Neo-Darwinian theory about evolution

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.



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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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.




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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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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A research paper in 2005 found that although there is only 1-2% difference in DNA sequence between humans and chimpanzees, 80% of the proteins of human and chimp are different. This was a very limited study. For starters they excluded from the study complex proteins that are synthesized from multiple genes, such as major histocompatibility complex (MHC) and immunoglobin, and mitochondrial proteins. Of the thousands of proteins in the body and brain of humans and chimp they ended up comparing just 127 proteins that have a one-on-one relation between DNA sequence and primary amino acid sequence in the protein. In other words the actual 3-D structures of the proteins were not compared which also would have a bearing on whether the proteins were different or the same. The report found that although only 25 out of the 127 proteins had identical amino acid sequences, most of the differences in the amino acid sequences were too small to explain the actual phenotype differences between human and chimp. In a lot of the proteins compared there were only a few differences in the amino acid polypeptide chains. The report suggests that phenotypic differences must be controlled by a small proportion of genes, either by regulatory genes or by major effect genes. Since 2005 the amount of data in the genetic databases would have increased exponentially and there is here an urgent need to do a follow up study in this area. This blog has been set up primarily to look into this issue in great depth. This issue holds the key to proving whether neo-Darwinism is right or wrong. We have to find these “regulatory genes or major effect genes” that are responsible for phenotype differences.

chimp photo



An article that was published in 1975, before the actual sequencing of the human and chimp genomes, entitled ‘Evolution at Two Levels in Humans and Chimpanzees’, had already made extensive enquiry into this vexed question that at the molecular level, that is to say our DNA and our proteins, the human and the chimp are even more similar than sibling species, and yet the phenotypes of the human and the chimp are so different. Sibling species are almost identical morphologically but are reproductively isolated, that is to say that cannot produce viable offspring (different sorts of fish or birds for example).

According to the article: ‘The molecular similarity between chimpanzees and humans is extraordinary because they differ far more than sibling species in anatomy and way of life. Although humans and chimpanzees are rather similar in the structure of the thorax and arms, they differ substantially not only in brain size but also in the anatomy of the pelvis, foot, and jaws, as well as in relative lengths of limbs and digits. Humans and chimpanzees also differ significantly in many other anatomical respects, to the extent that nearly every bone in the body of a chimpanzee is readily distinguishable in shape or size from its human counterpart. Associated with these anatomical differences there are, of course, major differences in posture (see cover picture), mode of locomotion, methods of procuring food, and means of communication. Because of these major differences in anatomy and way of life, biologists place the two species not just in separate genera but in separate families. So it appears that molecular and organismal methods of evaluating the chimpanzee- human difference yield quite different conclusions’.

The article concludes: ‘The contrasts between organismal and molecular evolution indicate that the two processes are to a large extent independent of one another. Is it possible, therefore, that species diversity results from molecular changes other than sequence differences in proteins? It has been suggested that major anatomical changes usually result from mutations affecting the expression of genes. According to this hypothesis, small differences in the time of activation or in the level of activity of a single gene could in principle influence considerably the systems controlling embryonic development. The organismal differences between chimpanzees and humans would then result chiefly from genetic changes in a few regulatory systems, while amino acid substitutions in general would rarely be a key factor in major adaptive shifts’.

What this means is that Neo-Darwinism (the post-Darwinian concept that species evolve by the natural selection of adaptive phenotypes caused by random mutation of genes) cannot explain how the human and chimp can be so similar in genotype and yet so dissimilar in phenotype. Are we expected to believe that over a period of six million years or so a small number of core regulatory genes created two separate and very different species with widely different phenotypes, and yet made minimal (and even negligible) mutational changes in the DNA and the proteins of these two species? Are we expected to believe that this process of species differentiation can possibly be random?

You will see in some of the articles on this website (Inner Self Located & Our Unconscious Soul) that the embryo cranium is bulging with midbrain and is firing spontaneously five weeks after conception. In my theories this is the soul or vital force. It’s my bet that the genes that are expressed in this early embryonic stage that cause the midbrain to fire, are the ‘regulatory’ genes responsible for the differentiation of the species.  

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You will see from my first post below that there is only a 1-2% difference in DNA sequence between human and chimpanzee. This post will perhaps only be meaningful to experts. These are research papers that describe specific genes that are expressed in the midbrain during development. The title to the paper appears in bold type. The next step for me is to go to the gene databases and to find the DNA sequence differences (if any) between these genes in the human and chimpanzee.

1. Differential Display of Genes Expressed at the Midbrain – Hindbrain Junction Identifies sprouty2: An FGF8-Inducible Member of a Family of Intracellular FGF Antagonists - A clone upregulated in cDNA derived from rhombomere 1 tissue showed a 91% identity at the nucleotide level to the putative human receptor tyrosine kinase antagonist: sprouty2. In situ hybridization on whole chick embryos showed chick sprouty2 to be expressed initially within the isthmus and rhombomere 1, spatially and temporally coincident with Fgf8 expression. However, at later stages this domain was more extensive than that of Fgf8. Introduction of ligand-coated beads into either midbrain or hindbrain region revealed that sprouty2 could be rapidly induced by FGF8. These data suggest that sprouty2 participates in a negative feedback regulatory loop to modulate the patterning activity of FGF8 at the isthmus

2. Cyclopia and defective axial patterning in mice lacking Sonic hedgehog gene function - Targeted gene disruption in the mouse shows that the Sonic hedgehog(Shh) gene plays a critical role in patterning of vertebrate embryonic tissues, including the brain and spinal cord, the axial skeleton and the limbs.

3. Pax-5 is expressed at the midbrain-hindbrain boundary during mouse development - Pax-5 was expressed in the developing brain, predominantly at the midbrain-hindbrain boundary, and in the neural tube. While the neural tube expression pattern overlapped completely with Pax-2 and Pax-8, the expression pattern in the brain was only partially overlapping. Unlike Pax-2 and Pax-8, Pax-5 was not expressed in the developing excretory system, thyroid, eye or ear. Our data suggest that Pax-5 has a role in the development of the central nervous system.

4. The midbrain-hindbrain phenotype of Wnt-1 (minus) mice results from stepwise deletion of engrailed-expressing cells by 9.5 days postcoitum - By examining embryonic expression of the mouse engrailed (En) genes, from 8.0 to 9.5 days postcoitum, we demonstrate that Wnt-1 primarily regulates midbrain development. The midbrain itself is required for normal development of the metencephalon. Wnt-1 and a related gene, Wnt-3a, are coexpressed from early somite stages in dorsal aspects of the myelencephalon and spinal cord. We suggest that functional redundancy between these two genes accounts for the lack of a caudal central nervous system phenotype.

5. Foxa1 and Foxa2 regulate multiple phases of midbrain dopaminergic neuron development in a dosage-dependent manner - The role of transcription factors in regulating the development of midbrain dopaminergic (mDA) neurons is intensively studied owing to the involvement of these neurons in diverse neurological disorders. Here we demonstrate novel roles for the forkhead/winged helix transcription factors Foxa1 and Foxa2 in the specification and differentiation of mDA neurons by analysing the phenotype of Foxa1 and Foxa2 single- and double-mutant mouse embryos. During specification, Foxa1 and Foxa2 regulate the extent of neurogenesis in mDA progenitors by positively regulating Ngn2 (Neurog2) expression. Subsequently, Foxa1 and Foxa2 regulate the expression of Nurr1 (Nr4a2) and engrailed 1 in immature neurons and the expression of aromatic l-amino acid decarboxylase and tyrosine hydroxylase in mature neurons during early and late differentiation of midbrain dopaminergic neurons. Interestingly, genetic evidence indicates that these functions require different gene dosages of Foxa1 and Foxa2.

6. A MicroRNA Feedback Circuit in Midbrain Dopamine Neurons - MicroRNAs (miRNAs) are evolutionarily conserved, 18- to 25-nucleotide, non–protein coding transcripts that posttranscriptionally regulate gene expression during development. miRNAs also occur in postmitotic cells, such as neurons in the mammalian central nervous system, but their function is less well characterized. We investigated the role of miRNAs in mammalian midbrain dopaminergic neurons (DNs). We identified a miRNA, miR-133b, that is specifically expressed in midbrain DNs.

7. Expression patterns of the homeo box-containing genes En-1 and En-2 and the proto-oncogene int-1 diverge during mouse development - We have compared the expression of the murine genes En-1,En-2, and in-1 during development by in situ hybridization. Expression of all three genes was first detected at 8.0 days in overlapping bands of the anterior neural folds. By 12.0 days the expression patterns diverged. En-1 and En-2 were expressed in a similar ring of cells in the central nervous system (CNS) at the midbrain/hindbrain junction.

8. Mutations in zebrafish genes affecting the formation of the boundary between midbrain and hindbrain - Mutations in two genes affect the formation of the boundary between midbrain and hindbrain (MHB): no isthmus (noi) and acerebellar (ace). noi mutant embryos lack the MHB constriction, the cerebellum and optic tectum, as well as the pronephric duct. Analysis of noi mutant embryos with neuron-specific antibodies shows that the MHB region and the dorsal and ventral midbrain are absent or abnormal, but that the rostral hindbrain is unaffected with the exception of the cerebellum. Using markers that are expressed during its formation (eng, wnt1 and pax-b), we find that the MHB region is already misspecified in noi mutant embryos during late gastrulation.

9. The caudal limit of Otx2 gene expression as a marker of the midbrain/hindbrain boundary: a study using in situ hybridisation and chick/quail homotopic grafts - Chick/quail homotopic grafts of various portions of the midbrain/hindbrain domain have shown that the progeny of the cells located in the caudal mesencephalic vesicle at stage HH10 are found within the rhombomere 1 as early as stage HH14. Furthermore, our results indicate that the cells forming the HH20 constriction (coinciding with the caudal Otx2 limit) are the progeny of those located at the caudal Otx2 limit at stage HH10 (within the mesencephalic vesicle). As a result, the Otx2-positive portion of the HH10 mesencephalic vesicle gives rise to the HH20 mesencephalon, while the Otx2-negative portion gives rise to the HH20 rostral rhombomere 1.

10. Inactivation of the (β)-catenin gene by Wnt1-Cre-mediated deletion results in dramatic brain malformation and failure of craniofacial development - ('bgr;)-Catenin is a central component of both the cadherin-catenin cell adhesion complex and the Wnt signaling pathway. We have investigated the role of (β)-catenin during brain morphogenesis, by specifically inactivating the (β)-catenin gene in the region of Wnt1 expression. To achieve this, mice with a conditional ('floxed') allele of (β)-catenin with required exons flanked by loxP recombination sequences were intercrossed with transgenic mice that expressed Cre recombinase under control of Wnt1 regulatory sequences. (β)-catenin gene deletion resulted in dramatic brain malformation and failure of craniofacial development. Absence of part of the midbrain and all of the cerebellum is reminiscent of the conventional Wnt1 knockout (Wnt1(−)(/)(−)), suggesting that Wnt1 acts through (β)-catenin in controlling midbrain-hindbrain development.


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