BAD NEW FOR NEO-DARWINISTS\u2014DNA MUST CODE FOR EMBRYOGENESIS<\/p>\r\n\r\n\r\n\r\n
CHROMATIN REGULATION OF EARLY EMBRYONIC LINEAGE SPECIFICATION<\/p>\r\n\r\n\r\n\r\n
Darwin\u2019s theory of evolution\u2014the creation of human beings by the natural selection of random mutations\u2014is a wholly inadequate scientific theory to explain the astronomically complex anatomy and physiology of human beings. Darwin based his theory of evolution on the morphology (shape) of different species. He knew nothing of genetics, embryology and molecular biology. Without incorporating these (and other) sciences, Darwin\u2019s theory necessarily fails as a mechanism for the creation of humans.<\/p>\r\n\r\n\r\n\r\n
Unfortunately, Neo-Darwinists who are aware of these sciences have no excuse for their acceptance of such an unsophisticated worldview of creation. If Neo-Darwinists expect us to believe that the current human genome is an accumulation of random mutations, they first need to explain how DNA codes for the constantly changing anatomy and physiology of an embryo, fetus, child and finally an adult. Naturally, no Neo-Darwinist has yet attempted this.<\/p>\r\n\r\n\r\n\r\n
Most unfortunate for Neo-Darwinists, every adult must begin as an embryo and very little is known about the function of DNA in embryology. Recently, elegant research has been done in this area and the complexity is awe-inspiring.<\/p>\r\n\r\n\r\n\r\n
\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Knott and Latham provide a collection of current research in Advances in Anatomy, Embryology and Cell Biology: Chromatin Regulation of Early Embryonic Lineage Specification <\/em>(Springer, 2018), which addresses the topic of how DNA effects embryologic development. It is my goal to provide a simple and very brief description of the research presented in order to illustrate the failure of Darwinism. This book consists of five research papers. I will present a short glossary of terms used by the authors, then a synopsis of four papers, and finally conclude with some thoughts on what that means for Darwinism. If the reader is expecting support for Darwinism, he or she may be disappointed\u2014or hopefully, enlightened.<\/p>\r\n\r\n\r\n\r\n EMBRYOLOGY PRIMER<\/p>\r\n\r\n\r\n\r\n \u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Before getting started, I would like to present a very brief embryology lesson so that the authors\u2019 findings will be more accessible. The journey from fertilization to an adult is extremely complex and is controlled at every step and every moment by countless genes. The authors illustrate this complexity when they state, \u201cEvery cell in an organism contains the same genome, and yet there are multiple distinct cell types, all of which exhibit different dynamic gene expression profiles. Therefore, when we consider cell fate choices, we are witnessing the rewiring of these gene regulatory networks (GRN) to create new stable cell types.\u201d[1]<\/a> The authors further elucidate the complexity involved. A cell\u2019s identity is defined by the genes it expresses and those it represses, therefore, to understand cell fate decisions we must understand how gene expression and gene repression are controlled.[2]<\/a><\/p>\r\n\r\n\r\n\r\n Within the first five days of development, a single-celled zygote grows by a very well-ordered series of cleavage divisions and successive differentiation events to create three lineages: trophectoderm (TE), epiblast and primitive endoderm (PrE).[3]<\/a> But how do cells \u201cknow\u201d how to respond appropriately to stimuli and ensure the correct expression of specific genes? The solution to this problem are the chromatin modifiers and remodelers. Chromatin modifiers and remodelers facilitate . . . the genes required in the new cell state and prevent aberrant expression of those that are undesirable.[4]<\/a> An important question is implicit, how are the signals decoded by the cells at the chromatin level? \u201cWhether a gene is transcribed or silent is largely dependent upon its chromatin environment.\u201d[5]<\/a> Thus we see the importance of chromatin in embryologic development. The following articles will expand upon other important molecular structures. But first:<\/p>\r\n\r\n\r\n\r\n GLOSSARY<\/p>\r\n\r\n\r\n\r\n Chromatin\u2014a complex of DNA, RNA and proteins from which chromosomes condense during cell division.<\/p>\r\n\r\n\r\n\r\n Epigenetic\u2014changes in an organism caused by modification of gene expression rather than alteration of the genetic code.<\/p>\r\n\r\n\r\n\r\n Inner Cell Mass\u2014the mass of cells in an embryo, which eventually become the fetus.<\/p>\r\n\r\n\r\n\r\n Primitive endoderm\u2014the layer of cells, which develop into the digestive tract.<\/p>\r\n\r\n\r\n\r\n Trophectoderm\u2014the membrane of cells that forms the wall of the early embryo, which provides nutrients to the embryo and later becomes the placenta.<\/p>\r\n\r\n\r\n\r\n ARTICLE \u00a0I<\/p>\r\n\r\n\r\n\r\n \u201cChromatin Remodelling Proteins and Cell Fate Decisions in Mammalian Preimplantation Development,\u201d Anzy Miller and Brian Hendrich.<\/p>\r\n\r\n\r\n\r\n \u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 The authors begin with a good review of the embryologic process. The very first cell divisions produce a ball of cells, each cell having the potential to form any cell in the developing embryo or placenta. As more and more cells are produced, some are located on the outside of the embryo and some are completely surrounded by other cells. It is here that cells undergo the very first lineage commitment event. The outer cells form the trophectoderm (TE) and lose the potential to form embryonic lineages. The inner cells form the Inner Cell Mass (ICM), which retain embryonic potential.[6]<\/a><\/p>\r\n\r\n\r\n\r\n \u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 The second cell-fate commitment occurs as the ICM transforms into extraembryonic primitive endoderm (PrE) and what is called a pluripotent epiblast (where pluripotent means each cell has the potential to become many different cell types; and epiblast is the ball of rapidly growing cells.)[7]<\/a> This enlarging embryo goes through several identifiable stages including preimplantation, implantation, placentation and gastrulation (the gastrula is the stage where the embryo consists of three layers\u2014ectoderm, mesoderm and endoderm). Growth from one stage to the next is controlled by many different factors which, \u201cmodulate embryonic chromatin structure, impose cellular polarity and direct distinct gene expression programs in the first cell lineages.\u201d[8]<\/a> Cell growth is defined by gene expression patterns, and gene expression is controlled by how the DNA is packaged into chromatin.[9]<\/a> And here lies an unavoidable reality; all of the information and programming needed for the embryo to grow into an adult is present at the beginning of first cell division. No further information is gained. A second fact with which Neo-Darwinists must deal is that a simple one-to-one relationship of DNA-to-morphology as Darwin\u2019s theory implies, cannot exist. (For a medical example involving vision see my book The Collapse of Darwinism, <\/em>chapter 9 Genetics, p. 184.)<\/p>\r\n\r\n\r\n\r\n From the beginning of cell division we are already dealing with complex \u201cgene expression patterns,\u201d \u201cgene expression programs,\u201d and \u201cmolecular mechanisms through which chromatin remodelers facilitate the successful completion of the first cell fate decisions.\u201d[10]<\/a> We are also dealing with vague and poorly understood processes naively referred to as \u201ccontrolled,\u201d \u201cimpose\u201d and \u201cdirect.\u201d All of these patterns, programs and molecular mechanisms along with their control, imposition and direction must be encoded within DNA and ready to go at fertilization. Darwinists are incapable of describing the accumulation of random mutations that led to this arrangement and function of DNA.<\/p>\r\n\r\n\r\n\r\n \u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Now the authors delve into the complex genetics, which I have very briefly and superficially summarized. Briefly, Chromatin remodelling complexes are divided into four classes (SWI\/SNF, ISWI, IN080 and CHD families). Each chromatin remodeler controls distinct aspects of chromatin biology.[11]<\/a> The complexity of chromatin remodelling is impressive. There are many complexes that belong to each family some of which contain as least 15 different subunits. And loss of subunits is incompatible with successful development.[12]<\/a> The authors suggest this when they state, \u201cThis work highlights two important points: that the essential targets of a chromatin remodeler may vary depending on the tissue and\/or developmental stage and that, while the developing embryo is fairly robust, only small changes in gene expression can be enough to culminate in developmental failure.\u201d[13]<\/a> Here we see that not only is chromatin complex, it is delicate. And this is merely the tip of the iceberg.<\/p>\r\n\r\n\r\n\r\n \u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 In summary, chromatin remodelling proteins ensure that cell fate decisions occur correctly throughout development, and importantly, very specific proteins are necessary for these cell fate decisions.[14]<\/a><\/p>\r\n\r\n\r\n\r\n ARTICLE II<\/p>\r\n\r\n\r\n\r\n \u201cCHDI Controls Cell Lineage Specification through Zygotic Genome Activation,\u201d Shinnosuke Suzuki and Naojiro Minami.<\/p>\r\n\r\n\r\n\r\n \u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 In this article the authors focus on cell lineage specification (the process of cell division and differentiation). Cell lineage specification is dependent on epigenetic factors (factors that regulate gene expression) and chromatin remodeling factor CHD1. Together, epigenetic factors and CHD1 are involved in gene expression networks.[15]<\/a> Immediately after fertilization, the zygote becomes a totipotent cell (a cell that can differentiate into every type of cell needed). This totipotent cell initiates a developmental program that eventually results in the production of a new organism, which consists of a myriad of differentiated cells after extensive reconfiguration.[16]<\/a> This reconfiguration process is dependent on transcripts and proteins that remodel maternal and paternal genomes.<\/p>\r\n\r\n\r\n\r\n \u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 The authors go into great detail describing the chemical structure, function and interdependency of numerous transcription factors involved in cell lineage specification. And of course these are only the factors about which we know anything. Although the authors go into excruciating detail discussing how some factors operate, and illuminate the incredible complexity of fetal development, they make it clear that this is merely the tip of the iceberg, \u201cHowever, it is still far from clear how the gene expression required for each developmental stage is controlled.\u201d[17]<\/a><\/p>\r\n\r\n\r\n\r\n \u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 For our purposes\u2014applying embryology to Darwin\u2019s theory\u2014this article clearly demonstrates the astronomically complex state of DNA controlled fetal development. This development requires highly controlled genetic networks that interact and are interdependent on poorly understood epigenetic factors and proteins. The likelihood of these dynamically functioning genetic networks having been created by Darwin\u2019s numerous successive slight modifications becomes increasingly remote with the discovery of every new molecule.<\/p>\r\n\r\n\r\n\r\n ARTICLE III<\/p>\r\n\r\n\r\n\r\n \u201cTranscriptional Regulation and Genes Involved in First Lineage Specification During Preimplantation Development,\u201d Wei Cui and Jesse Mager.<\/p>\r\n\r\n\r\n\r\n The authors investigate how successful development from a single-cell zygote into a complex multicellular organism requires precise coordination of various cell-fate decisions. They note that multiple transcription factors are enriched and others are upregulated. This article reviews transcriptional control mechanisms and the genes responsible for the distinct differences in first cell lineage specification, which are categorized into three separate major events.<\/p>\r\n\r\n\r\n\r\n The first major event to occur is the maternal-to-zygotic transition (MZT), which includes degradation of maternal mRNA\u2019s and replacement with zygotic transcripts.[18]<\/a> This requires \u201cdramatic reprogramming of gene expression.\u201d[19]<\/a> A second major event that must occur early is embryo compaction and polarization, which occurs in the eight-cell stage.[20]<\/a> Compaction must occur in a precise manner so that cell polarization and thus cell division-dependent repositioning may occur properly. A third critical event that must occur is blastomere allocation into two distinct types of cell divisions during the 8-16-cell transition, which requires \u201cappropriate regulation and mutually exclusive localization\u201d of transcription factors.[21]<\/a> The authors go on to explain in great detail how these transcription factors and genes interact and what can go wrong when any one of 53 genes do not interact appropriately.[22]<\/a><\/p>\r\n\r\n\r\n\r\n To illustrate the astronomically complex nature of early implantation the authors state, \u201cOur screen selected genes to target based solely on expression during preimplantation and resulted in 7.4% of genes (53\/712) with phenotypes. If there are ~11,000 genes expressed during preimplantation (Stanton and Green 2001), our results suggest that ~800 genes are required for lineage development and\/or specification during preimplantation-the majority of which have yet to be discovered.\u201d[23]<\/a> The authors conclude that first cell lineage decision is determined by many distinct mechanisms some of which act in parallel and some that act in networks.[24]<\/a> Despite everything described here, the authors conclude that, \u201cunderstanding of the genes required for the first lineage specification remains elusive.\u201d[25]<\/a> It seems quite unbelievable that Darwin\u2019s random mutations could produce such incredibly complex networks of genetic interaction. The sheer number of genes alone (not to mention the complexity of information) is pushing the likelihood of Darwin\u2019s mechanism to the point of infinity.<\/p>\r\n\r\n\r\n\r\n ARTICLE IV<\/p>\r\n\r\n\r\n\r\n \u201cROCK and RHO Playlist for Preimplantation Development: Streaming to HIPPO Pathway and Apicobasal Polarity in the First Cell Differentiation\u201d Vernadeth Alarcon and Yusuke Marikawa.<\/p>\r\n\r\n\r\n\r\n \u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 The authors begin by describing a mere embryologic observation that is misused by Neo-Darwinists as a mechanism, \u201cIn placental mammalian development, the first cell differentiation produces two distinct lineages that emerge according to their position within the embryo: the trophectoderm (TE, placenta precursor) differentiates in the surface while the inner cell mass (ICM, fetal body precursor) forms inside.\u201d[26]<\/a> They ask the question, \u201cWhat kinds of mechanisms would allow each cell to interpret its position within the embryo and to execute specific differentiation programs?\u201d[27]<\/a> When reading Neo-Darwinists explanation of embryology, one will all too frequently encounter statements that claim organs develop as a result of the three dimensional position cells take in a growing embryo (topography). A quick internet search provides numerous examples of this oversimplification including this from Scientific American, \u201cThus the position <\/strong>(location) of a cell in the early embryo largely determines <\/strong>what cell type it will become in the end of the process of the embryonic development [bold not mine].\u201d[28]<\/a> This feeble attempt to simplify embryology is also an attempt to avoid the extreme complexity inherent within embryology and antithetical to Darwin\u2019s theory. The authors state, \u201cActivities of RHO\/ROCK are required to promote TE differentiation and to concomitantly suppress ICM formation. RHO\/ROCK operate through the HIPPO signaling pathway, whose cell position-specific modulation is central to establishing unique gene expression profiles that confer cell fate\u201d[29]<\/a><\/p>\r\n\r\n\r\n\r\n \u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 When discussing the regulation of lineage-specific gene expressions, signaling both upstream and downstream, the authors state, \u201cThe genome content is equivalent among most cell types in the embryo, so that cell differentiation mainly occurs through differential gene expressions by transcriptional regulations of distinct sets of genes in a lineage-specific manner.\u201d[30]<\/a> The important concepts here are the phrases \u201cdifferential gene expression\u201d by \u201cdistinct sets of genes.\u201d There is no simple position-to-cell-type relationship as Neo-Darwinists would have it. There is in reality a massively complex set of interacting genetic programs. The authors describe over 30 genes and other genetic factors involved in just this study of preimplantation development during first cell division.<\/p>\r\n\r\n\r\n\r\n CONCLUSION:<\/p>\r\n\r\n\r\n\r\n This book presents complex information that is ignored by Neo-Darwinists. The creation of species through the natural selection of random mutations must occur in the DNA, and that DNA must direct development of an embryo, fetus, infant, child and finally an adult. As an example healthy, disease free vision requires input from every chromosome demonstrating there is no simple one-to-one relationship of DNA to functioning anatomy and physiology; and no computer model exists that can demonstrate which nucleotides mutated to what nucleotides to produce any organ, system or network in the human being. No Nobel Laureate, professor or politician can prove this last statement wrong, and by Darwin\u2019s own words his theory absolutely breaks down.<\/p>\r\n\r\n\r\n [1]<\/a> Anzy Miller and Brian Hendrich, \u201cChromation Remodelling Proteins and Cell Fate Decisions in Mammalian Preimplantation Development,\u201d Chromatin Regulatioin of Early Embryonic Lineage Specificaiton <\/em>(Cham: Springer, 2018), 4.<\/p>\r\n\r\n\r\n\r\n [2]<\/a> Id.<\/p>\r\n\r\n\r\n\r\n [3]<\/a> Id.<\/p>\r\n\r\n\r\n\r\n [4]<\/a> Id.<\/p>\r\n\r\n\r\n\r\n [5]<\/a> Id.<\/p>\r\n\r\n\r\n\r\n [6]<\/a> I., 3.<\/p>\r\n\r\n\r\n\r\n [7]<\/a> Id.<\/p>\r\n\r\n\r\n\r\n [8]<\/a> Id., 1.<\/p>\r\n\r\n\r\n\r\n [9]<\/a> Id., 3.<\/p>\r\n\r\n\r\n\r\n [10]<\/a> Id.<\/p>\r\n\r\n\r\n\r\n [11]<\/a> Id., 6.<\/p>\r\n\r\n\r\n\r\n [12]<\/a> Id., 8.<\/p>\r\n\r\n\r\n\r\n [13]<\/a> Id.<\/p>\r\n\r\n\r\n\r\n [14]<\/a> Id., 10.<\/p>\r\n\r\n\r\n\r\n [15]<\/a> Shinnosuke Suzuki and Naojiro Minami, \u201cCHD1 Controls Cell Lineage Specification Through Zygotic Genome Activation,\u201d Chromatin Regulation of Early Embryonic Lineage Specification <\/em>(Cham: Springer, 2018), 15.<\/p>\r\n\r\n\r\n\r\n [16]<\/a> Id.<\/p>\r\n\r\n\r\n\r\n [17]<\/a> Id., 25.<\/p>\r\n\r\n\r\n\r\n [18]<\/a> Wei Cui and Jesse Mager, \u201cTranscriptional Regulation and Genes Involved in First Lineage Specification During Preimplantation Development,\u201d Chromatin Regulation of Early Embryonic Lineage Specification <\/em>(Cham: Springer, 2018), 31.<\/p>\r\n\r\n\r\n\r\n [19]<\/a> Id., 33.<\/p>\r\n\r\n\r\n\r\n [20]<\/a> Id.<\/p>\r\n\r\n\r\n\r\n [21]<\/a> Id., 34.<\/p>\r\n\r\n\r\n\r\n [22]<\/a> Id., 39.<\/p>\r\n\r\n\r\n\r\n [23]<\/a> Id., 41.<\/p>\r\n\r\n\r\n\r\n [24]<\/a> Id.<\/p>\r\n\r\n\r\n\r\n [25]<\/a><\/p>\r\n\r\n\r\n\r\n [26]<\/a> Vernadeth Alarcon and Yusuke Marikawa, \u201cROCK and RHO Playlist for Preimplantation Development: Streaming to HIPPO Pathway and Apicobasal Polarity in the First Cell Differentiation,\u201d Chromatin Regulation of Early Embryonic Lineage Specification <\/em>(Cham: Springer, 2018), 47.<\/p>\r\n\r\n\r\n\r\n [27]<\/a> Id., 49.<\/p>\r\n\r\n\r\n\r\n [28]<\/a> Bora Zivkovic, \u201cBIO101-From Two Cells to Many: Cell Differentiation and Embryonic Development,\u201d Scientific American, <\/em>September 10, 2001. Accessed online at blogs.scientificamerican.com July 4, 2019.<\/p>\r\n\r\n\r\n\r\n
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