying how they do it, researchers hope to pinpoint factors affecting human longevity.
By Bob Holmes.
Life, for most of us, ends far too soon — hence the effort by biomedical researchers to find ways to delay the aging process and extend our stay on Earth. But there’s a paradox at the heart of the science of aging: The vast majority of research focuses on fruit flies, nematode worms and laboratory mice, because they’re easy to work with and lots of genetic tools are available. And yet, a major reason that geneticists chose these species in the first place is because they have short lifespans. In effect, we’ve been learning about longevity from organisms that are the least successful at the game.
Most important part comes at 1:49 where Liza talks about gene therapies for people to stop people from aging, reaching homeostasis, or even exceeding it a little bit.
In this video Liz introduces BioViva Science and how the company works with its partners in delivering gene therapies.
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To begin with, why do we use mice in medical and biological research? The answer to this question is fairly straight forward. Mice are cheap, they grow quickly, and the public rarely object to experimentations involving mice. However, mice offer something that is far more important than simple pragmatism, as despite being significantly smaller and externally dissimilar to humans, our two species share an awful lot of similarities. Almost every gene found within mice share functions with genes found within humans, with many genes being essentially identical (with the obvious exception of genetic variation found within all species). This means that anatomically mice are remarkably similar to humans.
Now, this is where for the sake of clarity it would be best to break down biomedical research into two categories. Physiological research and pharmaceutical research, as the success of the mouse model should probably be judges separately depending upon the research that is being carried out. Separating the question of the usefulness of the mouse model down into these two categories also solves the function of more accurately focusing the ire of its critics.
The usefulness of the mouse model in the field of physiological research is largely unquestioned at this point. We have quite literally filled entire textbooks with the information we have gained from studying mice, especially in the field of genetics and pathology. The similarities between humans and mice are so prevalent that it is in fact possible to create functioning human/mouse hybrids, known as ‘genetically engineered mouse models’ or ‘GEMMs’. Essentially, GEMMs are mice that have had the mouse version of a particular gene replaced with its human equivalent. This is an exceptionally powerful tool for medical research, and has led to numerous medical breakthroughs, including most notably our current treatment of acute promyelocytic leukaemia (APL), which was created using GEMMs.
There’s some really interesting CRISPR news out today, and it’s likely to be a forerunner of much more news to come. A research team has demonstrated what looks like robust, long-lasting effects in a primate model after one injection of the CRISPR enzymatic machinery. There have been plenty of rodent reports on various forms of CRISPR, and there are some human trials underway, but these is the first primate numbers that I’m aware of.
The gene they chose to inactivate is PCSK9, which has been a hot topic in drug discovery for some years now. It’s a target validated by several converging lines of evidence from the human population (see the “History” section of that first link). People with overactive PCSK9 have high LDL lipoproteins and cholesterol, and people with mutations that make it inactive have extremely low LDL and seem to be protected from a lot of cardiovascular disease. There are several drugs and drug candidates out there targeting the protein, as well there might be.
It’s a good proof-of-concept, then, because we know exactly what the effects of turning down the expression of active PCSK9 should look like. It’s also got the major advantage of being mostly a liver target – as I’ve mentioned several times on the blog already, many therapies aimed at gene editing or RNA manipulation have a pharmacokinetic complication. The formulations used to get such agents intact into the body (and in a form that they can penetrate cells) tend to get combed out pretty thoroughly by the liver – which after all, is (among other things) in the business of policing the bloodstream for weird, unrecognized stuff that is then targeted for demolition by hepatocytes. Your entire bloodstream goes sluicing through the liver constantly; you’re not going to able to dodge it if your therapy is out there in the circulation. It happens to our small-molecule drugs all the time: hepatic “first pass” metabolism is almost always a factor to reckon with.
Dr. Kate Adamala describes what synthetic cells are and how they can teach us the fundamental principles of life.
Life on Earth evolved once — this means that all biological systems on our planet are rooted in the same fundamental framework. This framework is extremely complex and we have yet to fully understand the processes inside each living cell. One way of understanding complex systems is to break them down into simpler parts. This is the principle of engineering the synthetic cell: to use our current knowledge of biology for building a living cell with the least amount of parts and complexity. Synthetic cells can be used to teach us about the basic principles of life and evolution, and they hold promise for a range of applications including biomaterials and drug development. Dr. Kate Adamala narrates an introduction to this exciting field.
0:00 Introduction. 2:22 How do we build a synthetic cell? 7:12 How can we use synthetic cells?
Speaker Biography: Dr. Kate Adamala is a synthetic biologist and a McKnight Land-Grant Assistant Professor in the Department of Genetics, Cell Biology and Development at the University of Minnesota. Her research interests include astrobiology, synthetic cell engineering and biocomputing. Adamala is a co-founder and steering group member of the international Build-a-Cell Initiative, which seeks to broaden the impact of synthetic cell engineering. Find more information on Adamala’s lab at: http://www.protobiology.org.
Credits: Brittany Anderton (iBiology): Producer. Eric Kornblum (iBiology): Videographer and Editor. Kate Adamala (UMN): Graphics and Narration.
