Podcasts about dna mtdna

* List of Discoveries Squeezing Evolution: Did you know that dinosaurs ate rice before rice evolved? That turtle shells existed forty million years before turtle shells began evolving? That insects evolved tongues for eating from flowers 70 million years before flowers evolved? And that birds appeared before birds evolved? The fossil record is a wonderful thing. And more recently, only a 40,000-year squeeze, Neanderthal had blood types A, B, and O, shocking evolutionists but expected to us here at Real Science Radio! Sit back and get ready to enjoy another instant classic, today's RSR "list show" on Evolution's Big Squeeze! Our other popular list shows include: - scientists doubting Darwin - evidence against whale evolution - problems with 'the river carved the canyon' - carbon 14 everywhere it shouldn't be - dinosaur still-soft biological tissue - solar system formation problems - evidence against the big bang - evidence for the global flood - genomes that just don't fit - and our list of not so old things! (See also rsr.org/sq2 and rsr.org/sq3!) * Evolution's Big Squeeze: Many discoveries squeeze the Darwinian theory's timeframe and of course without a workable timeframe there is no workable theory. Examples, with their alleged (and falsified) old-earth timeframes, include: - Complex skeletons existed 9 million years before they were thought to have evolved, before even the "Cambrian explosion".- Butterflies existed 10 million years before they were thought to have evolved. - Parrots existed "much earlier than had been thought", in fact, 25 million years before they were thought to have evolved. - Cephalopod fossils (squids, cuttlefish, etc.) appear 35 million years before they were able to propagate. - Turtle shells 40 million years before turtle shells began evolving - Trees began evolving 45 million years before they were thought to evolve - Spores appearing 50 million years before the plants that made them (not unlike footprints systematically appearing "millions of years before" the creatures that made them, as affirmed by Dr. Marcus Ross, associate professor of geology). - Sponges existed 60 million years before they were believed to have evolved. - Dinosaurs ate rice before it evolved Example - Insect proboscis (tongue) in moths and butterflies 70 million years before previously believed has them evolving before flowers. - Arthropod brains fully developed with central nervous system running to eyes and appendages just like modern arthropods 90 million years earlier than previously known (prior to 2021, now, allegedly 310mya) - 100 million years ago and already a bird - Fossil pollen pushes back plant evolution 100 million years. - Mammalian hair allegedly 100-million-years-old show that, "the morphology of hair cuticula may have remained unchanged throughout most of mammalian evolution", regarding the overlapping cells that lock the hair shaft into its follicle. - Piranha-like flesh-eating teeth (and bitten prey) found pushing back such fish 125 million years earlier than previously claimed   - Shocking organic molecules in "200 million-years-old leaves" from ginkgoes and conifers show unexpected stasis. - Plant genetic sophistication pushed back 200 million years. - Jellyfish fossils (Medusoid Problematica :) 200 million years earlier than expected; here from 500My ago. - Green seaweed 200 million years earlier than expected, pushed back now to a billion years ago!  - The acanthodii fish had color vision 300 million years ago, but then, and wait, Cheiracanthus fish allegedly 388 million years ago already had color vision. - Color vision (for which there is no Darwinian evolutionary small-step to be had, from monochromatic), existed "300 million years ago" in fish, and these allegedly "120-million-year-old" bird's rod and cone fossils stun researchers :) - 400-million-year-old Murrindalaspis placoderm fish "eye muscle attachment, the eyestalk attachment and openings for the optic nerve, and arteries and veins supplying the eyeball" The paper's author writes, "Of course, we would not expect the preservation of ancient structures made entirely of soft tissues (e.g. rods and cone cells in the retina...)." So, check this next item... :) - And... no vertebrates in the Cambrian? Well, from the journal Nature in 2014, a "Lower-Middle Cambrian... primitive fish displays unambiguous vertebrate features: a notochord, a pair of prominent camera-type eyes, paired nasal sacs, possible cranium and arcualia, W-shaped myomeres, and a post-anal tail" Primitive? - Fast-growing juvenile bone tissue, thought to appear in the Cretaceous, has been pushed back 100 million years: "This pushes the origin of fibrolamellar bone in Sauropterygia back from the Cretaceous to the early Middle Triassic..."- Trilobites "advanced" (not the predicted primitive) digestion "525 million" years ago - And there's this, a "530 million year old" fish, "50 million years before the current estimate of when fish evolved" - Mycobacterium tuberculosis 100,000 yr-old MRCA (most recent common ancestor) now 245 million- Fungus long claimed to originate 500M years ago, now found at allegedly 950 Mya (and still biological "the distant past... may have been much more 'modern' than we thought." :) - A rock contained pollen a billion years before plants evolved, according to a 2007 paper describing "remarkably preserved" fossil spores in the French Alps that had undergone high-grade metamorphism - 2.5 billion year old cyanobacteria fossils (made of organic material found in a stromatolite) appear about "200 million years before the [supposed] Great Oxidation Event". - 2.7 billion year old eukaryotes (cells with a nucleus) existed (allegedly) 1 billion years before expected - 3.5 billion year "cell division evidently identical to that of living filamentous prokaryotes." - And even older cyanobacteria! At 220 million years earlier than thought, per Nature's 3.7 billion year old dating of stromatolites! - The universe and life itself (in 2019 with the universe dated a billion, now, no, wait, two billion!, years younger than previously thought, that's not only squeezing biological but also astronomical evolution, with the overall story getting really tight) - Mantis shrimp, with its rudimentary color but advanced UV vision, is allegedly ancient. - Hadrosaur teeth, all 1400 of them, were "more complex than those of cows, horses, and other well-known modern grazers." Professor stunned by the find! (RSR predicts that, by 2030 just to put an end date on it, more fossils will be found from the geologic column that will be more "advanced" as compared to living organisms, just like this hadrosaur and like the allegedly 100M year old hagfish  fossil having more slime glands than living specimens.)  - Trace fossils "exquisitely preserved" of mobile organisms (motility) dated at 2.1 billion years ago, a full 1.5 billion earlier than previously believed - Various multicellular organisms allegedly 2.1 billion years old, show multicellularity 1.5 billion years sooner than long believed   - Pre-sauropod 26,000-pound dinosaur "shows us that even as far back as 200 million years ago, these animals had already become the largest vertebrates to ever walk the Earth." - The Evo-devo squeeze, i.e., evolutionary developmental biology, as with rsr.org/evo-devo-undermining-darwinism. - Extinct Siberian one-horned rhinos coexisted with mankind. - Whale "evolution" is being crushed in the industry-wide "big squeeze". First, geneticist claims whales evolved from hippos but paleontologists say hippos evolved tens of millions of years too late! And what's worse than that is that fossil finds continue to compress the time available for whale evolution. To not violate its own plot, the Darwinist story doesn't start animals evolving back into the sea until the cast includes land animals suitable to undertake the legendary journey. The recent excavation of whale fossils on an island of the Antarctic Peninsula further compresses the already absurdly fast 10 million years to allegedly evolve from the land back to the sea, down to as little as one million years. BioOne in 2016 reported a fossil that is "among the oldest occurrences of basilosaurids worldwide, indicating a rapid radiation and dispersal of this group since at least the early middle Eocene." By this assessment, various techniques produced various published dates. (See the evidence that falsifies the canonical whale evolution story at rsr.org/whales.) * Ancient Hierarchical Insect Society: "Thanks to some well-preserved remains, researchers now believe arthropod social structures have been around longer than anyone ever imagined. The encased specimens of ants and termites recently studied date back [allegedly] 100 million years." Also from the video about "the bubonic plague", the "disease is well known as a Middle Ages mass killer... Traces of very similar bacteria were found on [an allegedly] 20-million-year-old flea trapped in amber." And regarding "Caribbean lizards... Even though they are [allegedly] 20 million years old, the reptiles inside the golden stones were not found to differ from their contemporary counterparts in any significant way. Scientists attribute the rarity [Ha! A rarity or the rule? Check out rsr.org/stasis.] to stable ecological surroundings." * Squeezing and Rewriting Human History: Some squeezing simply makes aspects of the Darwinian story harder to maintain while other squeezing contradicts fundamental claims. So consider the following discoveries, most of which came from about a 12-month period beginning in 2017 which squeeze (and some even falsify) the Out-of-Africa model: - find two teeth and rewrite human history with allegedly 9.7 million-year-old teeth found in northern Europe (and they're like Lucy, but "three times older") - date blue eyes, when humans first sported them, to as recently as 6,000 years ago   - get mummy DNA and rewrite human history with a thousand years of ancient Egyptian mummy DNA contradicting Out-of-Africa and demonstrating Out-of-Babel - find a few footprints and rewrite human history with allegedly 5.7 million-year-old human footprints in Crete - re-date an old skull and rewrite human history with a very human skull dated at 325,000 years old and redated in the Journal of Physical Anthropology at about 260,000 years old and described in the UK's Independent, "A skull found in China [40 years ago] could re-write our entire understanding of human evolution." - date the oldest language in India, Dravidian, with 80 derivatives spoken by 214 million people, which appeared on the subcontinent only about 4,500 years ago, which means that there is no evidence for human language for nearly 99% of the time that humans were living in Asia. (Ha! See rsr.org/origin-of-language for the correct explanation.) - sequence a baby's genome and rewrite human history with a 6-week old girl buried in Alaska allegedly 11,500 years ago challenging the established history of the New World. (The family buried this baby girl just beneath their home like the practice in ancient Mesopotamia, the Hebrews who sojourned in Egypt, and in Çatalhöyük in southern Turkey, one of the world's most ancient settlements.) - or was that 130,000? years ago as the journal Nature rewrites human history with a wild date for New World site - and find a jawbone and rewrite human history with a modern looking yet allegedly 180,000-year-old jawbone from Israel which "may rewrite the early migration story of our species" by about 100,000 years, per the journal Science - re-date a primate and lose yet another "missing link" between "Lucy" and humans, as Homo naledi sheds a couple million years off its age and drops from supposedly two million years old to (still allegedly) about 250,000 years old, far too "young" to be the allegedly missing link - re-analysis of the "best candidate" for the most recent ancestor to human beings, Australopithecus sediba, turns out to be a juvenile Lucy-like ape, as Science magazine reports work presented at the American Association of Physical Anthropologists 2017 annual meeting - find skulls in Morocco and "rewrite human history" admits the journal Nature, falsifying also the "East Africa" part of the canonical story - and from the You Can't Make This Stuff Up file, NPR reports in April 2019, Ancient Bones And Teeth Found In A Philippine Cave May Rewrite Human History. :) - Meanwhile, whereas every new discovery requires the materialists to rewrite human history, no one has had to rewrite Genesis, not even once. Yet, "We're not claiming that the Bible is a science textbook. Not at all. For the textbooks have to be rewritten all the time!"  - And even this from Science: "humans mastered the art of training and controlling dogs thousands of years earlier than previously thought."- RSR's Enyart commented on the Smithsonian's 2019 article on ancient DNA possibly deconstructing old myths...  This Smithsonian article about an ancient DNA paper in Science Advances, or actually, about the misuse of such papers, was itself a misuse. The published research, Ancient DNA sheds light on the genetic origins of early Iron Age Philistines, confirmed Amos 9:7 by documenting the European origin of the biblical Philistines who came from the island of Caphtor/Crete. The mainstream media completely obscured this astounding aspect of the study but the Smithsonian actually stood the paper on its head. [See also rsr.org/archaeology.]* Also Squeezing Darwin's Theory: - Evolution happens so slowly that we can't see it, yet - it happens so fast that millions of mutations get fixed in a blink of geologic time AND: - Observing a million species annually should show us a million years of evolution, but it doesn't, yet - evolution happens so fast that the billions of "intermediary" fossils are missing AND: - Waiting for helpful random mutations to show up explains the slowness of evolution, yet - adaption to changing environments is often immediate, as with Darwin's finches Finches Adapt in 17 Years, Not 2.3 Million: Charles Darwin's finches are claimed to have taken 2,300,000 years to diversify from an initial species blown onto the Galapagos Islands. Yet individuals from a single finch species on a U.S. Bird Reservation in the Pacific were introduced to a group of small islands 300 miles away and in at most 17 years, like Darwin's finches, they had diversified their beaks, related muscles, and behavior to fill various ecological niches. So Darwin's finches could diversify in just 17 years, and after 2.3 million more years, what had they evolved into? Finches! Hear this also at rsr.org/lee-spetner and see Jean Lightner's review of the Grants' 40 Years. AND: - Fossils of modern organisms are found "earlier" and "earlier" in the geologic column, and - the "oldest" organisms are increasingly found to have anatomical, proteinaceous, prokaryotic, and eukaryotic sophistication and similarity to "modern" organisms AND: - Small populations are in danger of extinction (yet they're needed to fix mutations), whereas - large populations make it impossible for a mutation to become standard AND: - Mutations that express changes too late in an organism's development can't effect its fundamental body plan, and - mutations expressed too early in an organism's development are fatal (hence among the Enyart sayings, "Like evolving a vital organ, most major hurdles for evolutionary theory are extinction-level events.") AND: - To evolve flight, you'd get bad legs - long before you'd get good wings AND: - Most major evolutionary hurdles appear to be extinction-level events- yet somehow even *vital* organs evolve (for many species, that includes reproductive organs, skin, brain, heart, circulatory system, kidney, liver, pancreas, stomach, small intestines, large intestines, lungs -- which are only a part of the complex respiration system) AND: - Natural selection of randomly taller, swifter, etc., fish, mammals, etc. explains evolution yet - development of microscopic molecular machines, feedback mechanisms, etc., which power biology would be oblivous to what's happening in Darwin's macro environment of the entire organism AND: - Neo-Darwinism suggests genetic mutation as the engine of evolution yet - the there is not even a hypothesis for modifying the vast non-genetic information in every living cell including the sugar code, electrical code, the spatial (geometric) code, and the epigenetic code AND: - Constant appeals to "convergent" evolution (repeatedly arising vision, echolocation, warm-bloodedness, etc.) - undermine most Darwinian anatomical classification especially those based on trivialities like odd or even-toed ungulates, etc. AND: - Claims that given a single species arising by abiogenesis, then - Darwinism can explain the diversification of life, ignores the science of ecology and the (often redundant) biological services that species rely upon AND: - humans' vastly superior intelligence indicates, as bragged about for decades by Darwinists, that ape hominids should have the greatest animal intelligence, except that - many so-called "primitive" creatures and those far distant on Darwin's tee of life, exhibit extraordinary rsr.org/animal-intelligence even to processing stimuli that some groups of apes cannot AND: - Claims that the tree of life emerges from a single (or a few) common ancestors - conflict with the discoveries of multiple genetic codes and of thousands of orphan genes that have no similarity (homology) to any other known genes AND (as in the New Scientist cover story, "Darwin Was Wrong about the tree of life", etc.): - DNA sequences have contradicted anatomy-based ancestry claims - Fossil-based ancestry claims have been contradicted by RNA claims - DNA-based ancestry claims have been contradicted by anatomy claims - Protein-based ancestry claims have been contradicted by fossil claims. - And the reverse problem compared to a squeeze. Like finding the largest mall in America built to house just a kid's lemonade stand, see rsr.org/200 for the astounding lack of genetic diversity in humans, plants, and animals, so much so that it could all be accounted for in just about 200 generations! - The multiplied things that evolved multiple times - Etc. * List of Ways Darwinists Invent their Tree of Life, aka Pop Goes the Weasle – Head and Shoulders, Knees and Toes: Evolutionists change their selection of what evidence they use to show 'lineage', from DNA to fossils to genes to body plans to teeth to many specific anatomical features to proteins to behavior to developmental similarities to habitat to RNA, etc. and to a combination of such. Darwinism is an entire endeavor based on selection bias, a kind of logical fallacy. By anti-science they arbitrarily select evidence that best matches whichever evolutionary story is currently preferred." -Bob E. The methodology used to create the family tree edifice to show evolutionary relationships classifies the descent of organisms based on such attributes as odd-toed and even-toed ungulates. Really? If something as wildly sophisticated as vision allegedly evolved multiple times (a dozen or more), then for cryin' out loud, why couldn't something as relatively simple as odd or even toes repeatedly evolve? How about dinosaur's evolving eggs with hard shells? Turns out that "hard-shelled eggs evolved at least three times independently in dinosaurs" (Nature, 2020). However, whether a genus has an odd or even number of toes, and similar distinctions, form the basis for the 150-year-old Darwinist methodology. Yet its leading proponents still haven't acknowledged that their tree building is arbitrary and invalid. Darwin's tree recently fell anyway, and regardless, it has been known to be even theoretically invalid all these many decades. Consider also bipedalism? In their false paradigm, couldn't that evolve twice? How about vertebrate and non-vertebrates, for that matter, evolving multiple times? Etc., etc., etc. Darwinists determine evolutionary family-tree taxonomic relationships based on numbers of toes, when desired, or on hips (distinguishing, for example, dinosaur orders, until they didn't) or limb bones, or feathers, or genes, or fossil sequence, or neck bone, or..., or..., or... Etc. So the platypus, for example, can be described as evolving from pretty much whatever story would be in vogue at the moment...   * "Ancient" Protein as Advanced as Modern Protein: A book review in the journal Science states, "the major conclusion is reached that 'analyses made of the oldest fossils thus far studied do not suggest that their [allegedly 145-million year-old] proteins were chemically any simpler than those now being produced.'" 1972, Biochemistry of Animal Fossils, p. 125 * "Ancient" Lampreys Just Modern Lampreys with Decomposed Brain and Mouth Parts: Ha! Researches spent half-a-year documenting how fish decay. RSR is so glad they did! One of the lessons learned? "[C]ertain parts of the brain and the mouth that distinguish the animals from earlier relatives begin a rapid decay within 24 hours..." :) * 140-million Year Old Spider Web: The BBC and National Geographic report on a 140-million year old spider web in amber which, as young-earth creationists expect, shows threads that resemble silk spun by modern spiders. Evolutionary scientists on the otherhand express surprise "that spider webs have stayed the same for 140 million years." And see the BBC. * Highly-Credentialed Though Non-Paleontologist on Flowers: Dr. Harry Levin who spent the last 15 years of a brilliant career researching paleontology presents much evidence that flowering plants had to originate not 150 million years ago but more than 300 million years ago. (To convert that to an actual historical timeframe, the evidence indicates flowers must have existed prior to the time that the strata, which is popularly dated to 300 mya, actually formed.) * Rampant Convergence: Ubiquitous appeals to "convergent" evolution (vision, echolocation, warm-bloodedness, icthyosaur/dolphin anatomy, etc.), all allegedly evolving multiple times, undermines anatomical classification based on trivialities like odd or even-toed ungulates, etc. * Astronomy's Big Evolution Squeeze: - Universe a billion, wait, two billion, years younger than thought   (so now it has to evolve even more impossibly rapidly) - Sun's evolution squeezes biological evolution - Galaxies evolving too quickly - Dust evolving too quickly - Black holes evolving too quickly - Clusters of galaxies evolving too quickly. * The Sun's Evolution Squeezes Life's Evolution: The earlier evolutionists claim that life began on Earth, the more trouble they have with astrophysicists. Why? They claim that a few billion years ago the Sun would have been far more unstable and cooler. The journal Nature reports that the Faint young Sun paradox remains for the "Sun was fainter when the Earth was young, but the climate was generally at least as warm as today". Further, our star would shoot out radioactive waves many of which being violent enough to blow out Earth's atmosphere into space, leaving Earth dead and dry like Mars without an atmosphere. And ignoring the fact that powerful computer simulators cannot validate the nebula theory of star formation, if the Sun had formed from a condensing gas cloud, a billion years later it still would have been emitting far less energy, even 30% less, than it does today. Forget about the claimed one-degree increase in the planet's temperature from man-made global warming, back when Darwinists imagine life arose, by this just-so story of life spontaneously generating in a warm pond somewhere (which itself is impossible), the Earth would have been an ice ball, with an average temperature of four degrees Fahrenheit below freezing! See also CMI's video download The Young Sun. * Zircons Freeze in Molten Eon Squeezing Earth's Evolution? Zircons "dated" 4 to 4.4 billion years old would have had to freeze (form) when the Earth allegedly was in its Hadean (Hades) Eon and still molten. Geophysicist Frank Stacey (Cambridge fellow, etc.) has suggested they may have formed above ocean trenches where it would be coolest. One problem is that even further squeezes the theory of plate tectonics requiring it to operate two billion years before otherwise claimed. A second problem (for these zircons and the plate tectonics theory itself) is that ancient trenches (now filled with sediments; others raised up above sea level; etc.) have never been found. A third problem is that these zircons contain low isotope ratios of carbon-13 to carbon-12 which evolutionists may try to explain as evidence for life existing even a half-billion years before they otherwise claim. For more about this (and to understand how these zircons actually did form) just click and then search (ctrl-f) for: zircon character. * Evolution Squeezes Life to Evolve with Super Radioactivity: Radioactivity today breaks chromosomes and produces neutral, harmful, and fatal birth defects. Dr. Walt Brown reports that, "A 160-pound person experiences 2,500 carbon-14 disintegrations each second", with about 10 disintergrations per second in our DNA. Worse for evolutionists is that, "Potassium-40 is the most abundant radioactive substance in... every living thing." Yet the percentage of Potassium that was radioactive in the past would have been far in excess of its percent today. (All this is somewhat akin to screws in complex machines changing into nails.) So life would have had to arise from inanimate matter (an impossibility of course) when it would have been far more radioactive than today. * Evolution of Uranium Squeezed by Contrasting Constraints: Uranium's two most abundant isotopes have a highly predictable ratio with 235U/238U equaling 0.007257 with a standard deviation of only 0.000017. Big bang advocates claim that these isotopes formed in distant stellar cataclysms. Yet that these isotopes somehow collected in innumerable small ore bodies in a fixed ratio is absurd. The impossibility of the "big bang" explanation of the uniformity of the uranium ratio (rsr.org/bb#ratio) simultaneously contrasts in the most shocking way with its opposite impossibility of the missing uniform distribution of radioactivity (see rsr.org/bb#distribution) with 90% of Earth's radioactivity in the Earth's crust, actually, the continental crust, and even at that, preferentially near granite! A stellar-cataclysmic explanation within the big bang paradigm for the origin of uranium is severely squeezed into being falsified by these contrasting constraints. * Remarkable Sponges? Yes, But For What Reason? Study co-author Dr. Kenneth S. Kosik, the Harriman Professor of Neuroscience at UC Santa Barbara said, "Remarkably, the sponge genome now reveals that, along the way toward the emergence of animals, genes for an entire network of many specialized cells evolved and laid the basis for the core gene logic of organisms that no longer functioned as single cells." And then there's this: these simplest of creatures have manufacturing capabilities that far exceed our own, as Degnan says, "Sponges produce an amazing array of chemicals of direct interest to the pharmaceutical industry. They also biofabricate silica fibers directly from seawater in an environmentally benign manner, which is of great interest in communications [i.e., fiber optics]. With the genome in hand, we can decipher the methods used by these simple animals to produce materials that far exceed our current engineering and chemistry capabilities." Kangaroo Flashback: From our RSR Darwin's Other Shoe program: The director of Australia's Kangaroo Genomics Centre, Jenny Graves, that "There [are] great chunks of the human genome… sitting right there in the kangaroo genome." And the 20,000 genes in the kangaroo (roughly the same number as in humans) are "largely the same" as in people, and Graves adds, "a lot of them are in the same order!" CMI's Creation editors add that "unlike chimps, kangaroos are not supposed to be our 'close relatives.'" And "Organisms as diverse as leeches and lawyers are 'built' using the same developmental genes." So Darwinists were wrong to use that kind of genetic similarity as evidence of a developmental pathway from apes to humans. Hibernating Turtles: Question to the evolutionist: What happened to the first turtles that fell asleep hibernating underwater? SHOW UPDATE Of Mice and Men: Whereas evolutionists used a very superficial claim of chimpanzee and human genetic similarity as evidence of a close relationship, mice and men are pretty close also. From the Human Genome Project, How closely related are mice and humans?, "Mice and humans (indeed, most or all mammals including dogs, cats, rabbits, monkeys, and apes) have roughly the same number of nucleotides in their genomes -- about 3 billion base pairs. This comparable DNA content implies that all mammals [RSR: like roundworms :)] contain more or less the same number of genes, and indeed our work and the work of many others have provided evidence to confirm that notion. I know of only a few cases in which no mouse counterpart can be found for a particular human gene, and for the most part we see essentially a one-to-one correspondence between genes in the two species." * Related RSR Reports: See our reports on the fascinating DNA sequencing results from roundworms and the chimpanzee's Y chromosome! * Genetic Bottleneck, etc: Here's an excerpt from rsr.org/why-was-canaan-cursed... A prediction about the worldwide distribution of human genetic sequencing (see below) is an outgrowth of the Bible study at that same link (aka rsr.org/canaan), in that scientists will discover a genetic pattern resulting from not three but four sons of Noah's wife. Relevant information comes also from mitochondrial DNA (mtDNA) which is not part of any of our 46 chromosomes but resides outside of the nucleus. Consider first some genetic information about Jews and Arabs, Jewish priests, Eve, and Noah. Jews and Arabs Biblical Ancestry: Dr. Jonathan Sarfati quotes the director of the Human Genetics Program at New York University School of Medicine, Dr. Harry Ostrer, who in 2000 said: Jews and Arabs are all really children of Abraham … And all have preserved their Middle Eastern genetic roots over 4,000 years. This familiar pattern, of the latest science corroborating biblical history, continues in Dr. Sarfati's article, Genesis correctly predicts Y-Chromosome pattern: Jews and Arabs shown to be descendants of one man. Jewish Priests Share Genetic Marker: The journal Nature in its scientific correspondence published, Y Chromosomes of Jewish Priests, by scie

In this episode of Research Like a Pro, Diana and Nicole explore the use of mitochondrial DNA (mtDNA) and WikiTree in genealogical research. They explain that mtDNA is inherited from our mothers, with only females passing it on, and how it differs from autosomal DNA by coming from a distant maternal ancestor. They discuss how mtDNA testing reveals haplogroups, genetic population groups with a common ancestor, and share their personal testing experiences with 23andMe, FamilyTree DNA, and Living DNA, highlighting the northern European origins of their haplogroup, U5b1c2b. The hosts emphasize that while mtDNA changes very little over generations, making it difficult to pinpoint recent common ancestors, it is useful for confirming or refuting specific female ancestral lines. They discuss integrating DNA information into WikiTree, a collaborative and free online platform, which allows users to add mtDNA haplogroups to family profiles, enhancing genealogical research by sharing DNA data with other researchers. They provide practical tips for getting started on WikiTree, including creating a login, adding ancestors, and integrating DNA information from various testing services. They also highlight unique features of WikiTree, such as the DNA Ancestors view, which shows the inheritance of different types of DNA from ancestors. This episode offers valuable insights into using mtDNA and WikiTree as powerful tools in genealogical research. Links https://www.wikitree.com/ Honoring my Matrilineal Grandmothers: A Look at Mitochondrial DNA - https://familylocket.com/honoring-my-matrilineal-grandmothers-a-look-at-mitochondrial-dna/ WikiTree and My Mitochondrial DNA - https://familylocket.com/wikitree-and-my-mitochondrial-dna/ Sponsor – Newspapers.com For listeners of this podcast, Newspapers.com is offering new subscribers 20% off a Publisher Extra subscription so you can start exploring today. Just use the code “FamilyLocket” at checkout.  Research Like a Pro Resources Airtable Universe - Nicole's Airtable Templates - https://www.airtable.com/universe/creator/usrsBSDhwHyLNnP4O/nicole-dyer Airtable Research Logs Quick Reference - by Nicole Dyer - https://familylocket.com/product-tag/airtable/ Research Like a Pro: A Genealogist's Guide book by Diana Elder with Nicole Dyer on Amazon.com - https://amzn.to/2x0ku3d 14-Day Research Like a Pro Challenge Workbook - digital - https://familylocket.com/product/14-day-research-like-a-pro-challenge-workbook-digital-only/ and spiral bound - https://familylocket.com/product/14-day-research-like-a-pro-challenge-workbook-spiral-bound/ Research Like a Pro Webinar Series 2024 - monthly case study webinars including documentary evidence and many with DNA evidence - https://familylocket.com/product/research-like-a-pro-webinar-series-2024/ Research Like a Pro eCourse - independent study course -  https://familylocket.com/product/research-like-a-pro-e-course/ RLP Study Group - upcoming group and email notification list - https://familylocket.com/services/research-like-a-pro-study-group/ Research Like a Pro with DNA Resources Research Like a Pro with DNA: A Genealogist's Guide to Finding and Confirming Ancestors with DNA Evidence book by Diana Elder, Nicole Dyer, and Robin Wirthlin - https://amzn.to/3gn0hKx Research Like a Pro with DNA eCourse - independent study course -  https://familylocket.com/product/research-like-a-pro-with-dna-ecourse/ RLP with DNA Study Group - upcoming group and email notification list - https://familylocket.com/services/research-like-a-pro-with-dna-study-group/ Thank you Thanks for listening! We hope that you will share your thoughts about our podcast and help us out by doing the following: Write a review on iTunes or Apple Podcasts. If you leave a review, we will read it on the podcast and answer any questions that you bring up in your review. Thank you! Leave a comment in the comment or question in the comment section below. Share the episode on Twitter, Facebook, or Pinterest. Subscribe on iTunes, Stitcher, Google Podcasts, or your favorite podcast app. Sign up for our newsletter to receive notifications of new episodes - https://familylocket.com/sign-up/ Check out this list of genealogy podcasts from Feedspot: Top 20 Genealogy Podcasts - https://blog.feedspot.com/genealogy_podcasts/

We mark Memorial Day with the  PFC Lawrence Gordon Foundation's Jed Henry (https://www.pfclawrencegordonfoundati...) who, along with Operation Benjamin (https://www.operationbenjamin.org/nat..., recently recovered the remains of 1st Lt. Nathan Baskind, who was killed in Normandy near Utah Beach in 1944. In June 1944, Baskind was assigned to Company C, 899th Tank Destroyer Battalion, as a platoon commander of four M-10 tank destroyers. According to historical war records, 1st Lt. Baskind and another man from his company were scouting ahead of their tank destroyers when enemy forces descended upon them in an ambush. The other soldier, heavily wounded, escaped the firefight and made his way back to the main U.S. force, believing Baskind was killed in the attack. Several attempts were made to retrieve Baskind's body from the ambush point, but they could not locate his remains. Following the end of the war, the American Graves Registration Command (AGRC) was tasked with investigating and recovering missing American personnel in Europe. Investigators discovered a death and burial report for 1st Lt. Baskind among the foreign records recovered from the Germans, evidently filed after the war on May 29, 1945, in Meiningen, Germany. The record revealed 1st Lt. Baskind was captured and later died at a hospital for German air force personnel near Cherbourg on June 23, 1944. German forces then buried him in the military cemetery in the city. In early 1948, the International Committee of the Red Cross (ICRC) sent the U.S. Army one of 1st Lt. Baskind's identification tags. It is believed the German government likely submitted the tag to the ICRC, along with a death and burial report, following the war. In November 1957, the Volksbund, the German War Grave Commission, contacted the U.S. Army regarding 1st Lt. Baskind. While disinterring a mass grave of what were believed to be 24 Germans buried in the Cherbourg cemetery, a Volksbund team discovered one of 1st Lt. Baskind's identification tags and remnants of an American-type shirt with a first lieutenant rank and tank destroyer insignia. The remains in the mass grave were commingled, and the German team was unable to separate them into individual sets. The German investigators therefore placed the remains in seven burial pouches and then re-interred them in the Marigny German War Cemetery, 40 miles south of Cherbourg. Subsequent attempts to identify the remains of 1st Lt. Baskind by U.S. and German investigators were not successful. In 2023, the Volksbund and other interested private research organizations exhumed the commingled remains from Marigny War Cemetery for analysis. By February 2024, these researchers contacted DPAA to inform the agency that 1st Lt. Baskind's remains had been analyzed by a private U.S. laboratory and sought DPAA's concurrence. To verify Baskind's remains, scientists from the Armed Forces Medical Examiner System reviewed the mitochondrial DNA (mtDNA), Y chromosome DNA (Y-STR), and autosomal DNA (auSTR) analysis previously performed. 1st Lt. Baskind's name is recorded on the Walls of the Missing at Normandy American Cemetery, an American Battle Monuments Commission site in Colleville-sur-Mer, France, along with the others still missing from World War II. A rosette will be placed next to his name to indicate he has been accounted for. We also talk with veterans about whom they remember on Memorial Day. We're grateful to UPMC for Life and Tobacco Free Adagio Health for sponsoring this event! #memorialday #missinginaction #wwii #greatestgeneration  #happyhour #history #interview #veteran #veterans #veteransbreakfastclub #virtualevents #virtual #zoomevents #liveevents #webinar #militaryhistory #military #army #navy #marinecorps #marines  #coastguard #vbc #nonprofit #501c3  #vet #militaryhistory #usarmy #vietnam #usnavy #pilot #airforce #veteranowned #coastguard #aviators #militaryveterans #Iraq #vietnamveterans #veteransstories #veteranshistory #veteranshistoryproject #veteranstravel #veteranstrips #veteranshistoricaltours #veteransoralhistory #militaryretirees #armyretirees #navyretirees #warstories #airforce #vietnamwar #veteraninterview #greatestgeneration #wwii #ww2 #worldwarii #worldwar2 #war #americanhistory #oralhistory #veteraninterview

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.07.547791v1?rss=1 Authors: Pass, T., Ricke, K. M., Hofmann, P., Chowdhury, R., Nie, Y., Chinnery, P. F., Endepols, H., Neumaier, B., Carvalho, A., Rigoux, L., Steculorum, S., Prudent, J., Riemer, T., Aswendt, M., Brachvogel, B., Wiesner, R. J. Abstract: Degeneration of dopamine neurons in the substantia nigra and their striatal axon terminals causes cardinal motor symptoms of Parkinson's disease (PD). In idiopathic cases, high levels of mitochondrial DNA (mtDNA) mutations associated with mitochondrial dysfunction are a central feature of these vulnerable neurons. Here we present a mouse model expressing the K320E-variant of the mitochondrial helicase Twinkle in dopamine neurons, leading to accelerated mtDNA ageing. K320E-TwinkleDaN mice showed normal motor function at 20 months of age, although already ~70% of nigral dopamine neurons had perished. The remaining neuron population still preserved ~75% of axon terminals in the dorsal striatum, which enabled normal dopamine release. Transcriptome analysis and viral tracing confirmed compensatory axonal sprouting of surviving nigral dopamine neurons. We conclude that a small population of substantia nigra neurons can adapt to mtDNA mutations and maintain motor control in mice, holding chances for new treatment strategies in PD patients. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.02.547346v1?rss=1 Authors: Hong, Y., Zhang, Z., Yangzom, T., Chen, A., Lundberg, B. C., Fang, E. F., Sullivan, G. J., Tzoulis, C., Bindoff, L. A., Liang, K. X. Abstract: Alpers' syndrome is an early-onset neurodegenerative disorder usually caused by biallelic pathogenic variants in the gene encoding the catalytic subunit of polymerase-gamma (POLG), which is essential for mitochondrial DNA (mtDNA) replication. The disease is progressive, incurable, and inevitably it leads to death from drug-resistant status epilepticus. The neurological features of Alpers' syndrome are intractable epilepsy and developmental regression, with no effective treatment; the underlying mechanisms are still elusive, partially due to lack of good experimental models. Here, we generated the patient-derived induced pluripotent stem cells from one Alpers' patient carrying the compound heterozygous mutations of A467T (c.1399G greater than A) and P589L (c.1766C greater than T), and further differentiated them into cortical organoids and neural stem cells (NSCs) for mechanistic studies of neural dysfunction in Alpers' syndrome. Patient cortical organoids exhibited a phenotype that faithfully replicated the molecular changes found in patient postmortem brain tissue, as evidenced by cortical neuronal loss and depletion of mtDNA and complex I (CI). Patient NSCs showed mitochondrial dysfunction leading to ROS overproduction and downregulation of the NADH pathway. More importantly, the NAD+ precursor nicotinamide riboside (NR) significantly ameliorated mitochondrial defects in patient brain organoids. Our findings demonstrate that the iPSC model and brain organoids are good in vitro models of Alpers' disease; this first-in-its-kind stem cell platform for Alpers' syndrome enables therapeutic exploration and has identified NR as a viable drug candidate for Alpers' disease and, potentially, other mitochondrial diseases with similar causes. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.09.527880v1?rss=1 Authors: McShane, E., Couvillion, M., Ietswaart, R., Prakash, G., Smalec, B. M., Soto, I., Baxter-Koenigs, A. R., Choquet, K., Churchman, L. S. Abstract: Mitochondria play a critical role in cellular metabolism primarily through hosting the oxidative phosphorylation (OXPHOS) machinery that is encoded by mitochondrial DNA (mtDNA) and nuclear DNA, with each genome separately regulated in their respective compartments. To unravel how the two gene expression systems collaborate to produce the OXPHOS complexes, the regulatory principles controlling the production of mtDNA-encoded proteins need to be elucidated. Here, we performed a quantitative analysis of the mitochondrial messenger RNA (mt-mRNA) life cycle to gain insight into which steps of gene expression experience the most regulatory control. Our analysis revealed a unique balance between the rapid turnover and high accumulation of mt-mRNA, leading to a 700-fold higher transcriptional output than nuclear-encoded OXPHOS genes. Additionally, we observed that mt-mRNA processing and its association with the mitochondrial ribosome occur rapidly and that these processes are linked mechanistically. These data resulted in a model of mtDNA expression that is predictive across human cell lines, revealing that differential turnover and translation efficiencies are the major contributors to mitochondrial-encoded protein synthesis. Applying this framework to a disease model of Leigh syndrome, French-Canadian type, we found that disrupting the responsible nuclear-encoded gene, LRPPRC, perturbs OXPHOS biogenesis predominantly through altering mt-mRNA stability. Our findings provide a comprehensive view of the intricate regulatory mechanisms governing mtDNA-encoded protein synthesis, highlighting the importance of quantitatively analyzing the mitochondrial RNA life cycle for decoding the regulatory principles of mtDNA expression. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.01.28.526021v1?rss=1 Authors: Hong, Y., Kristiansen, C. K., Chen, A., NIDO, G. S., Hoyland, L. E., Ziegler, M., Sullivane, G. J., Bindoff, L. A., Liang, K. X. Abstract: Diseases caused by POLG mutations are the most common form of mitochondrial disease and associated with phenotypes of varying severity. Clinical studies have shown that patients with compound heterozygous POLG mutations have a lower survival rate than patients with homozygous mutations, but the molecular mechanisms behind this remain unexplored. Using an induced pluripotent stem cell (iPSC) model, we investigate differences between homozygous and compound heterozygous genotypes in different cell types, including patient-specific fibroblasts, iPSCs, and iPSC-derived neural stem cells (NSCs) and astrocytes. We found that compound heterozygous lines exhibited greater impairment of mitochondrial function in NSCs than homozygous NSCs, but not in fibroblasts, iPSCs, or astrocytes. Compared with homozygous NSCs, compound heterozygous NSCs exhibited more severe functional defects, including reduced ATP production, loss of mitochondrial DNA (mtDNA) copy number and complex I expression, disturbance of NAD+ metabolism, and higher ROS levels, which further led to cellular senescence and activation of mitophagy. RNA sequencing analysis revealed greater downregulation of mitochondrial and metabolic pathways, including the citric acid cycle and oxidative phosphorylation, in compound heterozygous NSCs. Our iPSC-based disease model can be widely used to understand the genotype-phenotype relationship of affected brain cells in mitochondrial diseases, and further drug discovery applications. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.11.30.517979v1?rss=1 Authors: Pena, N., Gonzalez-Hunt, C., Qi, R., Barlow, C., Shanks, N. F., Carlisle, H., Sanders, L. H. Abstract: Pathogenic mutations in LRRK2 cause Parkinson's disease (PD). The G2019S variant is the most common, which results in abnormally high kinase activity. Compounds that target LRRK2 kinase activity are currently being developed and tested in clinical trials. We recently found that G2019S LRRK2 causes mitochondrial DNA (mtDNA) damage and treatment with multiple classes of LRRK2 kinase inhibitors at concentrations associated with dephosphorylation of LRRK2 reversed mtDNA damage to healthy control levels. Because maintaining the normal function of LRRK2 in heterozygous G2019S LRRK2 carriers while specifically targeting the G2019S LRRK2 activity could have an advantageous safety profile, we explored the efficacy of a G2019S mutant selective LRRK2 inhibitor to reverse mtDNA damage in G2019S LRRK2 models and patient cells relative to non-selective LRRK2 inhibitors. Potency of LRRK2 kinase inhibition by EB-42168, a G2019S mutant LRRK2 kinase inhibitor, and MLi-2, a nonselective inhibitor, was determined by measuring phosphorylation of LRRK2 at Ser935 and/or Ser1292 using quantitative western immunoblot analysis. The Mito DNADX assay, a novel system that allows for the accurate real-time quantification of mtDNA damage in a 96-well platform, was performed in parallel. We confirmed that EB-42168 selectively inhibits LRRK2 phosphorylation on G2019S LRRK2 relative to wild-type LRRK2. On the other hand, MLi-2 was equipotent for wild-type and G2019S LRRK2. Acute treatment with EB-42168 inhibited LRRK2 phosphorylation and also restored mtDNA damage to healthy control levels. Precision medicine is a common approach in modern day cancer research that is not yet routinely applied to neurodegenerative diseases. Abrogation of mtDNA damage with mutant selective tool inhibitor EB-42168 demonstrates the promise of a precision medicine approach for LRRK2 G2019S PD. Levels of mtDNA damage may serve as a potential pharmacodynamic biomarker of altered kinase activity that could be useful for small molecule development and clinical trials. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.10.12.511955v1?rss=1 Authors: Newman, L. E., Tadepalle, N., Novak, S. W., Schiavon, C. R., Rojas, G. R., Chevez, J. A., Lemersal, I., Medina, M., Rocha, S., Towers, C. G., Grotjahn, D. A., Manor, U., Shadel, G. S. Abstract: Maternally inherited mitochondrial DNA (mtDNA) encodes essential subunits of the mitochondrial oxidative phosphorylation system, but is also a major damage-associated molecular pattern (DAMP) that engages innate immune sensors when released into the cytoplasm, outside of cells or into circulation1. This function of mtDNA contributes to antiviral resistance, but unfortunately also causes pathogenic inflammation in many disease contexts2. Cells experiencing mtDNA stress due to depletion of the mtDNA-packaging protein, Transcription Factor A, Mitochondrial (TFAM), or HSV-1 infection exhibit elongated mitochondria, mtDNA depletion, enlargement of nucleoids (mtDNA-protein complexes), and activation of cGAS/STING innate immune signaling via mtDNA released into the cytoplasm3. However, the relationships between altered mitochondrial dynamics and mtDNA-mediated activation of the cGAS-STING pathway remain unclear. Here, we show that entire enlarged nucleoids are released from mitochondria that remain bound to TFAM and colocalize with cGAS. These nucleoids arise at sites of mtDNA replication due to a block in mitochondrial fission at a stage when endoplasmic reticulum (ER) actin polymerization would normally commence, which we propose is a fission checkpoint to ensure that mtDNA has completed replication and is competent for segregation into daughter mitochondria. Released nucleoids also colocalize with the early endosomal marker RAB5 as well as the late endosomal marker RAB7 in TFAM-deficient cells and in response to mtDNA stress caused by the HSV-1 UL12.5 protein. Loss of RAB7 increases interferon stimulated gene (ISG) expression. Thus, we propose that defects in mtDNA replication and/or segregation enact a late mitochondrial fission checkpoint that, if persistent, leads to selective removal of dysfunctional nucleoids by a mitochondrial-endosomal pathway. Early steps in this pathway are prone to mtDNA release and cGAS-STING activation, but the immunostimulatory mtDNA is ultimately disposed of through a mechanism involving RAB7-containing late endosomes to prevent excessive innate immune signaling. This mtDNA quality control pathway might represent a therapeutic target to prevent mtDNA-mediated inflammation and associated pathology. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Dr. Stanley Lipkowitz and Dr. Yoshimi Endo Greer from the Women's Malignancies Branch at the National Cancer Institute discuss a research paper they co-authored that was published by Oncotarget in 2018, entitled, "ONC201 kills breast cancer cells in vitro by targeting mitochondria." DOI - https://doi.org/10.18632/oncotarget.24862 Correspondence to - lipkowis@mail.nih.gov Abstract We report a novel mechanism of action of ONC201 as a mitochondria-targeting drug in cancer cells. ONC201 was originally identified as a small molecule that induces transcription of TNF-related apoptosis-inducing ligand (TRAIL) and subsequently kills cancer cells by activating TRAIL death receptors. In this study, we examined ONC201 toxicity on multiple human breast and endometrial cancer cell lines. ONC201 attenuated cell viability in all cancer cell lines tested. Unexpectedly, ONC201 toxicity was not dependent on either TRAIL receptors nor caspases. Time-lapse live cell imaging revealed that ONC201 induces cell membrane ballooning followed by rupture, distinct from the morphology of cells undergoing apoptosis. Further investigation found that ONC201 induces phosphorylation of AMP-dependent kinase and ATP loss. Cytotoxicity and ATP depletion were significantly enhanced in the absence of glucose, suggesting that ONC201 targets mitochondrial respiration. Further analysis indicated that ONC201 indirectly inhibits mitochondrial respiration. Confocal and electron microscopic analysis demonstrated that ONC201 triggers mitochondrial structural damage and functional impairment. Moreover, ONC201 decreased mitochondrial DNA (mtDNA). RNAseq analysis revealed that ONC201 suppresses expression of multiple mtDNA-encoded genes and nuclear-encoded mitochondrial genes involved in oxidative phosphorylation and other mitochondrial functions. Importantly, fumarate hydratase deficient cancer cells and multiple cancer cell lines with reduced amounts of mtDNA were resistant to ONC201. These results indicate that cells not dependent on mitochondrial respiration are ONC201-resistant. Our data demonstrate that ONC201 kills cancer cells by disrupting mitochondrial function and further suggests that cancer cells that are dependent on glycolysis will be resistant to ONC201. Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.24862 Press release - https://www.oncotarget.com/index.php?journal=oncotarget&page=news&op=press&item=onc201-kills-breast-cancer-cells-in-vitro-by-targeting-mitochondria Keywords - ONC201, breast cancer, mitochondria About Oncotarget Oncotarget is a peer-reviewed, open access biomedical journal covering research on all aspects of oncology. To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: SoundCloud - https://soundcloud.com/oncotarget Facebook - https://www.facebook.com/Oncotarget/ Twitter - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/OncotargetYouTube LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Oncotarget is published by Impact Journals, LLC: https://www.ImpactJournals.com Media Contact MEDIA@IMPACTJOURNALS.COM 18009220957

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.11.13.381475v1?rss=1 Authors: Pabis, K. Abstract: The "theory of resistant biomolecules" posits that long-lived species show resistance to molecular damage at the level of their biomolecules. Here, we test this hypothesis in the context of mitochondrial DNA (mtDNA) as it implies that predicted mutagenic DNA motifs should be inversely correlated with species maximum lifespan (MLS). First, we confirmed that guanine-quadruplex (GQ) and direct repeat (DR) motifs are mutagenic, as they associate with mtDNA deletions in the human major arc of mtDNA, while also adding mirror repeat (MR) and intramolecular triplex motifs to a growing list of potentially mutagenic features. What is more, triplex motifs showed disease-specific associations with deletions and an apparent interaction with GQ motifs. Surprisingly, even though DR, MR and GQ motifs were associated with mtDNA deletions, their correlation with MLS was explained by the biased base composition of mtDNA. Only triplex motifs negatively correlated with MLS and these results remained stable even after adjusting for body mass, phylogeny, mtDNA base composition and effective number of codons. Taken together, our work highlights the importance of base composition for the comparative biogerontology of mtDNA and suggests that future research on mitochondrial triplex motifs is warranted. Copy rights belong to original authors. Visit the link for more info

For a long time, biologists believed that our DNA resided only in the nucleus, the large organelle acting as the control centre in our cells. It wasn't until 1963, when scientists Margrit and Sylvan Nass at Stockholm University discovered DNA fibres in mitochondria using electron microscopy. Our mitochondrial DNA (mtDNA) accounts for a small portion of our total DNA. In fact, it contains just 40 of the 20,000 to 25,000 protein-coding genes in our body, however, it is notably distinct from nuclear DNA. Unlike nuclear DNA, which comes from both parents, mitochondrial DNA comes only from the mother. In this podcast, I explain the significance of this key biological difference, and explore what other roles this fascinating molecule plays in our bodies. (With thanks to our sponsor 'Curriculum Press' for providing content for this podcast)

Meet Deborah Dunn, MD in the 2nd part of her interview. DNA and mitochondria have become such an important health topic and understanding this genetic information can optimize your well being.Deborah received her medical degree from the University of Texas and her master's in applied environmental public health from Tulane University. She completed a fellowship from Dr. Andrew Weil's Integrative Medicine program at the University of Arizona and completed training from The Institute of Functional Medicine. She is the founder of Genetic Eve, a company that interprets Mitochondrial DNA.Subscribe to YOUR TRUTH REVEALED weekly videos on YouTube - https://bit.ly/2MjsfdK➤RESOURCESFree Worksheet: https://www.YourTruthRevealed.comGenetic Eve: https://www.geneticeve.comMindful Self-Compassion https://amzn.to/34eYEHtWorkbook: https://amzn.to/34eYEHtStore: https://bit.ly/2H99Iwl ➤ SUMMARYWhy has DNA become such an interesting topic?There are 4 major reasons why analyzing DNA is popular.* DNA is far more expansive than your hair and eye color.* Analyzing DNA is now more affordable - in 2008 it cost $10 billion and now it can cost $200.* DNA tests are more available.* We're still figuring out the core value of analyzing DNA.What is mitochondrial DNA and its significance?* DNA, short for deoxyribonucleic acid, is the molecule that contains your genetic code.* Mitochondrial DNA is the DNA that is located in mitochondria that creates energy.* Mitochondria are small structures in cells that generate energy for the cell to use and are referred to as the "powerhouses" of the cell.* You inherit mitochondria exclusively from you mom that enables researchers to trace maternal lineage far back in time.How does mitochondrial DNA tie into your maternal haplogroup?* A maternal haplogroup is a family of mitochondrial DNA (mtDNA) that traces back to a single common maternal ancestor.* You share the same maternal haplogroup with any relative you share a direct maternal line with, including your mom, your brother, your maternal aunt, and so on.* Your maternal haplogroup traces back through the generations to a single mutation at a specific place and time to a shared maternal ancestor.How can you determine your maternal haplogroup? The process is easy to have your genetic DNA tested. Contact a testing company, and you will receive a DNA test kit in the mail.* The instructions will ask you to spit into a tube or wipe a swab around the inside of your mouth.* Then you mail the sample of your DNA to the lab.* Know that we all share 99.9% of the same genes. Testing companies show just .1% of your genetic makeup in the report.* These reports predict the ancestral origin of different parts of your DNA by comparing them to reference populations.* The report from 23andMe will provide your maternal haplogroup.Where does the name genetic eve come from?In human genetics, Genetic Eve refers to the the Mitochondrial Eve that is the matrilineal most recent common ancestor of all living human beings.* The most recent woman from whom all living humans descend in an unbroken line purely through your mom and your mom's mom, back until all lines converge on one woman.* The name “Mitochondrial Eve" alludes to biblical Eve.* Dr. Dunn's company is called Genetic Eve.Why does it matter in today's world that you carry ancient maternally inherited mutations?It's possible in the future that we will manipulate our genetics including our mitochondria.* If this happens, the ability to track the ancestry of people will be lost.* Manipulating genetics are life-altering interventions that can change the mitochondria to adapt to this modern world.

Meet Deborah Dunn, MD in the 1st part of her interview. DNA and mitochondria have become such an important health topic and understanding this genetic information can optimize your well being.Deborah received her medical degree from the University of Texas and her master's in applied environmental public health from Tulane University. She completed a fellowship from Dr. Andrew Weil's Integrative Medicine program at the University of Arizona and completed training from The Institute of Functional Medicine. She is the founder of Genetic Eve, a company that interprets Mitochondrial DNA.Subscribe to YOUR TRUTH REVEALED weekly videos on YouTube - https://bit.ly/2MjsfdK➤RESOURCESFree Worksheet: https://www.YourTruthRevealed.comGenetic Eve: https://www.geneticeve.comMindful Self-Compassion https://amzn.to/34eYEHtWorkbook: https://amzn.to/34eYEHtStore: https://bit.ly/2H99Iwl ➤ SUMMARYWhy has DNA become such an interesting topic?There are 4 major reasons why analyzing DNA is popular.* DNA is far more expansive than your hair and eye color.* Analyzing DNA is now more affordable - in 2008 it cost $10 billion and now it can cost $200.* DNA tests are more available.* We're still figuring out the core value of analyzing DNA.What is mitochondrial DNA and its significance?* DNA, short for deoxyribonucleic acid, is the molecule that contains your genetic code.* Mitochondrial DNA is the DNA that is located in mitochondria that creates energy.* Mitochondria are small structures in cells that generate energy for the cell to use and are referred to as the "powerhouses" of the cell.* You inherit mitochondria exclusively from you mom that enables researchers to trace maternal lineage far back in time.How does mitochondrial DNA tie into your maternal haplogroup?* A maternal haplogroup is a family of mitochondrial DNA (mtDNA) that traces back to a single common maternal ancestor.* You share the same maternal haplogroup with any relative you share a direct maternal line with, including your mom, your brother, your maternal aunt, and so on.* Your maternal haplogroup traces back through the generations to a single mutation at a specific place and time to a shared maternal ancestor.How can you determine your maternal haplogroup? The process is easy to have your genetic DNA tested. Contact a testing company, and you will receive a DNA test kit in the mail.* The instructions will ask you to spit into a tube or wipe a swab around the inside of your mouth.* Then you mail the sample of your DNA to the lab.* Know that we all share 99.9% of the same genes. Testing companies show just .1% of your genetic makeup in the report.* These reports predict the ancestral origin of different parts of your DNA by comparing them to reference populations.* The report from 23andMe will provide your maternal haplogroup.Where does the name genetic eve come from?In human genetics, Genetic Eve refers to the the Mitochondrial Eve that is the matrilineal most recent common ancestor of all living human beings.* The most recent woman from whom all living humans descend in an unbroken line purely through your mom and your mom's mom, back until all lines converge on one woman.* The name “Mitochondrial Eve" alludes to biblical Eve.* Dr. Dunn's company is called Genetic Eve.Why does it matter in today's world that you carry ancient maternally inherited mutations?It's possible in the future that we will manipulate our genetics including our mitochondria.* If this happens, the ability to track the ancestry of people will be lost.* Manipulating genetics are life-altering interventions that can change the mitochondria to adapt to this modern world.

As we thought, this became the longest episode we have recorded yet but then again, we had a lot to cover. Chapter IV is the part of Origin of Species where Darwin outlines how he believes natural selection, over long periods of time, can generate new species. It is a rich and complex chapter and our wide-ranging conversation explored a large number of the issues Darwin brings forth in the chapter.We discussed at great length the variety of ideas that Darwin encapsulates within the only figure in the book. James mentioned how Darwin first sketched the figure in his notebook B - Transmutation of Species with the understated "I think" title followed with "Case must be that one generation then should be as many living as now. To do this & to have many species in same genus (as is) requires extinction. Thus between A & B immense gap of relation. C & B the finest gradation, B & D rather greater distinction."   Image from Original Notebook at Darwin Online. Ultimately this image became refined for Origin of Species to look like this -In our discussion we noted that this image represents ideas like: a large number of extinction events, the lack of predictable direction in evolutionary change, no change (E & F), increase in species numbers, differential rates of evolution as indicated by the slope of the lines radiating out at a specified time era (e.g., era IV, z4), and that species can converge in character traits (e.g., how f lineage shifts to look like extinct d lineage). A larger version of the figure can be found here. Sarah noted how human evolution phylogenetic tree can show the same sort of pruned bushiness that Darwin represented in his figure. This figure is from the Smithsonian and is an interactive figure at their site that is worth checking out.Interestingly there has been recent researchers who reject the evolutionary tree model for human evolution. Instead of the classic tree structure they note that the mitochondrial DNA (mtDNA) analysis suggests all modern humans can be traced back to African ancestors who dispersed out of Africa only 100,000 years ago. However, those various subspecies of humans interbred and migrated back into Africa thereby creating a more reticulated, "trellis" evolutionary relationship than the classic branching independent lineages as represented in a tree. Follow this link to read a nice summary of the alternative view with a figure to illustrate the trellis view of human evolution. Sarah mentioned how quickly other scientists adopted Darwin's tree model to represent relatedness and she noted how the embryologist Ernst Haeckel drew up a phenomenal evolutionary tree. To truly appreciate this tree  you should see it in a larger format. We also discussed the rapid evolution of the Hawthorn maggot fly and its shift to feeding on introduced Apples and how that resulted in two populations with little genetic exchange between them. It is a beautiful house fly sized insect with painted wings which they flick to mimic the movement of jumping spiders. Photo Copyright © 2013 Harvey Schmidthttp://bugguide.net/node/view/817659Do you see the jumping spider in its wings?At the end of the podcast we attempted to read the epic opening sentence in Darwin's summary in a way that brings the words to life. Here it is for you to try.If under changing conditions of life organic beings present individual differences in almost every part of their structure, and this cannot be disputed; if there be, owing to their geometrical rate of increase, a severe struggle for life at some age, season, or year, and this certainly cannot be disputed; then, considering the infinite complexity of the relations of all organic beings to each other and to their conditions of life, causing an infinite diversity in structure, constitution, and habits, to be advantageous to them, it would be a most extraordinary fact if no variations had ever occurred useful to each being's own welfare, in the same manner as so many variations have occurred useful to man.

Background: Myanmar is the largest country in mainland Southeast Asia with a population of 55 million people subdivided into more than 100 ethnic groups. Ruled by changing kingdoms and dynasties and lying on the trade route between India and China, Myanmar was influenced by numerous cultures. Since its independence from British occupation, tensions between the ruling Bamar and ethnic minorities increased. Results: Our aim was to search for genetic footprints of Myanmar's geographic, historic and sociocultural characteristics and to contribute to the picture of human colonization by describing and dating of new mitochondrial DNA (mtDNA) haplogroups. Therefore, we sequenced the mtDNA control region of 327 unrelated donors and the complete mitochondrial genome of 44 selected individuals according to highest quality standards. Conclusion: Phylogenetic analyses of the entire mtDNA genomes uncovered eight new haplogroups and three unclassified basal M-lineages. The multi-ethnic population and the complex history of Myanmar were reflected in its mtDNA heterogeneity. Population genetic analyses of Burmese control region sequences combined with population data from neighboring countries revealed that the Myanmar haplogroup distribution showed a typical Southeast Asian pattern, but also Northeast Asian and Indian influences. The population structure of the extraordinarily diverse Bamar differed from that of the Karen people who displayed signs of genetic isolation. Migration analyses indicated a considerable genetic exchange with an overall positive migration balance from Myanmar to neighboring countries. Age estimates of the newly described haplogroups point to the existence of evolutionary windows where climatic and cultural changes gave rise to mitochondrial haplogroup diversification in Asia.

Alpha-synuclein (α-Syn) accumulation/aggregation and mitochondrial dysfunction play prominent roles in the pathology of Parkinson's disease. We have previously shown that postmortem human dopaminergic neurons from PD brains accumulate high levels of mitochondrial DNA (mtDNA) deletions. We now addressed the question, whether alterations in a component of the mitochondrial import machinery -TOM40- might contribute to the mitochondrial dysfunction and damage in PD. For this purpose, we studied levels of TOM40, mtDNA deletions, oxidative damage, energy production, and complexes of the respiratory chain in brain homogenates as well as in single neurons, using laser-capture-microdissection in transgenic mice overexpressing human wildtype α-Syn. Additionally, we used lentivirus-mediated stereotactic delivery of a component of this import machinery into mouse brain as a novel therapeutic strategy. We report here that TOM40 is significantly reduced in the brain of PD patients and in α-Syn transgenic mice. TOM40 deficits were associated with increased mtDNA deletions and oxidative DNA damage, and with decreased energy production and altered levels of complex I proteins in α-Syn transgenic mice. Lentiviral-mediated overexpression of Tom40 in α-Syn-transgenic mice brains ameliorated energy deficits as well as oxidative burden. Our results suggest that alterations in the mitochondrial protein transport machinery might contribute to mitochondrial impairment in α-Synucleinopathies.

Background: Deletions of the mitochondrial DNA (mtDNA) accumulate to high levels in dopaminergic neurons of the substantia nigra pars compacta (SNc) in normal aging and in patients with Parkinson's disease (PD). Human nigral neurons characteristically contain the pigment neuromelanin (NM), which is believed to alter the cellular redox-status. The impact of neuronal pigmentation, neurotransmitter status and brainstem location on the susceptibility to mtDNA damage remains unclear. We quantified mtDNA deletions (Delta mtDNA) in single pigmented and non-pigmented catecholaminergic, as well as non-catecholaminergic neurons of the human SNc, the ventral tegmental area (VTA) and the locus coeruleus (LC), using laser capture microdissection and single-cell real-time PCR. Results: In healthy aged individuals, Delta mtDNA levels were highest in pigmented catecholaminergic neurons (25.2 +/- 14.9%), followed by non-pigmented catecholamergic (18.0 +/- 11.2%) and non-catecholaminergic neurons (12.3 +/- 12.3%; p < 0.001). Within the catecholaminergic population, Delta mtDNA levels were highest in dopaminergic neurons of the SNc (33.9 +/- 21.6%) followed by dopaminergic neurons of the VTA (21.9 +/- 12.3%) and noradrenergic neurons of the LC (11.1 +/- 11.4%; p < 0.001). In PD patients, there was a trend to an elevated mutation load in surviving non-pigmented nigral neurons (27.13 +/- 16.73) compared to age-matched controls (19.15 +/- 11.06; p = 0.052), but levels where similar in pigmented nigral neurons of PD patients (41.62 +/- 19.61) and controls (41.80 +/- 22.62). Conclusions: Catecholaminergic brainstem neurons are differentially susceptible to mtDNA damage. Pigmented dopaminergic neurons of the SNc show the highest Delta mtDNA levels, possibly explaining the exceptional vulnerability of the nigro-striatal system in PD and aging. Although loss of pigmented noradrenergic LC neurons also is an early feature of PD pathology, mtDNA levels are not elevated in this nucleus in healthy controls. Thus, Delta mtDNA are neither an inevitable consequence of catecholamine metabolism nor a universal explanation for the regional vulnerability seen in PD.

Because of the widespread phenomenon of patrilocality, it is hypothesized that Y-chromosome variants tend to be more localized geographically than those of mitochondrial DNA ( mtDNA). Empirical evidence confirmatory to this hypothesis was subsequently provided among certain patrilocal and matrilocal groups of Thailand, which conforms to the isolation by distance mode of gene diffusion. However, we expect intuitively that the patterns of genetic variability may not be consistent with the above hypothesis among populations with different social norms governing the institution of marriage, particularly among those that adhere to strict endogamy rules. We test the universality of this hypothesis by analyzing Y-chromosome and mtDNA data in three different sets of Indian populations that follow endogamy rules to varying degrees. Our analysis of the Indian patrilocal and the matrilocal groups is not confirmatory to the sex- specific variation observed among the tribes of Thailand. Our results indicate spatial instability of the impact of different cultural processes on the genetic variability, resulting in the lack of universality of the hypothesized pattern of greater Y-chromosome variation when compared to that of mtDNA among the patrilocal populations.

Programmierter Zelltod oder Apoptose ist essentiell für die Entwicklung und Homöostase mehrzelliger Organismen. Störungen in der Regulierung dieser Prozesse können zu zahlreichen Erkrankungen führen, unter anderem zu Autoimmunerkrankungen und Krebs. In den letzten Jahren konnte in zahlreichen Arbeiten gezeigt werden, daß Mitochondrien eine wichtige Rolle bei der Steuerung der Apoptoseprozesse spielen. So wird Cytochrom c, ein Protein aus dem mitochondrialen Intermembranraum, durch einen pro-apoptotischen Stimulus als ein Caspase-Aktivierungsfaktor ins Cytosol freigesetzt. In der vorliegenden Arbeit wird die initiale Charakterisierung eines neuen murinen Proteins (mDAP-3) beschrieben. mDAP-3 wurde identifiziert bei dem Versuch molekulare Marker der Nierenentwicklung mit Hilfe einer modifizierten „differential display“ Polymerase Kettenreaktion zu finden. Die 1,7 kb große mDAP-3 mRNA kodiert für ein ca. 45 kDa großes Protein, das als funktionelles Motiv eine ATP/GTP-Bindungsstelle (P-Loop) besitzt. Die Analyse der Aminosäurensequenz von mDAP-3 ergab eine 81 %ige Identität zu dem humanen DAP-3 (Death Associated Protein 3), einem positiven Apoptose Mediator. Northern-Blot-Analyse von 20 µg Gesamt-RNA aus 11 Organen adulter Mäuse zeigte eine abundante mDAP-3 Expression in Niere, Herz, Leber, Thymus, Muskel, Milz, Darm und Bauch, mit einem Expressionsmaximum in Testis. Eine geringe bis fast fehlende Expression konnte in der Lunge und im Ovar gezeigt werden. Die Überexpression eines mDAP-3/EGFP Fusionproteins in murinen Mesangialzellen (MMC) führte zu einer Apoptoseinduktion bei 27,6% ± 2,6% (n=3) der Zellen gegenüber einer Apoptose Inzidenz von 11,9% ± 2,8% bei MMCs die mit einem Kontrollvektor transfiziert wurden. Die pro-apoptotische Funktion von mDAP-3 ist dabei abhängig von der Funktionalität des P-Loops. Die Überexpression eines P-Loop mutierten mDAP-3/EGFP Fusionproteins führte zu keiner Apoptoseinduktion. Sowohl das murine als auch das humane DAP-3 bleiben während der Apoptose intra-mitochondrial und werden nicht in das Cytosol freigesetzt. Für die Untersuchung der intrazellulären Lokalisation von mDAP-3 wurde ebenfalls das mDAP-3/EGFP-Fusionsprotein verwendet. Murine-Tubuluszellen (MTC) zeigten nach Transfektion mit dem Fusionsprotein ein punktiertes Signal im Fluoreszenz-Mikroskop. Im Gegensatz dazu zeigten Zellen nach Transfektion mit dem EGFP-Expressionsvektor alleine das für EGFP typische diffuse, zytosolische Fluoreszenzsignal. Sowohl im Fluoreszenz-Mikroskop als auch im konfokalen Laser-Scann-Mikroskop lokalisierte mDAP-3/EGFP zusammen mit einem mitochondrialen Farbstoff, jedoch nicht mit einem lysosomalen. Diese Ergebnisse weisen auf eine mitochondriale Lokalisation von mDAP-3 hin. Zellfraktionierungen bestätigten die mitochondriale Lokalisation von mDAP-3. Das endogene mDAP-3 Protein konnte nur in der mitochondrialen Fraktion, nicht jedoch in der endoplasmatischen Reticulum- oder der zytosolischen-Fraktion, nachgewiesen werden. Proteinase-K-Behandlung isolierter Mitochondrien führte zu keiner Reduktion der mDAP-3 Proteinmenge im Western-Blot. Dies ließ auf eine intra-mitochondriale Lokalisation von mDAP-3 schließen. Digitonin-Behandlung isolierter Mitochondrien zeigte eine Freisetzung von mDAP-3 aus den Mitochondrien bei relativ hohen Digitonin Konzentrationen (0,3%). Ganz im Gegensatz dazu wurde Cytochrom c bereits bei 0,075% Digitonin freigesetzt. Diese Daten weisen auf eine mDAP-3 Lokalisation in der mitochondrialen Matrix hin. Da die DAP-3 Proteinfamilie in Eukaryonten sehr konserviert ist und auch in nichtapoptotischen Organismen wie S. cerevisiae vertreten ist, muß DAP-3 eine weitere Funktion neben der pro-apoptotischen besitzen. Um die Rolle von DAP-3 näher zu definieren wurde eine Disruption des mDAP-3 Hefe-Orthologs YGL129c (yDAP-3) durchgeführt. Die yDAP-3 Nullmutanten zeigten keinen Wachstumsverlust auf nicht fermentierbaren Kohlenstoffquellen wie Glycerol oder Lactat. Dies deutet darauf hin, daß yDAP-3 für die mitochondriale Atmung nicht zwingend notwendig ist. Allerdings zeigten Hefen bei einer yDAP-3 Disruption einen signifikanten und progressiven Verlust ihrer mitochondrialen DNA (mtDNA) (46% in ∆yDAP-3 vs. 3% im Wildtyp). Dieser Verlust der mtDNA, der auf eine Funktion von yDAP- 3 für die mitochondriale Biogenese hinweist, ließ sich durch eine Transfektion der ∆yDAP-3 Hefen mit dem murinen DAP-3 teilweise verhindern. Damit konnte bewiesen werden, daß die Funktion, die DAP-3 für die Biogenese der Mitochondrien ausübt, unter Eukaryonten konserviert ist. Diese Daten identifizieren mDAP-3 als einen der ersten pro-apoptotischen Faktoren der mitochondrialen Matrix. Weiterhin kann eine duale Funktion für die Mitglieder der DAP-3 Proteinfamilie postuliert werden. Zum Einen spielen sie eine wichtige, evolutionär konservierte Rolle für die Biogenese von Mitochondrien, zum Anderen besitzen sie in mehrzelligen Organismen eine zusätzliche pro-apoptotische Funktion.