Technology
Ancient viral DNA helps human embryos develop
This episode explores groundbreaking research revealing how ancient viral DNA plays a crucial role in human embryo development and evolution. The findings suggest that these embedded viral sequences, ...
Ancient viral DNA helps human embryos develop
Technology •
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Hey, I'm a good dude. I fell for the first time working sphere,
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and I'm a head study volunteer, a difficult beginner for taking middle school,
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who is the ambassador of the high school who is interested in Maser Treshnon's job.
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I obviously have a very small job of financing for as part of a job.
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So today I'm developing a cultured business.
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At hard times, all my friends are studying It�� survival for 50 years.
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Sometimes you start dale 맛Con, while telling them I have a good house in sure around it.
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Like a knight.
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Each G师 were 1...
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..as well added.
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Welcome to the 900th edition of The Nature Podcast. This time, how viral DNA seems central
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to human development. And a DNA-based computer that's powered by heat. I'm Nick Poucher-Chau.
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And I'm Shamini Bundel.
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This week, a study shows evidence that an ancient viral infection appears to be playing an
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important role in human embryo development, and perhaps even a human evolution.
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Reporter Benjamin Thompson is here with more.
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When we think about our genome, we think of something that's uniquely us, human through
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and through. But in reality, a large portion of the human genome is made of DNA that originated
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elsewhere. Take retroviruses. These viruses infected our distant ancestors by slipping
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in their genetic material. And in some cases, it stuck around and was passed down through
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the generations. In fact, these endogenous retroviruses, as they're known, make up about
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8% of our genome. And if that sounds alarming, worry not, because these sequences have changed
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a fair bit over time, as Raquel Fueyau from Stanford University in the US explains.
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Because there's been many years, they acquire a lot of mutations, so they are not able
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to function as regular viruses. And very interestingly, they form part of regulatory parts of
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our genome. Yes, you heard that right. These viruses now seem to have a function in our
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genomes. But how are ancient, embedded viral DNA sequences regulating the activity of human
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genes? Well, because these viral genomes contain short DNA sequences that originally acted
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either as on-off switches or as volume controls, controlling the activity of viral genes,
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back when they started out. But over countless generations, some of them have been co-opted
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to be used to control the activity of human genes. These short sequences are dotted all
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over the human genome and can play important roles. Evidence from other species suggests
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that these viral sequences are important in embryo development, but not a huge amount
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was understood about the role they play in humans. That's where a new paper by Raquel and
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her colleagues comes in. They have used CRISPR to selectively alter the activity of specific
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viral associated sequences to see what their function is. Their work reveals that these
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genome insertions are vital for embryo development and might have played a role in making us, us.
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Now, studying human embryo development requires many practical and ethical considerations. So,
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in this case, the team-made use of structures called blastoids that are derived from a type
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of stem cell. These stem cell-derived blastoids don't develop into embryos, but they mimic
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the ball of cells that forms around day five of development. And they allow researchers
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to investigate the human specific processes going on shortly after fertilization.
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In this case, the team silenced the activity of a specific type of viral sequence inserted
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into the human genome called an LTR-5HS. There are hundreds of these, but using CRISPR
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techniques Raquel managed to target 90% of them in one go. What we saw is that when we repressed
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these insertions, the blastoids can't form at all, but not only that, we see that it's
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actually those dependent. If we silence more, we see less blastoid formation. If we silence less,
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they still have some capacity of forming blastoids, even though they are not normal. So, this
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gave us a hint that they may be essential for blastoid formation and of course, potentially
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for human embryogenesis. Similar to what had been seen in non-human work, the team show that
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these sequences are involved in controlling levels of gene expression. The team then deleted
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a handful of these LTR-5HS's one at a time to see what effect they were having on specific
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genes. Deleting one led to a fairly drastic outcome. Just by deleting this LTR, we saw that
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the cells started growing very, very slow and we said, okay, this is very interesting. What is
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this gene doing? It turns out that this specific LTR-5HS in this location was essential for the
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expression of a gene called zinc finger 729. A gene that is in evolutionary terms, quite young.
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This zinc finger 729 is a primate specific gene. So, you can see it in Macaxe a little bit,
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but it's not present before that. The zinc finger 729 gene encodes a protein that switches on
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a bunch of other genes, involved in basic cellular functions, things like metabolism and cell
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proliferation. So, important stuff. But usually, vital functions like these are evolutionarily
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ancient, so they are controlled by evolutionarily ancient mechanisms. To have them under the control
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of a young gene doesn't make sense at first glance. And things get even weirder. The original viral
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LTR-5HS sequence required for this zinc finger protein to be produced is an even more recent addition
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to our genome. So, this one LTR-5HS that had the phenotype that regulates the zinc finger 729
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is only present in humans. So, here we have this curious situation where critical cellular processes
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needed for early human embryo development are under the control of a relatively young gene
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only found in some primates, which is only switched on at high levels in humans thanks to a virus
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that left its mark on a specific place in our genomes, but not those of our closest ape cousins.
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Exactly how and when this system came to be is a puzzle, but Rekellen the team think that it might
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have endured because it gave cells in a developing embryo an advantage. It turns out that the zinc
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finger 729 protein is really good at binding to DNA and switching genes on. With its production
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turbocharged by the LTR-5HS sequence it may have been that this protein quickly outnumbered the
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original switches controlling the essential genes resulting in higher gene activity and maybe
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more rapid cell growth and division. It's also relevant that this zinc finger protein regulates
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cell proliferation genes. So, we also speculate that the cells that acquire these LTR-5HS
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elements could cycle faster maybe out competing the cells that didn't have the LTR-5HS in the
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embryo. They may have had like a competitive advantage. Rekellen says that while the essential
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processes involved in early embryogenesis are similar across mammalian species, the pattern
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of endogenous retrovirus sequences isn't. It could be that these patterns are driving species
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specific differences and those could help sculpt what our species is. She hopes these findings could
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help give new insights into early human embryo development and the issues that can arise during
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this time. Vincent Pask from KU-Lurven in Belgium works on the early development of human embryos.
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He's written a news and views article about the research and also stresses the need to understand
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this developmental stage as a first step that could ultimately result in clinical interventions
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for when embryos develop incorrectly. A lot of what we know about this process comes from animal
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studies but if we want to start to try to understand what is specific to humans then we must
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rely on experiments in humans and this paper really uses these stem cell based models blastoids
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to gain insight into human specific features of development. So that's what I really like about
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this study is that it really tells us something about what is specific to humans. Vincent says that
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experiments like these wouldn't have been possible were it not for the development of blastoid
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technology in the last few years but notes that it's important to remember that these stem cell
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based blastoids are analogues not the real thing. So one of the main in imitation of the paper is
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that the work is not done in human embryos. We still don't know if these human specific elements
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and ape specific genes are essential for the development of the embryo itself. So it will still
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be needed to validate these findings in embryos. These experiments are much harder to do but they will
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have to be done. Raquel readily agrees that there may be differences between their model system
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and human embryos but she says their work does offer further insights into our early developments
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and the role that indulgenous retroviruses. These echoes of ancient infections lodged in our genome
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play in making us who we are. How many human specific or ape specific function
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there may be regulating is an open question that actually now I will continue investigating because
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we have many more indulgenous retroviruses for me and many more insertions that are active.
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So I think we just like open a box and you know now we have the functional tools to ask these
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questions. That was Raquel Fueyau from Stanford University in the US. You also heard from Vincent
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Pask from KU-Leaven in Belgium. To read Raquel's paper and Vincent's news and views article look
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out for links in the show notes. Coming up researchers have been building DNA computers
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and now they found a way to power them using heat. Right now though it's time for the research
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highlights with Dan Fox. Longer whale mothers are more likely to produce female offspring compared
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to shorter mums according to new research. For species whose males compete for access to females
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scientists disagree about whether mothers with ample resources would benefit more from producing a
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sun who would have a better chance when competing against other males or a daughter who could give
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birth. To investigate whether whales manipulate the sex ratios of their offspring research has
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analysed archival wailing data describing over 200,000 whale fetuses from seven different species of whale.
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The team found that in the seven species they looked at, longer mothers who have more stored fat
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to power the demanding task of carrying and looking after young tended to produce more female offspring.
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This pattern could slow these species recovery from wailing because whalers tend to target larger
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animals if the surviving shorter females give birth to more males there will be fewer females available
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for reproduction. Read that research in full in the proceedings of the Royal Society B.
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Corpse flowers are mammoth plants that bloom about once every decade and when they do flower produce
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a stench like rotting meat perfect for attracting carry in loving pollinators. Now researchers have found
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that this stinkingness peaks on the first night of their spectacular blooms. Research has studied
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the chemicals that wafted off a corpse flower named Cosmo when it bloomed in May 2024. The emissions
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included a range of organic sulfur compounds. The sulfur emission rates rivaled those of landfills
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and wax and wained throughout the night. Most of the emissions came during the first night of the
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day can depart the following night. The male flowers which bloom on the second night
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emit a sweeter mild ascent. Knowing how and why corpse flowers produce their stink can help researchers
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to better preserve these rare plants. Don't kick up a stink trying to find that research.
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It's published in geophysical research letters.
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Let's face it, computers are pretty central to our lives. I sent my spend most of my life looking
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at one screen or another. And for good reason, they allow us to do all sorts of things that would
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have been near impossible decades ago. Podcasts probably would have been a hard sell in 1970.
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Don't come at me radio nerds. But what if computers could be much much smaller or maybe even
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integrated into our own bodies? Imagine medicine that self-diagnose complex diseases
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and release just the right therapeutics. This is Lulujin, a researcher working on computers made
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from DNA. Now, while self-diagnosing medicine is a long way off, different teams have been working
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on using DNA as a computer for a while. Because this is exactly the kind of application it promises
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in the long term. Rather than a competitor for regular computers, these molecular machines
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could be useful for doing complex calculations at the nanoscale. The way they work is instead
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of having physical switches that represent ones and zeros, like a regular computer, DNA strands
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with different sequences and of different concentrations, can represent those classic computing bits.
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Here single stranded bits of DNA would be inputs, which would then hybridize as the computations
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occur and then the outputs would be different strands of DNA. And because DNA is tiny and well
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home inside cells, all this processing could happen inside your body or on the surfaces of devices.
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But before we get there, there's something else researchers need to resolve.
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Like all machines, these molecular machines need a source of power. So how can such small systems
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keep going, responding again and again to their surroundings without just quickly running out of
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energy? This is a problem that researchers have been working on. Such DNA computers can be run
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on chemical energy or powered using enzymes. But these methods only work until that energy supply
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runs out and can lead to the build-up of waste products that interfere with the computations.
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They're also hard to scale up, as each different kind of computation requires a different
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chemical environment to function properly. We wondered could there be a universal power source
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for artificial molecular machines, something as reliable as, say, ATP in living cells or electricity
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in our everyday devices? And the perhaps surprising answer we found is heat.
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In a paper in this week's nature, Lulu and her team describe how to use heat to power DNA
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circuits. This method relies on two previous discoveries. The first is that DNA can be trapped
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in a state where it's primed ready to start reactions and perform computations, but can't until
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it's released. So imagine two DNA strands that are meant to bind together. But one of them is
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being held back by a surge strand that slows the reaction down. It's like a spring pressed
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down and held in place. The energy is there waiting. Now by adding a catalyst strand that releases
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the block, the spring is suddenly like a, and then the DNA strands pair quickly. It's like
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unleashing the stored energy to drive the system forward. The second discovery is that heat could
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potentially reset this process back to its original state. So when you heat up a test tube of DNA
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and then cool it down, the molecules don't always settle into their most favorable arrangement.
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Instead, especially when they have strong folded structures, the heating and cooling can actually
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reset them back to the spring loaded states, ready to release energy again. Getting this to actually
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work is quite tricky though. As each of the different strands of DNA, the inputs, the strands
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they interact with, and the outputs all have to work together in concert to perform their computations
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and reset without interfering with each other. So Lulu had to become a bit of a chemical conductor.
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We had to develop design rules so that different types of molecules could reset at different
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temperatures in the same heat-cool cycle without interfering with each other. This is a bit of
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like an orchestra tuning up. The violins, cellos and trumpets, they all need to land on the right
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notes without clashing, right? So the performance can be getting in harmony. This involved a
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mixture of DNA editing and clever chemistry, but eventually the team were able to make groups
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of different DNA molecules that perform different functions. For example, some of the DNA molecules
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were able to amplify signals or annihilate them, altogether this soup of DNA could perform computations.
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To put it through its paces, the team decided to create a neural network, a computing system
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inspired by neurons, to classify handwritten numbers, sixes and sevens. We showed that the DNA
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based in your network can indeed make the correct output classification decision and repeat that.
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The more important thing here is repeating that decision when the input patterns changes. For
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example, it changes from a six to a seven. So the system has to recompute and make the right
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decision again, right? So we showed that it was able to do that for 10 rounds and the performance
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was essentially the same. The first round and the tenth round we could not really identify any
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job in performance even after that many rounds of computation. DNA based neural networks have been
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demonstrated before, but the key here was that it was repeatable and only powered by heat.
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That, Lulu thinks, could open the door to DNA computing that could recharge whenever needed.
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This is John Reif, a computer scientist who works on DNA machines and wasn't associated with
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this paper. There have been a number of prior published papers on restoring DNA
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computations, including that I published, but I would say that this is the most I believe
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scalable methods so far determined. As this method relies on heat to recharge the DNA
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computations, it could potentially be scaled up. Lulu showed that many hundreds of different
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DNA strands could be mixed together and as long as the chemical orchestra is tuned, they could all
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perform their reactions. In theory, you could do many more. John, though, did point out that this
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heat-based method of DNA computation is not quite as quick as ones that use enzymes.
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When could argue it would be nice to have systems that could execute a little faster,
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but it's beautiful work. This heat-based system also avoids the buildup of waste products,
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and Lulu was able to repeat computations many times. But the world limits.
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So we estimated that if we use this high temperature, then essentially the system would stop working
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at a maximum of a thousand cycles. High temperatures eventually lead the DNA molecules to
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break down, so Lulu and the team are investigating whether they could get this to work at lower temperatures.
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The other problem is that none of this happens automatically. It requires someone there to carefully
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calibrate the temperature over time. In the future, Lulu hopes that they can find a consistent
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cycle of temperatures to powder reactions and allow the computations to repeat.
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But for now, the team has shown that heat can, in principle, power DNA computers.
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Something that Lulu hopes others will build on to help create the DNA-powered future, she imagines.
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What I hope will happen is that other researchers could utilize the principle of recharging and
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extend it from heat to other forms of universal energy sources, such like light, salt, or even
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acid gradients like those across cell membranes. Because in principle, any of these energy sources
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could serve for the same purpose. So this way, molecular machines could be designed to recharge
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themselves using, let's say, one of a few options. Whichever is available and functioning well
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in your changing environment. That's my dream. That was Lulu Chen from the California Institute
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of Technology in the US. You also heard from John Reif from Duke University, also in the US.
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For more on that study, check out the show notes for some links.
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Finally on the show, it's time for the briefing chat where we discuss a couple of articles
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that have been highlighted in the Nature Briefing, which is of course Nature's Daily Roundup
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of Science News. As a Nick, you go first. What have you got for us this time?
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So this week I was reading an article in Nature about some big news. It's a trial that shows
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a way to potentially treat Huntington's disease. Oh right. Well, that sounds pretty important.
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Can you give us a Huntington's disease, sort of recap primer?
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Yeah. So Huntington's disease is a neurological condition that tends to affect people between
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the ages of 35 to 55. That's when it starts its progression. And it progresses over time and
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symptoms become worse and worse. It may start with just some slight motor issues and a bit of
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forgetfulness and then eventually it progresses to confusion and mood swings and eventually death.
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So it's a really terrible condition for the people with effects and their families.
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And this story is about the closest evidence yet that the disease progression can be slowed
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with a one-time gene therapy treatment.
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Right. So is Huntington's well understood in terms of its sort of genetic causes?
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Yeah. So this is a condition that is caused just by a single gene. So this is a gene called Hunting
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ton. And in people with Huntington's it produces a protein that builds up and basically causes all
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of these problems that we've discussed. So it's been a target of gene therapies and things like it
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for a while. There was a lot of interest in something called anti-sense treatment. And this is
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where you put short strands of DNA or RNA to bind with the messenger RNA in the cell to stop the
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proteins that cause all these problems from being made in the first place. But that didn't end up
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panning out in a trial. It ended up performing worse than the placebo after showing some initial
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promise. Oh gosh, okay. Which is now led researchers to instead look to gene therapy.
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And the idea with gene therapy is you insert a bit of DNA into people's cells and then this
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represents a permanent change that can essentially tackle the condition. So in this case they used a
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harmless virus to deliver instructions to cells to make microRNAs, these are tiny little RNAs,
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that then bind to the messenger RNA and they stop this dysfunctional protein being produced
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in the first place. Okay, so it sounds simple enough in a way. And so this was a trial of
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how well this worked? Yeah, so this was a trial of 29 people to see how this works. And what I'll
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say is this isn't a cure. It doesn't stop it altogether. They've shown that it slows the disease
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progression over the course of three years. So compared to the control group, it slowed progression
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by 75%. So this was a small trial of 29 people performed by a company called UniQ,
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that's sput with a Q, by the way, which a gene therapy company based in Amsterdam. And so they've
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released a press release that has given the details of this trial, but this has not been peer-reviewed
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yet. There's not a full study as of yet. And obviously as only a few participants, but the
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researchers interviewed in this article think that this is a big step forward. So far as I've said,
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there is no treatment for Huntington. So if this is effective and is able to slow disease
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progression, then that could be really impactful for the people that Huntington's affects. And also
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based on the strength of this data, the company are looking to get regulatory approval next year.
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So this could be something that has an impact quite soon. And because this was a short term trial,
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that's not necessarily to say that it can't work to slow the disease over a longer time,
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or that further changes couldn't have bigger or more long-lasting effects.
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Yeah, there's a lot more to be understood about how exactly this works. And at what points it's best
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to do this. So this was done in people with early signs of Huntington's. And so you could imagine
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that you could try at different points to see how it would affect the disease progression. And as I
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say, it's not a cure either. Like the disease is still progressing just much slower. The issues
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for this, I would say, is this is quite an intense procedure. So I've simplified it somewhat by
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saying you put the DNA of iris, just whack it in there. So this is probably going to set it up.
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But it's actually, it's true that most people tolerated the therapy itself. There weren't the
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major concerns that have plagued gene therapy for other conditions. But you had to undergo
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surgery to do this. So they had to drill holes in the skull and insert a cannula to then, you know,
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direct the treatment to the parts of the brain that were most effective. And some people had headaches,
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pain, and other complications from the surgery, but not from the gene therapy itself. And because
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of this too, this means that this treatment is very expensive. So according to this article,
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it would cost upwards of a million US dollars per person. So that would make it probably out
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of reach for a lot of people and for many health services. But this is a start. Perhaps in the future
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that could change as, you know, more research is done. And there are different to try and give
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people this treatment. Well, that does sound promising at least for future Huntington's treatment.
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Thanks Nick. I actually also have a story about DNA. It's the thing of the week. We've accidentally
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had a really DNA heavy week. It's just these DNA scientists out there publishing their important
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DNA work that we really wanted to cover. But mine is about mitochondrial DNA. So I've been reading
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this article in nature about in each paper about how, or why exactly mitochondria do this thing,
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where they sometimes kick some of their DNA out out of them and into the cell that they're in.
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So we have mitochondria in all our cells. They're there being the powerhouse of the cell,
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as the saying goes. But yeah, it's been known for some time that there's this phenomenon where
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mitochondrial will just sort of eject some DNA from inside them. This is then mitochondrial DNA
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into the cell. And that can kick off inflammatory pathways associated with aging, which we don't love.
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Although, you know, this is an immune response. So it is supposed to be defending against pathogens.
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But, you know, we know that there's this chronic inflammation issue. And these researchers wanted
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to figure out kind of why the mitochondria were doing this and sort of figure out a little bit more
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about exactly what's going on there. Yeah, I mean, it's a good question because not only is this
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a weird thing that they seem to be doing, but also it seems to be bad for us. So understanding that
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that seems like a good step to me. Well, it's not bad for the mitochondria. So the mitochondria
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getting rid of sort of damaged or problematic DNA, but, you know, they want out. And, you know,
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this might be caused by certain drugs and the mitochondria being stressed. And it seems to happen
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in aging cells. So, you know, maybe this happens naturally during aging. And it's just one of these
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things. But these researchers had a mouse model that they basically used to kind of look into
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exactly what was going on here. And it's a mouse model of these genetically engineered mice
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that lack a certain enzyme. Right? This enzyme is the catchably named MGME1. And this enzyme actually
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is important for the mitochondria because it helps them make accurate copies of their genome.
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So you can already see the link here. But what is also known is that mice without these enzyme
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as they age, their kidneys become inflamed. So they're actually really useful models for inflammation.
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But looking into exactly what was going on, the researchers found that these enzyme lacking mice
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had loads of these loose DNA fragments than the kidney cells. And they saw that these loose pieces
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of DNA fragments bound to and turned on an enzyme that's a known contributor to inflammation
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in age tissues. So you can see that sort of connection there. But they also then looking closer,
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found out kind of what was wrong with these DNA fragments. Like why is it? Yeah, exactly.
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And basically the cells were lacking in the building blocks of DNA. So deoxyribonucleotides,
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you sort of get a sequence of them, put them together and then you make DNA. So obviously if you're
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replicating your genome, you need the building blocks in order to make another copy of the DNA.
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But because they were lacking these certain building blocks, they instead were using RNA building
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blocks. Oh, right. RNA ribonucleotides, incorporating that, it still works, but it's not as good.
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It sort of hinders future DNA replication. And it could be that this is why the mitochondria are
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basically getting rid of this DNA because it has way too many of the wrong stuff in essentially.
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And so now they figured out sort of why this happens. Do they think there's a way to prevent it or
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reverse it? Well, so one thing says that they were looking in a mouse model that was engineered to
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lack a certain enzyme on the last half, more kidney inflammation, right? So we don't know for
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sure is this relevant to normal physiology? Right. And also is this normal, I'll say in quotation
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marks, is this a natural part of aging or is there sort of specific conditions that then trigger
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this whole sequence that then is contributing to aging and inflammation or as it's sometimes called
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inflammation, which is apparently the chronic inflammation that occurs as people get older.
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Portmanteau there. But no, this is still, it's a cliche, but there's a lot to still figure out
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what's going on here. So for example, they don't really fully understand yet exactly how this
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discarded mitochondrial DNA then contributes to cellular aging and inflammation. So it looks
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like there's a lot of potential targets for if we wanted to try and slow down aging and prevent
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inflammation in the future. This study, you know, provides a lot more steps that we could look at and
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maybe potentially try to target. But yes, I think we're a bit of a way away from that at the moment.
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No, well fascinating stuff, Sharma. I always love hearing about mitochondria. It seems to be one of
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staples of the podcast as is DNA apparently. It is now DNA. All the DNA all the time. DNA
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podcast now. DNA podcast now. But I think that's all we've got time for on the briefing chat. This
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week, if you've enjoyed those stories and you want to get more like them, you can sign up to
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nature briefing to get more of them sent to your inbox and you can check out the show notes for
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some links to do that. And as always, you can reach out to us. You can say hi to us. Send us a
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message or an ex or a blue sky. We're at nature podcast is our handle there or you can just send us
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an email podcast at nature.com. I'm Sharma Bandele. And I'm Nick Patrick. How? Thanks a listening.
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