Spiritual Genome Blog

Neo-Darwinian theory about evolution

THE PROBABILITY WAVES OF LIGHT

Post in Quantum Computing group on Facebook 1st March, 2019.

It's just dawned on me the striking similarities between the 'two-slits' experiment and the DNA Phantom Effect. They both involve an experimenter shining light thru an apparatus and observing the wave pattern that appears on a screen behind. In other words they both involve this fundamental mystery of wave-particle duality. I have just realized that in both experiments we actually get to 'see' the probability waves of QM. When you think of it all the wave theory of light based on Fourier maths is in the nature of probability waves. The wave nature of light is what 'probably' happens and then miraculously when you observe a photon you find wonder of wonders that is what actually happens. For instance photons don't spread out in all directions from a bright orb billions of light years away and then travel indefinitely in perfectly straight lines sinusoidal oscillating from -1 to +1 on a Cartesian grid with no mass and no energy thru a void and then arrive in perfectly parallel 'rays' into the retina of our eyes so we see a perfectly coherent bright orb. Real physical photons would surely be no longer parallel and would be entering our eyes at an angle and should have spread out. I could list another dozen mysteries about light, The bottom line is 'wave-particle' duality mystery is precisely mysterious because we actually 'see' the probability waves of QM (if the experimenter doesn't make an observation then the probability waves travel thru both slits). And in the same way the DNA Phantom Effect is 'nature' enabling us to 'see' that the probability waves of QM are also occurring in the DNA.

Post in Quantum Computing group on Facebook on 2nd March, 2019

This entanglement experiment in New Scientist raises some interesting questions for quantum computing. Two entangled photons were sent off to labs AO and BO. They were measured by another set of entangled photons AOTest and AOSystem and BOTest and BOSystem. Then the original photon and the AOSystem photons sent on to lab A1 and other original photon and BOSystem sent to lab B1. Researchers claim the observer at AI got different results from 'observer' at AO and observer at B1 got different results from 'observer' at BO. In fact the 'observer' at AO and BO was not a conscious experimenter and the conscious experimenter at A1 and B1 was either choosing randomly to measure either the original photon or the A1System or B1System and the conscious experimenter at A1 and B1 got consistent 'results' with each other in as much as they significantly differed from the measurements of the 'observer' at AO and BO. All this proves in my opinion is that there is only one measurement within the meaning of QM at the end of process. Presumably in quantum computing there will be an infinitely large number of interactions like this between entangled photons before some sort of a 'result' appears on the screen. If the assumption made in this experiment were correct that an observation within the meaning of QM occurs every time there is an interaction between two photons such that the state of one photon changes the state of the other and the result of that 'observation' can disagree with 'observations' further down the line then you may as well close up shop right now cos quantum computing will never be possible. What would have been startling if the A1 results were 100% consistent with the AO 'results' and the B1 results diverged significantly from the BO 'results'. Then we would have to demolish the Copenhagen school and poor old Niels Bohr would turn over in his grave.

Post in Quantum Computing group on Facebook on 2nd March, 2019.

Well I’ve figured out this question of ‘probability’ waves in light within the meaning of quantum mechanics. Light occupies a unique position in as much as a single photon is clearly a ‘particle’ within the meaning of quantum mechanics and yet we can actually see light thru our sense of vision in the macroscopic world. In other words we do not need a measuring instrument so see light. So in the macroscopic world Fourier wave mechanics apply which will predict how light travels with 100% probability. It is not necessary to square the Fourier integral with it’s complex conjugate (Dirac’s <BRA KET> in order to get a ‘real’ probability and nor is it necessary to normalize the integral. Because the probability waves in the normal Earth based macroscopic world have 100% probability they ‘appear’ real. You can actually see them and predict them with certainty. Then comes Special Relativity and most especially the position of the observer. Special relativity states the probability that objects travelling near speed of light will appear different to a stationary observer here on Earth. It also predicts that the clocks will stop in an object travelling at the speed of light. So to an observer here on Earth it will appear that light from a distant galaxy has taken 10 billion light years to get here according to Fourier wave mechanics, but from the point of view of the photon itself time is simply not a factor. From the point of view of the photon itself it has traversed those 10 billion light years of space instantly and it is as young and as fresh as the instant it was emitted. When it comes to observing photons in the microscopic quantum world, that is to say photons that we can’t actually ‘see’ and now need a measuring instrument to give us a result, then quantum probability rules now apply. I puzzled over that finding that light slows down to 15 miles an hour in a Bose-Einstein condensate. What does that even mean? Light travelling at 15 miles an hour. Then I realized that they didn’t actually ‘see’ the light travelling at 15 miles an hour. There was a probability wave within the meaning of QM that told them the probability that light would travel at 15 miles an hour at near absolute zero and there was a measuring instrument that gave them that ‘result’. The point I’m trying to make is that all wave theory about light are probability waves. But different probabilities apply depending on where you are and what you’re trying to do. I think anyone trying to build a quantum computer in a Bose-Einstein condensate will have to factor this in.

Post in Quantum Computing group on facebook on 2nd March, 2019.

Sorry to be doing all these posts but I got quite a bit to say and if you make these posts too long nobody reads them. For my first post we need a definition of entangled photons. These are photons for which, from their own point of view, no time has passed. Even if they are sent to the two ends of the universe from their own point of view no time has passed. So in that experiment the original entangled photons went from their generation point to labs AO and BO and on to labs A1 and B1 and from their own point of view no time passed and the only measurement took place at labs A1 and B1 and those measurements would have been identical. At labs AO and BO a new set of entangled photons were generated, a test photon and a system photon and the system photon was then sent on with the original photon. Also from the point of view of the system photon no time has passed. The only point in the whole system where time passes is the minuscule amount of time to generate the test and system photons. So the system photon is ever so slightly out of phase with the original photon. From the point of view of all photons no time has passed but when the measurements were made by the conscious observers at labs A1 and B1 their measurements differed slightly from hypothetical measurements that would have been made at labs AO and BO. The point being that there was no observation and no measurement at AO and BO by a conscious experimenter so in the system there was only one point of view – the point of view of the entangled photons themselves and for them no time had passed. The fact that the system and original photons are slightly out of phase only becomes a factor when the measurement is made by the conscious observer and that is why they got a slight discrepancy in results. We can now solve quickly the second issue. The photons operating in a quantum computer in a Bose-Einstein condensate only have their own point of view so for them no time passes cos they’re travelling at the speed of light. They’ll do what they do instantaneously. But if a conscious observer decided to open the can and measure the speed of those photons, the measurement would show that they’re travelling at 15 mph.

Post in Quantum Computing group on Facebook on 3rd March, 2019.

Before someone says to me wait a minute there are lots of particles that are entangled that aren't travelling at the speed of light I'm gonna head you off at the pass. Photons play out in the macroscopic world so you need an explanation for entanglement of photons in standard physics and that's special relativity. Atomic and subatomic particles that are entangled don't need an explanation cos they just form part of a multiparticle wave function and when you collapse the wave function to observe one of them you will automatically get the state of the other. That's just standard Copenhagen. I think in a quantum computer you will need both forms of entanglement. For instance you generate highly polarized (horizontal or vertical) laser entangled photons one of which reads the data and the other manipulates the nucleus of the hydrogen atom as well as pushing the electron of the hydrogen atom into the conduction band. When that electron falls back into its hole it will emit a single spectral line photon which will read precisely whether that electron is up or down. I think the laser light manipulating the nucleus and reading the data has to be polarized horizontal or vertical cos they constitute orthogonal vectors that will read 0 or 1 (up or down spin). And I think you're gonna be able to use the DNA molecule itself as the semiconductor. It's my belief that visible laser light will push the hydrogen electron only into the conduction band. So all you gotta do is direct the laser light at eight hydrogen atoms in the DNA molecule and you will get a reading in spectral line photons of an 8 bit binary number.

Post in Quantum Computing group on Facebook on 5th March, 2019.

In previous posts I described how I thought you can make a quantum computer by generating two entangled laser photons one of which could read the input data and the other is directed at 8 hydrogen atoms that would then emit spectral lines of an 8 bit binary number. In other words this would be a solitonic (solitary) wave packet consisting of 8 spectral lines that contains an 8 bit binary number. This soliton would have non-adiabatic non-abelian geometric phase that contains information. This could then go thru these holonomic quantum gates that would execute some sort of algorithm or program. It would be a very nice concept if at the end of that process the geometric phase of that soliton has been changed into a different 8 bit binary number that represents the result. It's my feeling that a quantum computer must execute an algorithm or a program instantaneously like Shor's algorithm. I don't see how you could have RAM in the conventional sense in a quantum computer. If you've followed my ravings up to now one more crazy thought won't hurt. I've got this crazy notion that that result is still entangled with the other laser photon that read the input data and it now changes the hard drive data. The only way this could be justified is if the entire computing process represents a wave function that does not actually collapse until a result appears on the screen for a conscious human computer geek to read and that computer geek actually forms part of the wave function as well. In other words a quantum computer conceptually is just a very sophisticated measuring instrument. All the mysteries that apply to measuring conventional quantum processes will also apply to that quantum computer. You will think I am crazy but Niels Bohr would be proud of me!

Post in Quantum Computing group on Facebook on 8th March, 2019.

"One can recover the information dropped into the black hole by doing a massive quantum calculation on these outgoing Hawking photons," said Norman Yao, a UC Berkeley assistant professor of physics.

Berkely thought

<The trans-Planckian problem is the issue that Hawking's original calculation includes quantum particles where the wavelength becomes shorter than the Planck length near the black hole's horizon. This is due to the peculiar behavior there, where time stops as measured from far away. A particle emitted from a black hole with a finite frequency, if traced back to the horizon, must have had an infinite frequency, and therefore a trans-Planckian wavelength.>

This raises some nice issues about my new hobby horse about the probability waves of light. We'll take this as a pure thought experiment and assume that Einstein's field equations accurately reflect the fabric of space-time and inside that black hole there is some sort of 4-dimensional milieu that's accelerating. (the field equations are double differential equations) We drop a 3-D qubit that is stationary in there and then we measure the 'outgoing Hawking photons' that is to say we make an observation which collapses a wave function and we observe a photon in a particular state of polarization. We are entitled to surmise that that accurately reflects whether the 3-D qubit is now spin-up or spin-down in the 4-D space-time milieu. If nothing else it reflects the probability waves of all of physics. It's no more 'improbable' than the theory that light travels 13.5 billion years using 3-D Fourier wave mechanics at a constant speed thru 4-D space-time that is accelerating, and that this actually gives us the dimensions of a real physical universe.

 

Post in Quantum Computing group on Facebook 10th March, 2019

"and it's probable that there is some secret here which remains to be discovered" quote by C.S. Pierce at head of Eugene Wigner's article The Unreasonable Effectiveness of Mathematics in the Physical Sciences. I don't think you are going to make a quantum computer without discovering that 'secret'. And the secret is (drum roll) all of calculus is in the nature of probability waves whether in the macroscopic or the quantum world. By virtue of Planck's constant we know that all of matter is composed of discreet chunks ie. all of the physical world is discontinuous. Yet so much of physics involves differentiating waves that are 'real' and can't actually be differentiated because they are discontinuous. Once you realize that all of calculus involves probability wave functions and the only difference between quantum and macroscopic waves is the latter have 100% probability and therefore appear real, then we solve the 'observation' question in quantum mechanics. The fact is all of the 'physical sciences' require an 'observer'. A scientist comes up with a hypothesis, does the math, then goes and 'observes' whether the hypothesis is true or false. Scientists don't realize that the 'observation problem' applies in the macroscopic world because they have collapsed a wave function that has 100% probability of predicting the outcome of the observation. 

 

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ONCOGENES RESPONSIBLE FOR SPECIES DIFFERENTIATION?

Demon in the Machine

ONCOGENES RESPONSIBLE FOR SPECIES DIFFERENTIATION?

In earlier blogs you will see is the essential problem for Neo-Darwinism is that there is only a 1-2% difference in DNA sequence between human and chimpanzee. At the molecular level, genome and proteins, the human and the chimpanzee are more similar than sibling species and yet the phenotype of human and chimp are so vastly different that taxonomically they are placed not only in different genera but in different families.

In his new book The Demon in the Machine, Paul Davies proposes that oncogenes may be responsible for differentiation of the species. Oncogenes are the genes implicated in the development of cancer cells as well:

<Another reason that evolution hasn’t eliminated cancer is because of the link with embryogenesis. It has been known for thirty years that some oncogenes play a crucial role in development; eliminating them would be catastrophic. Normally, these developmental genes are silenced in the adult form, but if something reawakens them cancer results – an embryo gone wrong developing in adult tissue. The writer George Johnson summarizes this well by referring to tumours as the ‘embryo’s evil twin’. Significantly, the early stages of an embryo are when the organism’s basic body plan is laid down, representing the earliest phase of multicelled life. When the cancer switch is flipped, there will be systematic disruption in both the genetic and epigenetic regulators of information flow, as the cells recapitulate the very different circumstances of early embryo development. This will involve both changes to the way regulatory genes are wired together and changes in patterns of gene expression. Our research group is trying to find information signatures of these changes. We hope it will prove possible to identify distinct ‘informational hallmarks’ of cancer to go alongside the physical hallmarks I mentioned – a software indicator of cancer initiation that may precede the clinically noticeable changes in cell and tissue morphology, thus providing an early warning of trouble ahead.>

It should be a simple matter to compare the oncogenes of human and chimpanzee and see if there are any significant differences that might explain how humans and chimps can be so similar in genotype and yet so different in phenotype.

In addition Paul Davies in his book tells about the massive electrical activity both in cancerous tissue and in embryogenesis:

<Altering the electrical properties of so-called instructor cells had a dramatic effect, causing the pigmented cells to go crazy, spreading cancer-like into distant regions of the embryo. One perfectly normal tadpole developed a metastatic melanoma entirely from the electrical disruption, in the absence of any carcinogens or mutations. That tumours may be triggered purely epigenetically contradicts the prevailing view that cancer is a result of genetic damage, a story that I shall take up later in the chapter. All this was remarkable enough. But an even bigger surprise lay in store. In a different experiment at Tufts University, devised by Dany Adams, a microscope was fitted with a time-lapse camera to produce a movie of the shifting electric patterns during the development of Xenopus embryos. What it showed was spectacular. The movie began with a wave of enhanced electrical polarization sweeping across the entire embryo in about fifteen minutes. Then various patches and spots of hyperpolarization and depolarization appeared and became enfolded as the embryo reorganized its structure. The hyperpolarized regions marked out the future mouth, nose, ears, eyes and pharynx. By altering the patterns of these electrical domains and tracing how the ensuing gene expression and face patterning changed, the researchers concluded that the electrical patterns pre-figure structures scheduled to emerge much later in development, most strikingly in the face of the frog-to-be. Electrical pre-patterning appears to guide morphogenesis by somehow storing information about the three-dimensional final form and enabling distant regions of the embryo to communicate and make decisions about large-scale growth and morphology.>

In my article The Evolution of Consciousness on this website I argue that the DNA is a semiconducting nanowire, and that communication in the nucleus of the cell is mediated by UV light aka biophotons aka optogenetics. Quite simply a semiconducting nanowire will emit UV light when the electrons in the conduction band fall back into their holes in the valence band. A recent study notes some curious facts about the electromagnetic properties of DNA. For example, link DNA is said to “zig-zag” back and forth between “stacks” of these mini-coils, while the histone cores of the mini-coils are reported to link with each other. There is said to be a “permanent dipole moment” between each mini-coil that generates “electric dipolar oscillation” between them. The capacity for mutual induction of electromotive force (emf) in the nucleosomal fiber would be virtually infinite. In addition, the current that has been detected in the nucleosomal fiber is “oscillating;” that is to say, it is an alternating current with frequencies between 2 and 50MHz.

In other words the genome is capable of generating its own electricity and this electrical activity mediates communication in the cell thru UV photons aka optogenetics.  We find that oncogenes play a prominent role in embryogenesis and cancer cells. It seems likely that these three processes are linked in a fundamental way: the oncogenes are directing the electrical activity to produce coherent UV photons to control embryogenesis, and corrupted oncogenes result in incoherent UV photons which sends out scrambled signals to the cells which results in cancer. Quite simply the proper program they run in embryogenesis goes haywire. Which leads us back to Paul Davies’ initial thesis in his book that all of life is information processing.

QED

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PLAYING DOUBLE JEOPARDY WITH SOLIPSISM

Demon in the Machine


RUPERT SHELDRAKE'S BANNED TED TALK - THE SCIENCE DELUSION

AN OPEN LETTER TO PAUL DAVIES AUTHOR OF THE DEMON IN THE MACHINE

Dear Professor Davies I have a few concerns which tends to make me doubt that the universe is physical, but it is actually a virtual reality. I am hoping that you can convince me that the universe really is physical because sometimes I think I must be going crazy. Although your new book claims that all of life is computer processing so maybe you have a few thoughts that the universe could be computer generated yourself.

  1. It seems to me that scientists explain all matter in the universe in terms of electromagnetic radiation. Atoms are just little ‘chunks’ of positive charge and negative charge and are invisible. Light is also electromagnetic radiation which just happens to be in a small band of frequency in the whole spectrum which would otherwise itself be invisible as well. So it seems to me that if an alien from another universe were to travel thru our universe it would see absolutely nothing at all. For an alien trying to see stuff in our universe would be like us trying to see or be aware of the mobile phone network.
  2. On the subject of other universes that mainstream scientists talk about a lot. May I ask you whether these other universes all come out of the same singularity that our universe came out of or were there multiple singularities that all did whatever it was they did at the same time and place to create all the universes. Also if there are multiple universes as so many reputable mainstream scientists believe, are these universes all superimposed over each other or are they all spatially separated. I have real problems with this because if they are all superimposed over each other then it seems to me that they all must be virtual, and if they are all spatially separated then they all must have different constants of nature in order to be different universes and I can’t for the life of me see how a particle in our universe could branch off into a different universe if it has different constants of nature. Also there could only be a limited number of different universes bordering our universe, so our particles might have to travel through whole universes in order to get to other universes further out.
  3. The Bible says in the beginning there was the Word. Scientists say in the beginning there was a word – singularity. The Bible says God created the universe in a rather improbable way, and the scientists say that the universe appeared in a rather improbable and physically impossible way. The Bible says three wise men came from the East and scientists say that the four fundamental forces separated off like the four horsemen of the Apocalypse before there was any matter for these forces to act upon. Sometimes I think scientists just rewrote the Bible and just threw in a few fancy mathematical equations to delude us into thinking that they knew what they were talking about. Kind of like the Catholic mass in Latin so nobody could actually understand it. I think someone must have said it, I couldn’t think of anything so clever, but the more unbelievable a theory is, the more likely people are to believe it.
  4. Then there is this vexed question of time. It seems to me that ultimately we find ourselves spinning around a bright light in the middle of nowhere. If you were some sort of superintelligence and you were going to design an illusionary world where pseudophysical robots could live and interact ‘as if’ they were physical, that would be the perfect way to do it. The robots would count every time they did a full revolution of that bright light and they would think a year had passed. In other words time is nothing but an illusion of human construct based on the speed at which we revolve around the sun.
  5. Related to the problem of time is the problem of gravity. It seems to me that gravity is purely a fictitious force. I seem to recall that Einstein himself said that at some stage. Science has other fictitious forces, principally the centrifugal force, so there is no reason why gravity can not also be fictitious. Indeed there are some distinct parallels to be drawn precisely between gravity and the centrifugal force. They both involve things spinning around things (sic). On the subject of gravity there is the vexed problem of Einstein’s General Theory of Reality. It seems to me for space’ to maintain its curvature every ‘point’ in space would have to double differentiate itself wrt every other ‘point’ in space at every ‘moment’ in time (perhaps every interval of Planck time – because if I believe in anything Science has produced, I believe in Quantum Mechanics).
  6. Which leads me to the vexed problem of quantum mechanics. The essence of quantum mechanics is if a physicist does the math and works out the probability that a particle will be in a certain state and then goes looking for that particle he/she will find it. The problem I have is I don’t understand how a virtual particle can integrate itself and then square itself to work out where it might probably be underneath a bell curve. And I really don’t understand how that same virtual particle has to perform essentially the same maths every ‘time’ it moves from point A to point B. And given the fact that ‘time’ and ‘space’ don’t actually exist as we know it at the quantum level, all the equations in quantum mechanics actually plug in the x,y,z coordinates of Cartesian space and the t for time. And indeed many of the most crucial quantum mechanics equations actually resort to Pythagorean geometry. I just can’t believe that right angled triangles actually exist in the quantum world nor that subatomic particles actually know the speed at which the Earth revolves around the sun so it can count off ten seconds in Earthly time. It seems to me when Einstein described entanglement as ‘spooky’ this is precisely what he was alluding to. At the quantum level things are not ‘physical’.
  7. Also light is not in the quantum world. We see light in the macroscopic world. We don’t need any measuring instrument to see light. But what are we actually seeing? Is light a particle or a wave? Obviously the light we see coming from distant galaxies must be a wave, precisely a sinusoidal wave, because it has to oscillate from +1 to -1 on a Cartesian graph in a perfectly straight line for 13.5 billion light years to come to us all the way from the Big Bang. I find it hard to believe that there is a Cartesian graph with +1 and -1 coordinates connecting us with the Andromeda galaxy, our nearest galactic neighbor, let alone galaxies at the ‘edge’ of the Universe. The other problem I have with light is here on Earth light rays spread out in all directions from a globe and yet all these light rays are perfectly straight. I don’t understand how we can see, how a sufficient number of photons will strike the retinae of our eyes, if these perfectly straight light rays are coming from a distant galaxy and spreading out in all directions. Surely by the time they got to planet Earth these light rays would no longer be parallel but would be travelling at an angle in relation to each other. A sufficient number of photons should not strike the retinae of our eyes for us to see a coherent twinkling, twinkling little star.
  8. I have real problems with Cartesian dualism as well. You will know that Descartes originally claimed that we have a mental ‘soul’ and a physical body. In modern terms this has been changed to the mind-body problem. We have a mind which is not physical and a body which is physical. As I understand it most scientists do not agree with Cartesian dualism. They invariably make the claim therefore that there is only physical matter and mental or spiritual things are impossible. Essentially they are saying therefore that consciousness is impossible because whatever else it is, it is clearly not physical. They are also saying that our dreams are impossible because they also are clearly not physical. So if you deny Cartesian dualism and opt only for physical, you have to deny consciousness and dreams. My problem is that I am more certain that I have consciousness and dreams than I am that the world is physical. I find myself also denying Cartesian dualism so I have to deny that there is anything physical, everything is of mental construct.
  9. Which brings me to George Berkeley, the Bishop of Cloyne. His claim that nothing exists unless it is observed by a conscious mind. Boswell had the temerity to ask Dr. Johnson how to prove Berkeley wrong, whereupon Johnson, an intellectual giant, said “I prove it thus” and went and kicked a rock. Boswell meekly observed that still it was impossible to prove logically that Berkeley was wrong. Berkeley was widely ridiculed at the time and ever since. Everyone said how absurd this is because that would mean that anything that was not being observed by a conscience mind would cease to exist. This of course was centuries before computers were developed, so all Berkeley could say in reply was that unobserved things continue to exist in the mind of God. Which brings to mind one of your earlier books about the mind of God and your most recent book that all of life is information processing. Of course if Berkeley had known about computers he could have just simply said that things not being observed will continue to exist as data.
  10. Finally there is the problem of Neo-Darwinism. Darwin’s famous book offered an explanation how finches on different neighboring islands had different shaped beaks, which is essentially a Lamarkian explanation, and Darwin actually explained the origin of nothing. From this humble origin (sic) a magnificent conjectural and unprovable edifice of pseudoscience has arisen which involves tens of thousands of research papers and countless books and articles, called Neo-Darwinism: the natural selection of adaptive phenotypes caused by random chemical mutations of genes. In the beginning was the Word – a primordial swamp. No talk about how the elements carbon, oxygen, hydrogen and nitrogen actually managed to become a primordial swamp so they may as well have said in the beginning there was a singularity that resembled what we know today as a swamp. And the conjectures escalate exponentially from there. Which brings us to the current era with all our magnificent science and we have found that the human and the chimpanzee are more similar at the molecular level, genome and proteins, than sibling species and yet taxonomically they are placed not only in different genera but in different families, because of their profoundly different phenotypes. The fable of Neo-Darwinism has brought us to the point where I would sooner believe in the Book of Genesis in the Bible. And I am not even a Christian or a Jew!    
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10 GENES EXPRESSED IN THE PLACENTA

neodarwinism

You will see from earlier posts that the issue is a research article that was published in 2005 that found that there is 1-2% difference in DNA sequence between humans and chimps and yet 80% of the proteins are different. From the limited number of comparisons that were made at that time it emerged that for most of these proteins the differences were very small say 2% between human and chimp proteins. The article states that these differences were too small to account for the difference in phenotype between humans and chimps. The fact that there was such a small difference in DNA sequence and such a small difference in the quality not the quantity of the proteins in the chimp suggested that all is at it should be and Neo-Darwinism could stand. The article suggested that the difference in phenotype (which I put at about 60% at least) must be due to small differences in a few regulatory genes in early development. Indeed they must be small differences because there is only 1-2% difference in DNA sequence overall, and this is already needed to account for the differences in 80% of the proteins.

So I have now identified 10 genes that are expressed in the mammalian placenta and I am going to compare in the gene databases the proteins synthesized from these genes. I suspect however that again I will find that there is about a 1% difference in the DNA sequence and a 2-3% difference in the amino acid sequence of the proteins. My own theory about this is that the fact that there is a small percentage of difference in so many proteins (80%) does indeed account for the fact that there is a 60% (at least) difference in phenotype between human and chimp. Take a simple example: If there is a 2% difference in proteins between 80% of the proteins in two species then that could arguably account for an 80 x 2= 160% difference in phenotype between the two species. This is not strictly a formal mathematical permutation or combination but still as a matter of common sense it could account for the fact that there is a 60% (at least) difference in phenotype between human and chimp. Basically very small differences in a large proportion of all the proteins in an organism are responsible for its phenotype.

Which means that six million years ago in just one generation all these small insignificant mutations must have all occurred simultaneously for the human being to differentiate from the chimpanzee. The image above which presents the standard theory of Neo-Darwinism that the human gradually evolved over six million years and started to stand upright simply doesn't stack up with the fact that the differences in DNA sequence and the great bulk of the proteins in human and chimp are insignificantly small. It doesn't stack up because if these insignificantly small mutations happened randomly in dribs and drabs over millions of years then there could not have been a complete differentiation between the two species. They would have been able to continue to interbreed and the fossil record would show all sorts of intermediate hybrids. The only way to account for the 60% (at least) difference in phenotype between human and chimp is if all the insignificantly small mutations happened at once to create two different creatures. It is submitted that this demonstrates that Neo-Darwinism is clearly wrong, and if you can't accept that then surely you must concede that Neo-Darwinism offers no explanation for the fact that two creatures so similar in their genome and proteins could be two separate species so totally different and distinct in their phenotype.

In fact the orthodox explanation that a small difference in a few developmental genes in embryogenesis are responsible for the differentiation of human and chimp species would be the strongest argument possible for intelligent design, for these same small differences in only one or a few regulatory genes would be responsible for the differentiation of all the mammal species and these could not possibly be random cheemical mutations.

 

SCHRÖDINGER’S QUANTUM THEORY OF MUTATION VS. NEODARWINISM

TEN GENES EXPRESSED IN THE PLACENTA

Global gene expression analysis and regulation of the principal genes expressed in bovine placenta in relation to the transcription factor AP-2 family

We detected gestational-stage-specific gene expression profiles in bovine placentomes using a combination of microarray and in silico analysis. In silico analysis indicated that the AP-2 family may be a consensus regulator for the gene cluster that characteristically appears in bovine placenta as gestation progresses. In particular, TFAP2A and TFAP2B may be involved in regulating binucleate cell-specific genes such as CSH1, some PAG or SULT1E1. These results suggest that the AP-2 family is a specific transcription factor for clusters of crucial placental genes. This is the first evidence that TFAP2A may regulate the differentiation and specific functions of BNC in bovine placenta.

A Human Placenta-specific ATP-Binding Cassette Gene (ABCP) on Chromosome 4q22 That Is Involved in Multidrug Resistance

We characterized a new human ATP-binding cassette (ABC) transporter gene that is highly expressed in the placenta. The gene, ABCP, produces two transcripts that differ at the 5′ end and encode the same 655-amino acid protein. The predicted protein is closely related to the Drosophila white and yeast ADP1 genes and is a member of a subfamily that includes several multidrug resistance transporters. ABCPwhite, and ADP1 all have a single ATP-binding domain at the NH2terminus and a single COOH-terminal set of transmembrane segments. ABCP maps to human chromosome 4q22, between the markers D4S2462 and D4S1557, and the murine gene (Abcp) is located on chromosome 6 28–29 cM from the centromere. ABCP defines a new syntenic segment between human chromosome 4 and mouse chromosome 6. The abundant expression of this gene in the placenta suggests that the protein product has an important role in transport of specific molecule(s) into or out of this tissue.

Identification of a novel member of the TGF-beta superfamily highly expressed in human placenta

While conducting a gene discovery effort targeted to transcripts of the prevalent and intermediate frequency classes in placenta throughout gestation, we identified a novel member of the TGF-β superfamily that is expressed at high levels in human placenta. Hence, we named this factor `Placental Transforming Growth Factor Beta' (PTGFB). The full-length sequence of the 1.2-kb PTGFB mRNA has the potential of encoding a putative pre-pro-PTGFB protein of 295 amino acids and a putative mature PTGFB protein of 112 amino acids. Multiple sequence alignments of PTGFB and representative members of all TGF-β subfamilies evidenced a number of conserved residues, including the seven cysteines that are almost invariant in all members of the TGF-β superfamily. The single-copy PTGFB gene was shown to be composed of only two exons of 309 bp and 891 bp, separated by a 2.9-kb intron. The gene was localized to chromosome 19p12-13.1 by fluorescence in-situ hybridization. Northern analyses revealed a complex tissue-specific pattern of expression and a second transcript of 1.9 kb that is predominant in adult skeletal muscle. Most importantly, the 1.2-kb PTGFB transcript was shown to be expressed in placenta at much higher levels than in any other human fetal or adult tissue surveyed.

Expression of P-glycoprotein in Human Placenta: Relation to Genetic Polymorphism of the Multidrug Resistance (MDR)-1 Gene

To evaluate whether mutations in the human multidrug resistance (MDR)-1 gene correlate with placental P-glycoprotein (PGP) expression, we sequenced the MDR-1 cDNA and measured PGP expression by Western blotting in 100 placentas obtained from Japanese women.  When genotype results were compared between Caucasians and Japanese, ethnic differences in the frequency of polymorphism in the MDR-1 gene were suspected.

Human epidermal growth factor receptor cDNA sequence and aberrant expression of the amplified gene in A431 epidermoid carcinoma cells

The complete 1,210-amino acid sequence of the human epidermal growth factor (EGF) receptor precursor, deduced from cDNA clones derived from placental and A431 carcinoma cells, reveals close similarity between the entire predicted ν-erb-B mRNA oncogene product and the receptor transmembrane and cytoplasmic domains. 

Differential expression of HLA-E, HLA-F, and HLA-G transcripts in human tissue

The data presented here demonstrated that the HLA-G class I gene is unique among the members of the human class I gene family in that its expression is restricted to extraembryonic tissues during gestation. Furthermore, the pattern of HLA-G expression in these tissues changes as gestation proceeds. During first trimester HLA-G is expressed within the placenta and not within the extravillous membrane. At term, the pattern of the HLA-G expression is reversed, extravillous membrane expressed HLA-G while placenta does not. Another non-HLA-A, -B, -C class I gene, HLA-E, is also expressed by extraembryonic tissues. Unlike HLA-G, HLA-E is expressed by both placenta and extravillous membrane at first trimester and at term. These results raise the intriguing possbility that the HLA-G-encoded molecule has a role in embryonic development and/or the fetal-maternal immune response.

Cloning of a New Member of the Insulin Gene Superfamily (INSL4) Expressed in Human Placenta

A new member of the insulin gene superfamily was identified by screening a subtracted cDNA library of first-trimester human placenta and, hence, was tentatively named early placenta insulin-like peptide (EPIL). In this paper, we report the cloning and sequencing of the EPIL cDNA and the EPIL gene (INSL4). Comparison of the deduced amino acid sequence of the early placenta insulin-like peptide revealed significant overall and structural homologies with members of the insulin-like hormone superfamily. Moreover, the organization of the early placenta insulin-like gene, which is composed of two exons and one intron, is similar to that of insulin and relaxin. Byin situhybridization, the INSL4 gene was assigned to band p24 of the short arm of chromosome 9. RT-PCR analysis of EPIL tissue distribution revealed that its transcripts are expressed in the placenta and uterus.

Identification of a novel MHC class I gene, Mamu-AG, expressed in the placenta of a primate with an inactivated G locus.

In this study, we report the identification of a novel nonclassical MHC class I locus expressed in the placenta of the rhesus monkey, Mamu-AG (Macaca mulatta-AG). Although unrelated to HLA-G, Mamu-AG encodes glycoproteins with all of the characteristics of HLA-G. These Mamu-AG glycoproteins are limited in their diversity, possess truncated cytoplasmic domains, are the products of alternatively spliced mRNAs, and their expression is restricted to the placenta. Taken together, these data suggest that convergent evolution may have resulted in the expression of a unique nonclassical MHC class I molecule in the rhesus monkey placenta, and that the common structural features of Mamu-AG and HLA-G may be functionally significant.

Secreted placental alkaline phosphatase: a powerful new quantitative indicator of gene expression in eukaryotic cells

This paper describes a novel eukaryotic reporter gene, secreted alkaline phosphatase (SEAP). In transient expression experiments using transfected mammalian cells, we demonstrate that SEAP yields results that are qualitatively and quantitatively similar, at both the mRNA and protein levels, to parallel results obtained using established reporter genes. 

PPARγ Is Required for Placental, Cardiac, and Adipose Tissue Development

The nuclear hormone receptor PPARγ promotes adipogenesis and macrophage differentiation and is a primary pharmacological target in the treatment of type II diabetes. Here, we show that PPARγ gene knockout results in two independent lethal phases. Initially, PPARγ deficiency interferes with terminal differentiation of the trophoblast and placental vascularization, leading to severe myocardial thinning and death by E10.0. Supplementing PPARγ null embryos with wild-type placentas via aggregation with tetraploid embryos corrects the cardiac defect, implicating a previously unrecognized dependence of the developing heart on a functional placenta.

Human cholesterol side-chain cleavage enzyme, P450scc: cDNA cloning, assignment of the gene to chromosome 15, and expression in the placenta

 P450scc cDNA was used to probe DNA from a panel of mouse-human somatic cell hybrids, showing that the single human P450scc gene lies on chromosome 15. The human P450scc gene is expressed in the placenta in early and midgestation; primary cultures of placental tissue indicate P450scc mRNA accumulates in response to cyclic AMP.

 

 

 

 

 

 

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THE DEMON IN THE MACHINE

Demon in the Machine

 

A review I wrote for Paul Davies' new book The Demon in the Machine. This book has the potential to overturn Neo-Darwinism. But you have to know how to interpret the book. Essentially intelligence and consciousness is in the DNA in its own right as an organism. The DNA is 'thoughtfully' orchestrating its own evolution.

THE BIG QUESTION

LIFE’S SECRET INGREDIENT: A RADICAL THEORY OF WHAT MAKES THINGS ALIVE

In his new book The Demon in the Machine, Paul Davies attempts to provide an answer to Schrödinger’s question “What is life?” posed in a series of famous lectures that he delivered in Dublin in 1943. An auspicious date because unbeknown to him across the Irish Sea in England Alan Turing had just made the first computer. In those lectures, Schrödinger as one of the founding fathers of quantum mechanics was obviously angling to somehow reconcile quantum mechanics with organic matter and he was not optimistic and actually thought that some ‘new physics’ would have to be developed that would explain life.

Paul Davies offers as an answer to Schrödinger’s question that energy can in some way be equated with or be responsible for information; that the energy in a system directly encapsulates the information in the system. However when he comes to giving precise details about how the energy in a biological system can in some way generate the information in the system he reverts to conventional biological energy that drives cellular processes, namely ATP. Nowhere in his book does Davies point out that Schrödinger’s own famous wave equation is precisely about the calculation of energy in a system. Schrödinger’s wave equation is a complex differential equation that will enable a physicist to calculate the energy in a system. The hydrogen molecule which consists of two hydrogen atoms bonded together is the largest system for which a solution can be found for Schrödinger’s equation, but the fact is that every molecule whether organic or inorganic, has this wave equation including the extremely complex aperiodic DNA molecule.

Davies describes in detail how ATP drives a certain cellular component. The ‘information’ he gives comes as a result of a biologist ‘observing’ this process using no-doubt a variety of sophisticated measuring instruments, and just a basic knowledge of the principles of quantum mechanics should alert him to the fact that this act of observation has resulted in a collapse of the wave function not only at the DNA level but at the cellular level. This perhaps is not the right terminology. It involves the collapse of a wave function that encompasses the genome, the cell, the measuring equipment and the observing biologist. If you are looking for ‘information’ to answer the question ‘What is life?’ you need go no further than this one act of observation. There is more information here than all the computers in the world working in parallel could compute.

While we are on the subject of computers processing ‘information’ I read Davies book carefully thru from beginning to end, and not once did I come across the word semiconductor. May I humbly suggest to him that Schrödinger’s famous question ‘What is life?’ can actually be answered in one word – carbon. Carbon, like silicon, has four electrons in its valence shell and is a classic semiconductor. In 1943 however Schrödinger did not know this. The new physics that Schrödinger was seeking to explain life is simply semiconducting technology which leads to electronics and nanotechnology and ultimately to information technology. The result is that Davies correctly answers Schrödinger’s question without actually explaining precisely how that could be so. Davies has resort to complex self-regulating ‘up-down’ neural networks that somehow produce all this coherent ‘information’ that we take to be the real world, whereas all that was required to convince us that biology is about information is to point out that the DNA is essentially a carbon nanowire.

Well perhaps not simply that, he would also have to explain how the DNA could act as a semiconducting nanowire. And herein lies the other conundrum. After having read his book thru carefully from start to finish, I did not come across the word ‘optogenetics’. The fact is that there are thousand of research papers in mainstream journals detailing how the DNA absorbs electromagnetic radiation, everywhere from UV light down to ELF radiowaves (aka brainwaves), and Davis as a physicist will surely know that when a semiconducting nanowire absorbs electromagnetic radiation it pushes the electrons out of the valence band and into the conduction band. He will also know that when these electrons fall back into their ‘holes’ in the valence band they emit electromagnetic radiation (usually in the UV to visible light range aka biophotons).

Effectively Davis has correctly answered Schrödinger’s question ‘What is life?’ without knowing how or why. We shall call it inspiration. Davies has always impressed me as more than just a popularizer of science, but as a philosopher, dare I say a prophet. I distinctly remember one of his earlier books that the universe is the ‘mind of God’, which impressed me then although he fell short of recognizing that the universe is indeed a virtual reality of mental construct, and that our reality is no more than a sustained and consistent dream.

I particularly commend Davies for his ‘radical’ attempt to question Neo-Darwinism. He quotes with approval what Nobel Prize winner Barbara McClintock says that the DNA seems to be ‘thoughtfully’ orchestrating its own evolution, which clearly implies that both ‘consciousness’ and ‘intelligence’ are in the DNA as an organism in its own right. Davies puts this forward that life is about ‘information’ and once we understand that the DNA is actually a semi-conducting carbon nanowire it’s easy to see how this could be so. Indeed Schrödinger himself puts forward the same proposition in a latter series of lectures, Mind and Matter, which took place at Trinity College, Cambridge in 1956. I’m surprised that Davies did not mention this, as Schrödinger also offers an early theory of mutation based on the fact that the DNA is a semiconducting nanowire in those lectures as well.

In his treatment of Neo-Darwinism, Davies is also aware that there is only a 1-2% difference in DNA sequence between human and chimpanzee, and yet the phenotypes of human and chimp are vastly different. It has been said of human and chimp that at the molecular level, genome and proteins, they are even more similar than sibling species yet taxonomically human and chimp are not only in different genera but in different families. Davies recognizes that Neo-Darwinism is clearly wrong, or at least not the whole story. Davies suggests that epigenetic factors may be responsible for the profound difference in phenotype between human and chimp, and thus raises the spectre of Lamarckism as a more satisfactory explanation for evolution than Neo-Darwinism. As a mainstream internationally known scientist mouthing such a heresy, he has earned my undying respect and admiration. However I would point out to him that epigenetic factors affect the expression of genes, and if it was truly epigenetic factors that has caused the very profound difference in phenotype between human and chimp then this would be reflected in profound differences in the proteins.

This does not appear to be the case with simple proteins where there is a one-on-one relationship between DNA sequence and amino acid sequence, but there is certainly here an area of enquiry to see how complex proteins that are synthesized from more than one gene compare in human and chimp. Indeed if epigenetic factors are at work then this is most likely where they would show up.

I can’t remember when was the last time I read a book that I couldn’t put down, but Paul Davies book The Demon in the Machine is such a book. New Scientist has described his theory as ‘radical’ and indeed it is. I detect in this book a complete paradigm shift. Paul Davies has sufficient stature in the scientific community that if he cared to write a sequel and develop his ‘inspiration’ further, and perhaps call it The Ghost in the Machine, he could find himself on the same pedestal that occupies Schrödinger himself.

                                                                                                                                                Bradley York Bartholomew

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GENES EXPRESSED IN THE EMBRYO BRAIN RESPONSIBLE FOR DEVELOPMENT OF HIGHER CORTICAL REGIONS

chimp photo

You will see from the posts below that there is only a 1-2% difference in DNA sequence between human and chimpanzee and 80% of the proteins of human and chimpanzee are different. The burning question is what are the differences (if any) between the genes expressed in embryogenesis, because these are the genes most likely responsible for the radical phenotype differences between human and chimp. The next step for me is to go to the gene databases and compare the genes below in human and chimp. These genes are all different from the 10 genes listed in the post below this one.

1. Changes in cerebral cortex size are governed by fibroblast growth factor during embryogenesis - We show that fibroblast growth factor 2 (FGF2) and FGF receptors are transiently expressed by cells of the pseudostratified ventricular epithelium (PVE) during early neurogenesis. A single microinjection of FGF2 into cerebral ventricles of rat embryos at E15.5 increased the volume and total number of neurons in the adult cerebral cortex by 18% and 87%, respectively. Microinjection of FGF2 by the end of neurogenesis, at E20.5, selectively increased the number of glia. Mice lacking the FGF2 gene had fewer cortical neurons and glia at maturity. BrdU studies in FGF2-microinjected and FGF2-null animals suggested that FGF2 increases the proportion of dividing cells in the PVE without affecting the cell-cycle length. Thus, FGF2 increases the number of rounds of division of cortical progenitors.

2. Ventricular zone gene-1 (vzg-1) encodes a lysophosphatidic acid receptor expressed in neurogenic regions of the developing cerebral cortex. - Neocortical neuroblast cell lines were used to clone G-protein-coupled receptor (GPCR) genes to study signaling mechanisms regulating cortical neurogenesis. One putative GPCR gene displayed an in situ expression pattern enriched in cortical neurogenic regions and was therefore named ventricular zone gene-1 (vzg-1). These analyses identify the vzg-1 gene product as a receptor for LPA, suggesting the operation of LPA signaling mechanisms in cortical neurogenesis. Vzg-1 therefore provides a link between extracellular LPA and the activation of LPA-mediated signaling pathways through a single receptor and will allow new investigations into LPA signaling both in neural and nonneural systems.

3. An RNA gene expressed during cortical development evolved rapidly in humans - The developmental and evolutionary mechanisms behind the emergence of human-specific brain features remain largely unknown. However, the recent ability to compare our genome to that of our closest relative, the chimpanzee, provides new avenues to link genetic and phenotypic changes in the evolution of the human brain. We devised a ranking of regions in the human genome that show significant evolutionary acceleration. Here we report that the most dramatic of these ‘human accelerated regions’, HAR1, is part of a novel RNA gene (HAR1F) that is expressed specifically in Cajal–Retzius neurons in the developing human neocortex from 7 to 19 gestational weeks, a crucial period for cortical neuron specification and migration. HAR1F is co-expressed with reelin, a product of Cajal–Retzius neurons that is of fundamental importance in specifying the six-layer structure of the human cortex. HAR1 and the other human accelerated regions provide new candidates in the search for uniquely human biology.

4. Neuronal Subtype-Specific Genes that Control Corticospinal Motor Neuron Development In Vivo - Within the vertebrate nervous system, the presence of many different lineages of neurons and glia complicates the molecular characterization of single neuronal populations. In order to elucidate molecular mechanisms underlying the specification and development of corticospinal motor neurons (CSMN)..  Loss-of-function experiments in null mutant mice for Ctip2 (also known as Bcl11b), one of the newly characterized genes, demonstrate that it plays a critical role in the development of CSMN axonal projections to the spinal cord in vivo, confirming that we identified central genetic determinants of the CSMN population.

5. Functional and Evolutionary Insights into Human Brain Development through Global Transcriptome Analysis - Our understanding of the evolution, formation, and pathological disruption of human brain circuits is impeded by a lack of comprehensive data on the developing brain transcriptome. A whole-genome, exon-level expression analysis of 13 regions from left and right sides of the mid-fetal human brain revealed that 76% of genes are expressed, and 44% of these are differentially regulated. Of particular relevance to cognitive specializations, we have characterized the transcriptional landscapes of prefrontal cortex and perisylvian speech and language areas, which exhibit a population-level global expression symmetry. We show that differentially expressed genes are more frequently associated with human-specific evolution of putative cis-regulatory elements. These data provide a wealth of biological insights into the complex transcriptional and molecular underpinnings of human brain development and evolution.

6. Genomic imprinting and the differential roles of parental genomes in brain development - Certain genes are expressed either from the maternal or the paternal genome as a result of genomic imprinting, a process that confers functional differences on parental genomes during mammalian development. In this study we focus on the cumulative effects of imprinted genes on brain development by examining the fate of androgenetic (Ag: duplicated paternal genome) and parthenogenetic/gynogenetic (Pg/Gg: duplicated maternal genome) cells in chimeric embryos. Striking cell autonomous differences in the phenotypic properties of the uniparental cells were observed. Ag cells contributed substantially to the hypothalamic structures and not the cortex. By contrast, Pg/Gg cells contributed substantially to the cortex, striatum and hippocampus but not to the hypothalamic structures. Furthermore growth of the brain was enhanced by Pg/Gg and retarded by Ag cells. We propose that genomic imprinting may be responsible for a change in strategy controlling brain development in mammals. In particular, genomic imprinting may have facilitated a rapid non-linear expansion of the brain, especially the cortex, during development over evolutionary time.

7. Cell-cycle control and cortical development - The spatio-temporal timing of the last round of mitosis, followed by the migration of neuroblasts to the cortical plate leads to the formation of the six-layered cortex that is subdivided into functionally defined cortical areas. Whereas many of the cellular and molecular mechanisms have been established in rodents, there are a number of unique features that require further elucidation in primates. Recent findings both in rodents and in primates indicate that regulation of the cell cycle, specifically of the G1 phase has a crucial role in controlling area-specific rates of neuron production and the generation of cytoarchitectonic maps… Embryonic thalamocortical projections are likely to influence areal specification during early stages of corticogenesis by modulating proliferation.

8. Embryonic signaling centers expressing BMP, WNT and FGF proteins interact to pattern the cerebral cortex - Because noggin can induce Fgf8 expression, we examined noggin and BMP signaling in the Emx2 mutant. As the telencephalic vesicle closed, Nog expression was expanded and BMP activity reduced, potentially leading to FGF8 upregulation. Our findings point to a cross-regulation of BMP, FGF, and WNT signaling in the early telencephalon, integrated by EMX2, and required for normal cortical development. When endogenous BMP signaling is inhibited by noggin, robust Fgf8 expression appears ectopically in the cortical primordium.

9. Regional and Cellular Patterns of reelin mRNA Expression in the Forebrain of the Developing and Adult Mouse - The reelin gene encodes an extracellular protein that is crucial for neuronal migration in laminated brain regions. During embryogenesis,reelin was detected in the cerebral cortex in Cajal-Retzius cells but not in the GABAergic neurons of layer I. At prenatal stages, reelin was also expressed in the olfactory bulb, and striatum and in restricted nuclei in the ventral telencephalon, hypothalamus, thalamus, and pretectum. At postnatal stages, reelin transcripts gradually disappeared from Cajal-Retzius cells, at the same time as they appeared in subsets of GABAergic neurons distributed throughout neocortical and hippocampal layers. In other telencephalic and diencephalic regions,reelin expression decreased steadily during the postnatal period.

10. Independent Expression of the α and β c-erbA Genes in Developing Rat Brain - Thyroid hormone is important for normal brain development. Cellular responses to thyroid hormone are mediated by multiple nuclear receptors, classified into α- and β-subtypes. In the rat, expression of both the α and β genes results in several translation products.  The differential temporal and spatial distribution as well as coexpression at comparable levels in certain brain regions suggest different roles for the c-erbA proteins during brain development and in the mature animal.

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