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Ann Gauger on betting against design

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She remembers her days as a biochemistry sophomore:

One day we were having a discussion about the marvelous things that were being found in biology. It was only a decade since the genetic code had been cracked, and the first DNA and the first protein had been sequenced. These were remarkable achievements. The development of the tools that made genetic engineering possible was happening there and then, at MIT at the time. I didn’t really realize how momentous it all was. One thing Dr. X said stuck in my brain. He said, “We will find marvelous things in biology because nature is very inventive. But one thing we will never find is a wheel.” Maybe he thought that the wheel was a manmade machine, smooth, round, and designed. Biology was made of bumpy, lumpy proteins and was most emphatically not designed. But I speculate. He never gave his reasoning Let us a have a moment of silence for such hubris, overturned so neatly by reality. Let me count the ways “unintelligent” nature has made circles, rotors, wheels, and gears

Ann Gauger, “Making Predictions Against Design” at Evolution News and Views

Someone should do a film, featuring just the wheels of life.

See also: Ann Gauger Talks About Adam And Eve With World Editor Marvin Olasky

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20 Replies to “Ann Gauger on betting against design

  1. 1
    OLV says:

    Jumping retroviruses nudge TADs apart

    Far from being junk DNA, the pervasive retrotransposons that populate the genome have a powerful capacity to influence genes and chromatin. A new study demonstrates how the transcription of one such element, HERV-H, can modify the higher-order 3D structure of chromatin during early primate development.

     
    Transcriptionally active HERV-H retrotransposons demarcate topologically associating domains in human pluripotent stem cells

    Chromatin architecture has been implicated in cell type-specific gene regulatory programs, yet how chromatin remodels during development remains to be fully elucidated. Here, by interrogating chromatin reorganization during human pluripotent stem cell (hPSC) differentiation, we discover a role for the primate-specific endogenous retrotransposon human endogenous retrovirus subfamily H (HERV-H) in creating topologically associating domains (TADs) in hPSCs. Deleting these HERV-H elements eliminates their corresponding TAD boundaries and reduces the transcription of upstream genes, while de novo insertion of HERV-H elements can introduce new TAD boundaries. The ability of HERV-H to create TAD boundaries depends on high transcription, as transcriptional repression of HERV-H elements prevents the formation of boundaries. This ability is not limited to hPSCs, as these actively transcribed HERV-H elements and their corresponding TAD boundaries also appear in pluripotent stem cells from other hominids but not in more distantly related species lacking HERV-H elements. Overall, our results provide direct evidence for retrotransposons in actively shaping cell type- and species-specific chromatin architecture.

     

     

     

     

  2. 2
    martin_r says:

    “We will find marvelous things in biology because nature is very inventive. But one thing we will never find is a wheel.”

    Nature is very inventive ? 🙂 ohh… these biologists…. these geniuses…

    I can’t believe that all this nonsense is still happening in 21st century …

    I like when a biologist talks about bad design or engineering…

    We will never find a wheel ? NO ?

    WHAT A SURPRISE :))

    What we found is much more advanced than a wheel….

    Moreover, with joint limbs you can access places you can’t with wheels (a biologist will never realize that, because a biologist never made anything … )

    Try to do the following with wheels:

    https://i.pinimg.com/originals/f4/65/ca/f465caf8a6dc3469b396ca9bb09d0206.jpg

    Or have a look at a cheetah … it can accelerate like a sports car, no wheels needed, no combustion engine needed … WHAT A DESIGN !!!

    and then comes a biologist along, and talks about bad design… a biologist who never made anything… what a biologist is good at, is inventing convincing just-so-stories about how very advanced designs self-assembled…

  3. 3
    martin_r says:

    now, who believes in miracles ?

    how many of you know, that a flagellum allegedly evolved at least 3 times independently ?

    Wikipedia:

    “The evolution of flagella is of great interest to biologists because the three known varieties of flagella (eukaryotic, bacterial, and archaeal) each represent a sophisticated cellular structure that requires the interaction of many different systems.”

    Bacterial flagellum
    Eubacterial flagellum
    Archaeal flagellum

    These 3 are not related, allegedly evolved independently…..

    now, who believes in miracles ?

    See my new blog for more miracles

    http://www.stuffhappens.info

  4. 4
    Bob O'H says:

    Yes, the flagellum is a rotary motor, but it isn’t a wheel, is it?

  5. 5
    ET says:

    A rotary motor is by far a better example of design than a wheel…

  6. 6
    OLV says:

    Martin_r,

    Thanks for your contributions.
    BTW, can you provide the link to your website again? Thanks.

  7. 7
    kairosfocus says:

    BO’H: a rotary motor is necessarily a wheel. It applies the wheel to the creation of rotary motion through a torque-generating mechanism; in turn, that imposes a host of geometric and moment of inertia constraints and linked symmetry issues — recall, why wheels on cars often required adding balance weights to counteract wobbling and vibration. Ponder the rate of revolution involved. KF

  8. 8
    bornagain77 says:

    As to:

    Gauger: Maybe he thought that the wheel was a manmade machine, smooth, round, and designed. (Maybe he thought) Biology was made of bumpy, lumpy proteins and was most emphatically not designed.

    Darwinists, because of their reductive materialistic framework, have falsely presupposed there to be far more ‘random thermodynamic jostling’ of the atoms and molecules in biology than there is actually turning out to be.

    In fact, Darwinists have tried to directly undermine the inference to Intelligent Design by appealing to their false presupposition of pervasive ‘random thermodynamic jostling’ of atoms and molecules in cells:

    In 2006 Harvard University, via a production company called “BioVisions”, made a video entitled The Inner Life of the Cell

    The Inner Life of the Cell
    http://www.xvivo.net/animation.....-the-cell/

    The video by Harvard BioVisions was one of the first videos on the web that animated some of the amazing molecular machines that are now being found in cells.
    As you can see, the overwhelming impression of the intelligent design of the cell literally leaps out of the video at you. Since the Intelligent Design of the cell is readily apparent for all to see, Dr. William Dembski, one of the pioneers of the Intelligent Design movement, would, circa 2007, show the video in some of his talks to students on Intelligent Design:

    Inner Life of a Cell w William Dembski commentary – video
    https://www.youtube.com/watch?v=jNs5kBE66Xo

    When Harvard BioVisions found out about Dr. Dembski using the video in his lectures to his students they ‘warned him’ not to use the video anymore.

    William A. Dembski
    Excerpt: The Inner Life of the Cell copyright controversy,,
    David Bolinsky, creator of the video, wrote that Dembski was warned about using the video without permission,,,
    https://en.wikipedia.org/wiki/William_A._Dembski

    Their effort to stop Dembski was futile since the video soon went viral on the web and anyone with access to a computer could download the video and watch it whenever they wanted to, and see for themselves the amazing design that is readily apparent in the cell.

    The Darwinists at Harvard Biovisions who had originally made the video apparently did not like this development one bit. And in 2013, apparently trying to undo the damage that was done to Darwinian thinking by their original video, Harvard BioVisions then made a subsequent video entitled ‘Inner Life of the Cell: Protein Packing’.

    In 2013, we released The Inner Life of the Cell: Protein Packing, which illustrates the crowded molecular environment present in cells.
    http://www.xvivo.net/animation.....-the-cell/

    In the 2013 video, as you can see, Harvard Biovisions tried to make the inner workings of the cell look as random, chaotic, and haphazard as possible so as to try to dispel any impression of design in the cell that they had inadvertently created in their first video.

    Inner Life of a Cell | Protein Packing
    https://www.youtube.com/watch?v=uHeTQLNFTgU

    In fact, in 2014 New York Times itself ran an article on the ‘Protein Packing’ video. I’m sure many ID advocates wish they could get such free promotion for their videos on intelligent design in the New York Times. But anyways, in the article Carl Zimmer stated that ‘ “In the 2006 version, we can’t help seeing intention in the smooth movements of the molecules” but of the 2013 video he said that the molecules of the cell ‘flail blindly in the crowd.” And that “Our cells work almost in spite of themselves.’

    Watch Proteins Do the Jitterbug – Carl Zimmer – APRIL 10, 2014
    Excerpt: In the 2006 version, we can’t help seeing intention in the smooth movements of the molecules; it’s as if they’re trying to get from one place to another. In reality, however, the parts of our cells don’t operate with the precise movements of the springs and gears of a clock. They flail blindly in the crowd. Our cells work almost in spite of themselves.
    https://www.nytimes.com/2014/04/10/science/watch-proteins-do-the-jitterbug.html

    Yet, regardless of their overt bias against anyone daring to see Intelligent Design in the cell, the fact of the matter is that we now have several lines of empirical evidence firmly establishing the fact that the cell is not nearly as random and haphazard in its makeup as Darwinists would prefer people to believe

    For instance, in the following article from 2014, Dr Jonathan Wells takes direct issue with Carl Zimmer’s claim that biological molecules are ‘flailing blindly in the crowd’ and states,, But that’s not what the biological evidence shows. In fact, kinesin moves quickly, with precise movements, to get from one place to another,,,

    Flailing Blindly: The Pseudoscience of Josh Rosenau and Carl Zimmer – Jonathan Wells – April 17, 2014
    Excerpt: The new animation (like the old) also includes a kinesin molecule hauling a vesicle, but this time the kinesin’s movements are characterized (in Zimmer’s words) by
    “barely constrained randomness. Every now and then, a tiny molecule loaded with fuel binds to one of the kinesin “feet.” It delivers a jolt of energy, causing that foot to leap off the molecular cable and flail wildly, pulling hard on the foot that’s still anchored. Eventually, the gyrating foot stumbles into contact again with the cable, locking on once more — and advancing the vesicle a tiny step forward. This updated movie offers a better way to picture our most intricate inner workings…. In the 2006 version, we can’t help seeing intention in the smooth movements of the molecules; it’s as if they’re trying to get from one place to another. In reality, however, the parts of our cells don’t operate with the precise movements of the springs and gears of a clock. They flail blindly in the crowd.”
    But that’s not what the biological evidence shows. In fact, kinesin moves quickly, with precise movements, to get from one place to another. A kinesin molecule takes one 8-nanometer “step” along a microtubule for every high-energy ATP molecule it uses, and it uses about 80 ATPs per second. On the scale of a living cell, this movement is very fast. To visualize it on a macroscopic scale, imagine a microtubule as a one-lane road and the kinesin molecule as an automobile. The kinesin would be traveling over 200 miles per hour!
    https://iconsofevolution.com/flailing-blindly/

    Moreover, in the following 2016 paper, it was found that “crowding in cells doesn’t hamper protein binding as much as they thought it did.” In fact, finding a lack of ‘collisions’ in the crowded cell was a ‘counterintuitive surprise’ for the researchers: Specifically one of the researchers stated: “This was a surprise,” “It’s counterintuitive, because one would think collisions between a protein and other molecules on DNA would slow it down. But the system is so dynamic, it doesn’t appear to be an issue.”

    Proteins put up with the roar of the crowd – June 23, 2016
    Excerpt: It gets mighty crowded around your DNA, but don’t worry: According to Rice University researchers, your proteins are nimble enough to find what they need.
    Rice theoretical scientists studying the mechanisms of protein-DNA interactions in live cells showed that crowding in cells doesn’t hamper protein binding as much as they thought it did.,,,
    If DNA can be likened to a library, it surely is a busy one. Molecules roam everywhere, floating in the cytoplasm and sticking to the tightly wound double helix. “People know that almost 90 percent of DNA is covered with proteins, such as polymerases, nucleosomes that compact two meters into one micron, and other protein molecules,” Kolomeisky said.,,,
    That makes it seem that proteins sliding along the strand would have a tough time binding, and it’s possible they sometimes get blocked. But the Rice team’s theory and simulations indicated that crowding agents usually move just as rapidly, sprinting out of the way.
    “If they move at the same speed, the molecules don’t bother each other,” Kolomeisky said. “Even if they’re covering a region, the blockers move away quickly so your protein can bind.”
    In previous research, the team determined that stationary obstacles sometimes help quicken a protein’s search for its target by limiting options. This time, the researchers sought to define how crowding both along DNA and in the cytoplasm influenced the process.
    “We may think everything’s fixed and frozen in cells, but it’s not,” Kolomeisky said. “Everything is moving.”,,,
    Floating proteins appear to find their targets quickly as well. “This was a surprise,” he said. “It’s counterintuitive, because one would think collisions between a protein and other molecules on DNA would slow it down. But the system is so dynamic, it doesn’t appear to be an issue.”
    http://phys.org/news/2016-06-p.....crowd.html

    In fact, instead of a biological systems being “dominated by randomly colliding individual protein molecules”, the fact of the matter is that biological systems are now shown to be extremely resistant to random background noise. As the following article on photosynthesis stated, ‘These biological systems can direct a quantum process,,, in astoundingly subtle and controlled ways – showing remarkable resistance to the aggressive, random background noise of biology and extreme environments.’

    Unlocking nature’s quantum engineering for efficient solar energy – January 7, 2013
    Excerpt: Certain biological systems living in low light environments have unique protein structures for photosynthesis that use quantum dynamics to convert 100% of absorbed light into electrical charge,,,
    “Some of the key issues in current solar cell technologies appear to have been elegantly and rigorously solved by the molecular architecture of these PPCs – namely the rapid, lossless transfer of excitons to reaction centres.”,,,
    These biological systems can direct a quantum process, in this case energy transport, in astoundingly subtle and controlled ways – showing remarkable resistance to the aggressive, random background noise of biology and extreme environments. “This new understanding of how to maintain coherence in excitons, and even regenerate it through molecular vibrations, provides a fascinating glimpse into the intricate design solutions – seemingly including quantum engineering – ,,, and which could provide the inspiration for new types of room temperature quantum devices.”
    http://phys.org/news/2013-01-n.....nergy.html

  9. 9
    bornagain77 says:

    Likewise the following article on human vision stated that, “Research,, has shown that humans can detect the presence of a single photon, the smallest measurable unit of light”.,,, “it is remarkable: a photon, the smallest physical entity with quantum properties of which light consists, is interacting with a biological system consisting of billions of cells, all in a warm and wet environment,”,, and the researched added, “The response that the photon generates survives all the way to the level of our awareness despite the ubiquitous background noise. Any man-made detector would need to be cooled and isolated from noise to behave the same way.”,,, “What we want to know next is how does a biological system achieve such sensitivity? How does it achieve this in the presence of noise?”

    Study suggests humans can detect even the smallest units of light – July 21, 2016
    Excerpt: Research,, has shown that humans can detect the presence of a single photon, the smallest measurable unit of light. Previous studies had established that human subjects acclimated to the dark were capable only of reporting flashes of five to seven photons.,,,
    it is remarkable: a photon, the smallest physical entity with quantum properties of which light consists, is interacting with a biological system consisting of billions of cells, all in a warm and wet environment,” says Vaziri. “The response that the photon generates survives all the way to the level of our awareness despite the ubiquitous background noise. Any man-made detector would need to be cooled and isolated from noise to behave the same way.”,,,
    The gathered data from more than 30,000 trials demonstrated that humans can indeed detect a single photon incident on their eye with a probability significantly above chance.
    “What we want to know next is how does a biological system achieve such sensitivity? How does it achieve this in the presence of noise?”
    http://phys.org/news/2016-07-humans-smallest.html

    Moreover, in direct contradiction to Carl Zimmer’s claim of molecules flailing blindly in a crowd, in the following article subtitled ‘how bio-molecular machines can generate nontrivial quantum states’, the authors state that entanglement can be maintained even in the presence of very intense noise,

    Persistent dynamic entanglement from classical motion: how bio-molecular machines can generate nontrivial quantum states
    Gian Giacomo Guerreschi, Jianming Cai1, Sandu Popescu and Hans J Briegel
    Published 29 May 2012
    Excerpt: Very recently (Cai et al 2010 Phys. Rev. E 82 021921), a simple mechanism was presented by which a molecule subjected to forced oscillations, out of thermal equilibrium, can maintain quantum entanglement between two of its quantum degrees of freedom. Crucially, entanglement can be maintained even in the presence of very intense noise, so intense that no entanglement is possible when the forced oscillations cease. This mechanism may allow for the presence of nontrivial quantum entanglement in biological systems. Here we significantly enlarge the study of this model. In particular, we show that the persistent generation of dynamic entanglement is not restricted to the bosonic heat bath model, but can also be observed in other decoherence models, e.g. the spin gas model, and in non-Markovian scenarios. We also show how conformational changes can be used by an elementary machine to generate entanglement even in unfavorable conditions. In biological systems, similar mechanisms could be exploited by more complex molecular machines or motors.
    http://iopscience.iop.org/arti.....53043/meta

    And in the following article, the authors even go on to state that ‘this reverses the previous orthodoxy, which held that quantum effects could not exist in biological systems because of the amount of noise in these systems’,,, Environmental noise here drives a persistent and cyclic generation of new entanglement.

    Quantum entanglement in hot systems
    Excerpt: The authors remark that this reverses the previous orthodoxy, which held that quantum effects could not exist in biological systems because of the amount of noise in these systems,,,
    Environmental noise here drives a persistent and cyclic generation of new entanglement.
    http://quantum-mind.co.uk/quan.....t-systems/

    Thus instead of the molecular machines of the cell being dominated by random noise in the cell, as Carl Zimmer had falsely claimed in his New York Times article, the molecular machines of the cell are instead shown to have ‘remarkable resistance to the aggressive, random background noise of biology and extreme environments.’ Moreover, molecular machines are apparently designed in such an ingenious way so as to feed off the random noise in the cell. Quote unquote, “Environmental noise here drives a persistent and cyclic generation of new entanglement.”

    Moreover, in the following microscopic pictures of the bacterial flagellum, you can see for yourself that the molecular machines of a cell are not nearly as chaotic and haphazard looking as Harvard’s ‘Protein Packing’ video had falsely tried to portray them to be.

    Electron Microscope Photograph of Flagellum Hook-Basal Body
    http://www.skeptic.com/eskepti.....gure03.jpg

    Bacterial Flagellum: Visualizing the Complete Machine In Situ
    Excerpt: Electron tomography of frozen-hydrated bacteria, combined with single particle averaging, has produced stunning images of the intact bacterial flagellum, revealing features of the rotor, stator and export apparatus.
    http://www.sciencedirect.com/s.....220602286X

    Even the protein molecules themselves that make up the building blocks of the molecular machines of the cell do not find their final folded form by the supposed random collision of particles within the cell. As the following article states, “when one calculates the number of possible topological (rotational) configurations for the amino acids in even a small (say, 100 residue) unfolded protein, random search could never find the final folded conformation of that same protein during the lifetime of the physical universe.”

    The Humpty-Dumpty Effect: A Revolutionary Paper with Far-Reaching Implications – Paul Nelson – October 23, 2012
    Excerpt: Anyone who has studied the protein folding problem will have met the famous Levinthal paradox, formulated in 1969 by the molecular biologist Cyrus Levinthal. Put simply, the Levinthal paradox states that when one calculates the number of possible topological (rotational) configurations for the amino acids in even a small (say, 100 residue) unfolded protein, random search could never find the final folded conformation of that same protein during the lifetime of the physical universe. Therefore, concluded Levinthal, given that proteins obviously do fold, they are doing so, not by random search, but by following favored pathways. The challenge of the protein folding problem is to learn what those pathways are.
    http://www.evolutionnews.org/2.....65521.html

    And yet, proteins obviously do not take the lifetime of the universe to randomly find their final folded form. In fact, most small proteins fold,, ‘on a millisecond or even microsecond time scale.’

    Levinthal’s paradox
    Excerpt: The “paradox” is that most small proteins fold spontaneously on a millisecond or even microsecond time scale.
    https://en.wikipedia.org/wiki/Levinthal%27s_paradox

    Thus however proteins themselves may be managing to find their final folded form, they obviously are not being hampered in any significant way by any random noise that may be present in the cell.

    In fact, in the following article, the authors found that the long standing mystery of exactly how a protein is able to find its final folded form so quickly can be easily explained if protein folding is allowed to be a “quantum affair” where the “protein could ‘jump’ from one shape to another without necessarily forming the shapes in between.”,,,.

    Physicists Discover Quantum Law of Protein Folding – February 22, 2011
    Quantum mechanics finally explains why protein folding depends on temperature in such a strange way.
    Excerpt: First, a little background on protein folding. Proteins are long chains of amino acids that become biologically active only when they fold into specific, highly complex shapes. The puzzle is how proteins do this so quickly when they have so many possible configurations to choose from.
    To put this in perspective, a relatively small protein of only 100 amino acids can take some 10^100 different configurations. If it tried these shapes at the rate of 100 billion a second, it would take longer than the age of the universe to find the correct one. Just how these molecules do the job in nanoseconds, nobody knows.,,,
    Today, Luo and Lo say these curves can be easily explained if the process of folding is a quantum affair. By conventional thinking, a chain of amino acids can only change from one shape to another by mechanically passing through various shapes in between.
    But Luo and Lo say that if this process were a quantum one, the shape could change by quantum transition, meaning that the protein could ‘jump’ from one shape to another without necessarily forming the shapes in between.,,,
    Their astonishing result is that this quantum transition model fits the folding curves of 15 different proteins and even explains the difference in folding and unfolding rates of the same proteins.
    That’s a significant breakthrough. Luo and Lo’s equations amount to the first universal laws of protein folding. That’s the equivalent in biology to something like the thermodynamic laws in physics.
    http://www.technologyreview.co.....f-protein/

    Moreover, the following 2015 article experimentally confirmed that proteins are indeed based on quantum principles. More specifically, the following study observed that quantum processes “concentrate all of the vibrational energy in a biological protein into its lowest-frequency vibrational mode.”

    Quantum coherent-like state observed in a biological protein for the first time – October 13, 2015
    Excerpt: If you take certain atoms and make them almost as cold as they possibly can be, the atoms will fuse into a collective low-energy quantum state called a Bose-Einstein condensate. In 1968 physicist Herbert Fröhlich predicted that a similar process at a much higher temperature could concentrate all of the vibrational energy in a biological protein into its lowest-frequency vibrational mode. Now scientists in Sweden and Germany have the first experimental evidence of such so-called Fröhlich condensation (in proteins).,,,
    The real-world support for Fröhlich’s theory (for proteins) took so long to obtain because of the technical challenges of the experiment, Katona said.
    http://phys.org/news/2015-10-q.....otein.html

  10. 10
    bornagain77 says:

    And in the following more recent 2015 paper entitled, “Quantum criticality in a wide range of important biomolecules” it was found that “Most of the molecules taking part actively in biochemical processes are tuned exactly to the transition point and are critical conductors,” and the researchers further commented that “finding even one (biomolecule) that is in the quantum critical state by accident is mind-bogglingly small and, to all intents and purposes, impossible.,, of the order of 10^-50 of possible small biomolecules and even less for proteins,”,,,

    Quantum criticality in a wide range of important biomolecules – Mar. 6, 2015
    Excerpt: “Most of the molecules taking part actively in biochemical processes are tuned exactly to the transition point and are critical conductors,” they say.
    That’s a discovery that is as important as it is unexpected. “These findings suggest an entirely new and universal mechanism of conductance in biology very different from the one used in electrical circuits.”
    The permutations of possible energy levels of biomolecules is huge so the possibility of finding even one (biomolecule) that is in the quantum critical state by accident is mind-bogglingly small and, to all intents and purposes, impossible.,, of the order of 10^-50 of possible small biomolecules and even less for proteins,”,,,
    “what exactly is the advantage that criticality confers?”
    https://medium.com/the-physics-arxiv-blog/the-origin-of-life-and-the-hidden-role-of-quantum-criticality-ca4707924552

    And as the follow up article stated, “There is no obvious evolutionary reason why a protein should evolve toward a quantum-critical state, and there is no chance at all that the state could occur randomly.,,,”

    Quantum Critical Proteins – Stuart Lindsay – Professor of Physics and Chemistry at Arizona State University – 2018
    Excerpt: The difficulty with this proposal lies in its improbability. Only an infinitesimal density of random states exists near the critical point.,,
    Gábor Vattay et al. recently examined a number of proteins and conducting and insulating polymers.14 The distribution for the insulators and conductors were as expected, but the functional proteins all fell on the quantum-critical distribution. Such a result cannot be a consequence of chance.,,,
    WHAT OF quantum criticality? Vattay et al. carried out electronic structure calculations for the very large protein used in our work. They found that the distribution of energy-level spacings fell on exactly the quantum-critical distribution, implying that this protein is also quantum critical. There is no obvious evolutionary reason why a protein should evolve toward a quantum-critical state, and there is no chance at all that the state could occur randomly.,,,
    http://inference-review.com/ar.....l-proteins
    Gábor Vattay et al., “Quantum Criticality at the Origin of Life,” Journal of Physics: Conference Series 626 (2015);
    Gábor Vattay, Stuart Kauffman, and Samuli Niiranen, “Quantum Biology on the Edge of Quantum Chaos,” PLOS One 9, no. 3 (2014)

    Here are a few more factoids, besides Quantum criticallity and/or quantum coherence, that show us that cells are far more ‘in tune’ with the vibrations of the cell than the simplistic Darwinian model of cells being dominated by random noise::

    Symphony of Life, Revealed: New Imaging Technique Captures Vibrations of Proteins, Tiny Motions Critical to Human Life – Jan. 16, 2014
    Excerpt: To observe the protein vibrations, Markelz’ team relied on an interesting characteristic of proteins: The fact that they vibrate at the same frequency as the light they absorb.
    This is analogous to the way wine glasses tremble and shatter when a singer hits exactly the right note. Markelz explained: Wine glasses vibrate because they are absorbing the energy of sound waves, and the shape of a glass determines what pitches of sound it can absorb. Similarly, proteins with different structures will absorb and vibrate in response to light of different frequencies.
    So, to study vibrations in lysozyme, Markelz and her colleagues exposed a sample to light of different frequencies and polarizations, and measured the types of light the protein absorbed.
    This technique, , allowed the team to identify which sections of the protein vibrated under normal biological conditions. The researchers were also able to see that the vibrations endured over time, challenging existing assumptions.
    “If you tap on a bell, it rings for some time, and with a sound that is specific to the bell. This is how the proteins behave,” Markelz said. “Many scientists have previously thought a protein is more like a wet sponge than a bell: If you tap on a wet sponge, you don’t get any sustained sound.”
    http://www.sciencedaily.com/re.....084838.htm

    The Puzzling Role Of Biophotons In The Brain – Dec. 17, 2010
    Excerpt: In recent years, a growing body of evidence shows that photons play an important role in the basic functioning of cells. Most of this evidence comes from turning the lights off and counting the number of photons that cells produce. It turns out, much to many people’s surprise, that many cells, perhaps even most, emit light as they work.
    In fact, it looks very much as if many cells use light to communicate. There’s certainly evidence that bacteria, plants and even kidney cells communicate in this way. Various groups have even shown that rats brains are literally alight thanks to the photons produced by neurons as they work.,,,
    ,,, earlier this year, one group showed that spinal neurons in rats can actually conduct light.
    ,, Rahnama and co point out that neurons contain many light sensitive molecules, such as porphyrin rings, flavinic, pyridinic rings, lipid chromophores and aromatic amino acids. In particular, mitochondria, the machines inside cells which produce energy, contain several prominent chromophores.
    The presence of light sensitive molecules makes it hard to imagine how they might not be not influenced by biophotons.,,,
    They go on to suggest that the light channelled by microtubules can help to co-ordinate activities in different parts of the brain. It’s certainly true that electrical activity in the brain is synchronised over distances that cannot be easily explained. Electrical signals travel too slowly to do this job, so something else must be at work.,,,
    (So) It’s a big jump to assume that photons do this job.
    http://www.technologyreview.co.....the-brain/

    Thus, although Darwinists, because of their reductive materialistic framework, are forced to believe that the cell is dominated by random thermodynamic jostling of atoms and molecules, the reality of the situation is, once again, turning out to be far different that what they presupposed.

    Supplemental note

    Darwinian Materialism vs. Quantum Biology – Part II – video
    https://www.youtube.com/watch?v=oSig2CsjKbg

  11. 11
    Axel says:

    ‘what a biologist is good at, is inventing convincing just-so-stories about how very advanced designs self-assembled…’
    That’s cruel, Martin_r, but bizarre, in that it desperately needs to be said – like so such else of thier fantasy world. That one fatal assumption, to which they pin everthing, dooms their thought-processes to eternal ridicule. Logic, like God, is not mocked.

  12. 12
    martin_r says:

    OVL

    the link to my blog is

    http://www.stuffhappens.info

  13. 13
    OLV says:

    Martin_r,

    Got it. I like it. Thanks.

  14. 14
    OLV says:

    This was published 13 years ago:

    Imaging the choreography of lymphocyte trafficking and the immune response
    Michael D. Cahalan, Ian Parker
    Current Opinion in Immunology

    Volume 18, Issue 4, August 2006, Pages 476-482
    DOI: 10.1016/j.coi.2006.05.013

    The functioning of the immune system depends upon exquisitely choreographed interactions between its cellular constituents.

     It is clear that the next few years will bring a new level of complexity to our understanding of the cellular choreography between visitors and permanent residents within the lymph node and numerous other tissues.

    This was more recently:

    Structure and function of the immune system in the spleen

    Steven M. Lewis, Adam Williams and Stephanie C. Eisenbarth

    Science Immunology Vol. 4, Issue 33, eaau6085
    DOI: 10.1126/sciimmunol.aau6085

    The spleen is the largest secondary lymphoid organ in the body and, as such, hosts a wide range of immunologic functions alongside its roles in hematopoiesis and red blood cell clearance. The physical organization of the spleen allows it to filter blood of pathogens and abnormal cells and facilitate low-probability interactions between antigen-presenting cells (APCs) and cognate lymphocytes. APCs specific to the spleen regulate the T and B cell response to these antigenic targets in the blood. This review will focus on cell types, cell organization, and immunologic functions specific to the spleen and how these affect initiation of adaptive immunity to systemic blood-borne antigens. Potential differences in structure and function between mouse and human spleen will also be discussed.

     

  15. 15
    OLV says:

    Non-canonical B cell functions in transplantation

    Jeffrey L. Platt, Marilia Cascalho

    DOI: 10.1016/j.humimm.2019.04.006

    B cells are differentiated to recognize antigen and respond by producing antibodies. These activities, governed by recognition of ancillary signals, defend the individual against microorganisms and the products of microorganisms and constitute the canonical function of B cells. Despite the unique differentiation (e.g. recombination and mutation of immunoglobulin gene segments) toward this canonical function, B cells can provide other, “non-canonical” functions, such as facilitating of lymphoid organogenesis and remodeling and fashioning T cell repertoires and modifying T cell responses. Some non-canonical functions are exerted by antibodies, but most are mediated by other products and/or direct actions of B cells. The diverse set of non-canonical functions makes the B cell as much as any cell a central organizer of innate and adaptive immunity. However, the diverse products and actions also confound efforts to weigh the importance of individual non-canonical B cell functions. Here we shall describe the non-canonical functions of B cells and offer our perspective on how those functions converge in the development and governance of immunity, particularly immunity to transplants, and hurdles to advancing understanding of B cell functions in transplantation.

    B-1 cell responses to infections
    Smith FL, Baumgarth N

    Current Opinion in Immunology
    DOI: 10.1016/j.coi.2018.12.001
    Volume 57, April 2019, Pages 23-31

    B-1 cells represent an innate-like early-developing B cell population, whose existence as an independent lymphocyte subset has been questioned in the past. Recent molecular and lineage tracing studies have not only confirmed their unique origins and differentiation paths, they have also provided a rationale for their distinctive functionalities compared to conventional B cells. This review summarizes our current understanding of B-1 cell development, and the activation events that regulate B-1 cell responses to self and foreign antigens. We discuss the unresolved question to what extent BCR engagement, that is, antigen-specificity versus innate signaling contributes to B-1 cell’s participation in tissue homeostasis and immune defense as providers of ‘natural’ and antigen-induced antibody responses, and as cytokine-producing immune regulators.

  16. 16
    OLV says:

    B cell receptor and Toll-like receptor signaling coordinate to control distinct B-1 responses to both self and the microbiota
    Lieselotte SM Kreuk, Meghan A Koch, Leianna C Slayden, Nicholas A Lind, Sophia Chu, Hannah P Savage, Aaron B Kantor, Nicole Baumgarth, Gregory M Barton 

    doi: 10.7554/eLife.47015

    eLife. 2019; 8: e47015.

    B-1a cells play an important role in mediating tissue homeostasis and protecting against infections. They are the main producers of ‘natural’ IgM, spontaneously secreted serum antibodies predominately reactive to self antigens, like phosphatidylcholine (PtC), or antigens expressed by the intestinal microbiota. The mechanisms that regulate the B-1a immunoglobulin (Ig) repertoire and their antibody secretion remain poorly understood. Here, we use a novel reporter mouse to demonstrate that production of self- and microbiota-reactive antibodies is linked to BCR signaling in B-1a cells. Moreover, we show that Toll-like receptors (TLRs) are critical for shaping the Ig repertoire of B-1a cells as well as regulating their antibody production. Strikingly, we find that both the colonization of a microbiota as well as microbial-sensing TLRs are required for anti-microbiota B-1a responses, whereas nucleic-acid sensing TLRs are required for anti-PtC responses, demonstrating that linked activation of BCR and TLRs controls steady state B-1a responses to both self and microbiota-derived antigens.

  17. 17
    OLV says:

    Where’s the “evo” in evo-devo?

    Molecular and cellular mechanisms underlying the evolution of form and function in the amniote jaw

    The amniote jaw complex is a remarkable amalgamation of derivatives from distinct embryonic cell lineages. During development, the cells in these lineages experience concerted movements, migrations, and signaling interactions that take them from their initial origins to their final destinations and imbue their derivatives with aspects of form including their axial orientation, anatomical identity, size, and shape. Perturbations along the way can produce defects and disease, but also generate the variation necessary for jaw evolution and adaptation. We focus on molecular and cellular mechanisms that regulate form in the amniote jaw complex, and that enable structural and functional integration. Special emphasis is placed on the role of cranial neural crest mesenchyme (NCM) during the species-specific patterning of bone, cartilage, tendon, muscle, and other jaw tissues. We also address the effects of biomechanical forces during jaw development and discuss ways in which certain molecular and cellular responses add adaptive and evolutionary plasticity to jaw morphology. Overall, we highlight how variation in molecular and cellular programs can promote the phenomenal diversity and functional morphology achieved during amniote jaw evolution or lead to the range of jaw defects and disease that affect the human condition.

    Conclusion

    In 1916, E.S. Russell posed the question in his now classic book, Form and Function[18], “Is function the mechanical result of form, or is form merely the manifestation of function or activity? What is the essence of life, organisation or activity? (p.v).” A broad range of experimental strategies across different model systems have revealed that NCM is an essential player in most, if not all, of the decisive events that generate the primary organization of the amniote jaw complex. NCM not only provides the raw materials for the cartilages, bones, and other essential components that comprise the jaws, but NCM is also required for the critical signaling interactions that imbue these tissues with the multidimensional aspects of patterning from which their form is derived. Deficiencies in NCM or perturbing these interactions on the molecular or cellular level alters the form of the jaw complex in profound ways, which illuminates why the jaw complex is both highly evolvable and extremely susceptible to developmental defects [164]. Moreover, while NCM and neighboring epithelia typically collaborate to pattern the cartilages and bones of the jaws, and while NCM and mesodermal mesenchyme work together to pattern the jaw muscles, NCM seems to act as the dominant source of information that gives all of these jaw structures their species-specific size and shape. In this role, NCM is the common denominator that underlies the structural integration of the jaw apparatus, generates species-specific variation, and likely serves as a responsive target of natural selection during evolution [737138140191]. Moreover, NCM has augmented the evolutionary potential (i.e., adaptability) of the pharyngeal and rostral portions of the head and imparts the jaw skeleton with developmental plasticity, as evidenced by the ability of the NCM-derived skeleton to respond to mechanical forces like in the case of secondary cartilage. Initially, the form of the jaw appears to dictate function, but then through embryonic motility, function modulates form. In other words, NCM sets up the species-specific “organisation” of the jaw apparatus prior to the onset of muscle “activity.” But once jaw activity starts, the form of the skeleton adapts to support its functional needs. The species-specific form of the duck jaw apparatus, especially the geometry of the NCM-mediated muscle attachments, produces mechanical forces that differentially regulate FGF and TGF? signaling and cause secondary cartilage to form on the coronoid process. In this regard, NCM not only mediates form but also helps shape the biomechanical environment. Additionally, the patterning abilities and plasticity found in NCM-derived jaw progenitors facilitate seamless integration of form and function during embryonic development and evolution. These same processes are likely perturbed in cases of injury or disease. Overall, elucidating the molecular and cellular mechanisms through which NCM governs the species-specific patterning of cartilage, bone, tendon, and muscle has shed light on the evolutionary integration of form and function in the amniote jaw complex, and in the near future could help remedy an unmet clinical need to repair and regenerate jaw tissues affected by birth defects, disease, or injury.

     
    Conserved gene signalling and a derived patterning mechanism underlie the development of avian footpad scales
     
    Abstract

    Background
    Vertebrates possess a diverse range of integumentary epithelial appendages, including scales, feathers and hair. These structures share extensive early developmental homology, as they mostly originate from a conserved anatomical placode. In the context of avian epithelial appendages, feathers and scutate scales are known to develop from an anatomical placode. However, our understanding of avian reticulate (footpad) scale development remains unclear.
    Results
    Here, we demonstrate that reticulate scales develop from restricted circular domains of thickened epithelium, with localised conserved gene expression in both the epithelium and underlying mesenchyme. These domains constitute either anatomical placodes, or circular initiatory fields (comparable to the avian feather tract). Subsequent patterning of reticulate scales is consistent with reaction–diffusion (RD) simulation, whereby this primary domain subdivides into smaller secondary units, which produce individual scales. In contrast, the footpad scales of a squamate model (the bearded dragon, Pogona vitticeps) develop synchronously across the ventral footpad surface.
    Conclusions
    Widely conserved gene signalling underlies the initial development of avian reticulate scales. However, their subsequent patterning is distinct from the footpad scale patterning of a squamate model, and the feather and scutate scale patterning of birds. Therefore, we suggest reticulate scales are a comparatively derived epithelial appendage, patterned through a modified RD system.

    Conclusion

    Overall, we demonstrate that the development of avian epithelial appendages, including feathers, scutate and reticulate scales, is regulated by the signalling of conserved developmental genes. During reticulate scale development, circular domains of localised gene expression are observed along the ventral footpad at E10.5, constituting either anatomical placodes or circular initiatory fields. These domains subsequently subdivide into individual reticulate scales, following a patterning mechanism consistent with RD simulation. This is distinct from the patterning of squamate (P. vitticeps) ventral footpad scales. Therefore, we suggest that reticulate scales are derived epithelial appendages patterned through a modified RD system.

    Unravelling the genes forming the wing pattern supergene in the polymorphic butterfly Heliconius numata
     
    Abstract

    Background
    Unravelling the genetic basis of polymorphic characters is central to our understanding of the origins and diversification of living organisms. Recently, supergenes have been implicated in a wide range of complex polymorphisms, from adaptive colouration in butterflies and fish to reproductive strategies in birds and plants. The concept of a supergene is now a hot topic in biology, and identification of its functional elements is needed to shed light on the evolution of highly divergent adaptive traits. Here, we apply different gene expression analyses to study the supergene P that controls polymorphism of mimetic wing colour patterns in the neotropical butterfly Heliconius numata.
    Results
    We performed de novo transcriptome assembly and differential expression analyses using high-throughput Illumina RNA sequencing on developing wing discs of different H. numata morphs. Within the P interval, 30 and 17 of the 191 transcripts were expressed differentially in prepupae and day-1 pupae, respectively. Among these is the gene cortex, known to play a role in wing pattern formation in Heliconius and other Lepidoptera. Our in situ hybridization experiments confirmed the relationship between cortex expression and adult wing patterns.
    Conclusion
    This study found the majority of genes in the P interval to be expressed in the developing wing discs during the critical stages of colour pattern formation, and detect drastic changes in expression patterns in multiple genes associated with structural variants. The patterns of expression of cortex only partially recapitulate the variation in adult phenotype, suggesting that the remaining phenotypic variation could be controlled by other genes within the P interval. Although functional studies on cortex are now needed to determine its exact developmental role, our results are in accordance with the classical supergene hypothesis, whereby several genes inherited together due to tight linkage control a major developmental switch.

     
    Conclusions

    Here, we developed the first transcriptome resource for H. numata and performed differential expression analyses during wing development to identify genes involved in forming the supergene and contributing to the expression of differentiated phenotypes. Our analyses confirm the role of cortex in the formation of black wing pattern elements. Our results are consistent with the hypothesis that other genes in the P region may play a role in colour variation in H. numata. Functional studies on the gene cortex and exploration of longer developmental time series will now be required to conclude whether the supergene P is a classical supergene, or whether cortex alone fully controls the developmental switches involved in colour pattern polymorphism in H. numata.

     

     

  18. 18
    OLV says:

    Where’s the “evo” in evo-devo?

    Unravelling the genes forming the wing pattern supergene in the polymorphic butterfly Heliconius numata
     
    Abstract

    Background
    Unravelling the genetic basis of polymorphic characters is central to our understanding of the origins and diversification of living organisms. Recently, supergenes have been implicated in a wide range of complex polymorphisms, from adaptive colouration in butterflies and fish to reproductive strategies in birds and plants. The concept of a supergene is now a hot topic in biology, and identification of its functional elements is needed to shed light on the evolution of highly divergent adaptive traits. Here, we apply different gene expression analyses to study the supergene P that controls polymorphism of mimetic wing colour patterns in the neotropical butterfly Heliconius numata.
    Results
    We performed de novo transcriptome assembly and differential expression analyses using high-throughput Illumina RNA sequencing on developing wing discs of different H. numata morphs. Within the P interval, 30 and 17 of the 191 transcripts were expressed differentially in prepupae and day-1 pupae, respectively. Among these is the gene cortex, known to play a role in wing pattern formation in Heliconius and other Lepidoptera. Our in situ hybridization experiments confirmed the relationship between cortex expression and adult wing patterns.
    Conclusion
    This study found the majority of genes in the P interval to be expressed in the developing wing discs during the critical stages of colour pattern formation, and detect drastic changes in expression patterns in multiple genes associated with structural variants. The patterns of expression of cortex only partially recapitulate the variation in adult phenotype, suggesting that the remaining phenotypic variation could be controlled by other genes within the P interval. Although functional studies on cortex are now needed to determine its exact developmental role, our results are in accordance with the classical supergene hypothesis, whereby several genes inherited together due to tight linkage control a major developmental switch.

     
    Conclusions

    Here, we developed the first transcriptome resource for H. numata and performed differential expression analyses during wing development to identify genes involved in forming the supergene and contributing to the expression of differentiated phenotypes. Our analyses confirm the role of cortex in the formation of black wing pattern elements. Our results are consistent with the hypothesis that other genes in the P region may play a role in colour variation in H. numata. Functional studies on the gene cortex and exploration of longer developmental time series will now be required to conclude whether the supergene P is a classical supergene, or whether cortex alone fully controls the developmental switches involved in colour pattern polymorphism in H. numata.

     Conservation and flexibility in the gene regulatory landscape of heliconiine butterfly wings
     
    Abstract

    Background
    Many traits evolve by cis-regulatory modification, by which changes to noncoding sequences affect the binding affinity for available transcription factors and thus modify the expression profile of genes. Multiple examples of cis-regulatory evolution have been described at pattern switch genes responsible for butterfly wing pattern polymorphism, including in the diverse neotropical genus Heliconius,but the identities of the factors that can regulate these switch genes have not been identified.
    Results
    We investigated the spatial transcriptomic landscape across the wings of three closely related butterfly species, two of which have a convergently evolved co-mimetic pattern and the other having a divergent pattern. We identified candidate factors for regulating the expression of wing patterning genes, including transcription factors with a conserved expression profile in all three species, and others, including both transcription factors and Wnt pathway genes, with markedly different profiles in each of the three species. We verified the conserved expression profile of the transcription factor homothorax by immunofluorescence and showed that its expression profile strongly correlates with that of the selector gene optix in butterflies with the Amazonian forewing pattern element ‘dennis.’
    Conclusion
    Here we show that, in addition to factors with conserved expression profiles like homothorax, there are also a variety of transcription factors and signaling pathway components that appear to vary in their expression profiles between closely related butterfly species, highlighting the importance of genome-wide regulatory evolution between species.

     
    Conclusion

    Our understanding of the regulatory evolution of wing pattern in butterflies is dependent on a clear picture of the expression of developmental factors around the time of wing pattern specification. This study has provided a picture of gene expression along one axis of developing wings in a manner unbiased by our understanding of wing development in non-lepidopteran systems. At the within-species level, we can broadly rule out the hypothesis that trans-regulatory factors change their expression profiles in different pattern forms (Fig. 1d) based on genetic mapping, but we are not able to rule out this phenomenon at the between-species level—it is likely that both processes play a role, either through selection or drift. Our deeper understanding of factors that are expressed in the wing in correlation with pattern elements will permit us to decode the regulatory linkages that lead to the differential expression of pattern switch genes like optix, WntA and cortex, and it is clear that we should look to both conserved and diverging regulatory factors as the causative agents of cis-regulatory evolution.

  19. 19
    jawa says:

    Where’s the “evo” in evo-devo?

    Bar, stripe and spot development in sand-dwelling cichlids from Lake Malawi
     
    Abstract

    Background
    Melanic patterns such as horizontal stripes, vertical bars and spots are common among teleost fishes and often serve roles in camouflage or mimicry. Extensive research in the zebrafish model has shown that the development of horizontal stripes depends on complex cellular interactions between melanophores, xanthophores and iridophores. Little is known about the development of horizontal stripes in other teleosts, and even less is known about bar or spot development. Here, we compare chromatophore composition and development of stripes, bars and spots in two cichlid species of sand-dwellers from Lake Malawi—Copadichromis azureus and Dimidiochromis compressiceps.
    Results
    (1) In D. compressiceps, stripes are made of dense melanophores underlaid by xanthophores and overlaid by iridophores. Melanophores and xanthophores are either loose or absent in interstripes, and iridophores are dense. In C. azureus, spots and bars are composed of a chromatophore arrangement similar to that of stripes but are separated by interbars where density of melanophores and xanthophores is only slightly lower than in stripes and iridophore density appears slightly greater. (2) Stripe, bar and spot chromatophores appear in the skin at metamorphosis. Stripe melanophores directly differentiate along horizontal myosepta into the adult pattern. In contrast, bar number and position are dynamic throughout development. As body length increases, new bars appear between old ones or by splitting of old ones through new melanophore appearance, not migration. Xanthophore and iridophore distributions follow melanophore patterns. (3) Metamorphic pigmentation arises in cichlids in a fashion similar to that described in zebrafish: melanophore progenitors derived from the medial route of neural crest migration migrate from the vicinity of the neural tube to the skin during metamorphosis.
    Conclusion
    The three pigment cell types forming stripes, bars and spots arise in the skin at metamorphosis. Stripes develop by differentiation of melanophores along horizontal myosepta, while bars do not develop along patent anatomical boundaries and increase in number in relation with body size. We propose that metamorphic melanophore differentiation and migratory arrest upon arrival to the skin lead to stripe formation, while bar formation must be supported by extensive migration of undifferentiated melanophores in the skin.

     
    Conclusion

    The three same chromatophore types make up D. compressiceps and C. azureusbody coloration: melanophores, iridophores and xanthophores. In D. compressiceps,stripes are made of dense melanophores underlaid by xanthophores and overlaid by iridophores. Melanophores and xanthophores are either loose or absent in interstripes, and iridophores are dense. In C. azureus, spots and bars are composed of a chromatophore arrangement similar to that of stripes but are separated by interbars where density of melanophores and xanthophores is only slightly lower than in stripes and iridophore density appears slightly greater.

    Differences in pigmentation between C. azureus and D. compressiceps arise at metamorphosis when melanophores appear in the skin as arrangements prefiguring stripes, bars or spots. In D. compressiceps, stripe melanophores differentiate along horizontal myosepta and the adult pattern is essentially in place by the end of the larval period. In contrast, the number of bars developing in C. azureus larvae is smaller than in adults. Bars appear as a series of lateral melanophore patches that progressively elongate dorso-ventrally by new melanophore additions. New bars appear either between old ones, or through splitting of old ones. The place of new melanophore appearance, not migration, determines new bar formation. Increase in xanthophore density in developing bars and stripes follows that of melanophores. Iridophores appear in interstripes after stripe formation, while their appearance in interbars is concomitant with bar formation.

    Analysis of neural crest migration by ISH indicates that melanophore progenitors migrate from the vicinity of the neural tube to the skin along myosepta at metamorphosis, as previously described in zebrafish [13]. Time-lapse analysis of bar development during metamorphosis shows that melanophores do not migrate after differentiation. We thus propose that metamorphic melanophore differentiation and migratory arrest upon arrival to the skin lead to stripe formation, while bar formation must be supported by extensive dorsal and/or ventral migration of undifferentiated melanophores in the skin.

  20. 20
    jawa says:

    The question “Where’s the ‘evo’ in evo-devo?” refers mainly to what is also known as macro-evolution.

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