BAD NEW FOR NEO-DARWINISTS\u2014DNA MUST CODE\nFOR EMBRYOGENESIS<\/p>\n\n\n\n
CHROMATIN REGULATION OF EARLY EMBRYONIC\nLINEAGE SPECIFICATION<\/p>\n\n\n\n
Darwin\u2019s\ntheory of evolution\u2014the creation of human beings by the natural selection of\nrandom mutations\u2014is a wholly inadequate scientific theory to explain the\nastronomically complex anatomy and physiology of human beings. Darwin based his\ntheory of evolution on the morphology (shape) of different species. He knew\nnothing of genetics, embryology and molecular biology. Without incorporating\nthese (and other) sciences, Darwin\u2019s theory necessarily fails as a mechanism\nfor the creation of humans.<\/p>\n\n\n\n
Unfortunately, Neo-Darwinists who are\naware of these sciences have no excuse for their acceptance of such an unsophisticated\nworldview of creation. If Neo-Darwinists expect us to believe that the current\nhuman genome is an accumulation of random mutations, they first need to explain\nhow DNA codes for the constantly changing anatomy and physiology of an embryo,\nfetus, child and finally an adult. Naturally, no Neo-Darwinist has yet\nattempted this. <\/p>\n\n\n\n
Most unfortunate for Neo-Darwinists, every\nadult must begin as an embryo and very little is known about the function of\nDNA in embryology. Recently, elegant research has been done in this area and\nthe complexity is awe-inspiring. <\/p>\n\n\n\n
Knott and Latham provide a\ncollection of current research in Advances\nin Anatomy, Embryology and Cell Biology: Chromatin Regulation of Early\nEmbryonic Lineage Specification <\/em>(Springer, 2018), which addresses the topic\nof how DNA effects embryologic development. It is my goal to provide a simple\nand very brief description of the research presented in order to illustrate the\nfailure of Darwinism. This book consists of five research papers. I will\npresent a short glossary of terms used by the authors, then a synopsis of four\npapers, and finally conclude with some thoughts on what that means for\nDarwinism. If the reader is expecting support for Darwinism, he or she may be\ndisappointed\u2014or hopefully, enlightened. <\/p>\n\n\n\n EMBRYOLOGY\nPRIMER<\/p>\n\n\n\n Before getting started, I would like\nto present a very brief embryology lesson so that the authors\u2019 findings will be\nmore accessible. The journey from fertilization to an adult is extremely\ncomplex and is controlled at every step and every moment by countless genes.\nThe authors illustrate this complexity when they state, \u201cEvery cell in an\norganism contains the same genome, and yet there are multiple distinct cell\ntypes, all of which exhibit different dynamic gene expression profiles.\nTherefore, when we consider cell fate choices, we are witnessing the rewiring\nof these gene regulatory networks (GRN) to create new stable cell types.\u201d[1]<\/a>\nThe authors further elucidate the complexity involved. A cell\u2019s identity is\ndefined by the genes it expresses and those it represses, therefore, to\nunderstand cell fate decisions we must understand how gene expression and gene\nrepression are controlled.[2]<\/a>\n<\/p>\n\n\n\n Within the first five days of\ndevelopment, a single-celled zygote grows by a very well-ordered series of\ncleavage divisions and successive differentiation events to create three\nlineages: trophectoderm (TE), epiblast and primitive endoderm (PrE).[3]<\/a>\nBut how do cells \u201cknow\u201d how to respond appropriately to stimuli and ensure the\ncorrect expression of specific genes? The solution to this problem are the\nchromatin modifiers and remodelers. Chromatin modifiers and remodelers facilitate\n. . . the genes required in the new cell state and prevent aberrant expression\nof those that are undesirable.[4]<\/a>\nAn important question is implicit, how are the signals decoded by the cells at\nthe chromatin level? \u201cWhether a gene is transcribed or silent is largely\ndependent upon its chromatin environment.\u201d[5]<\/a>\nThus we see the importance of chromatin in embryologic development. The\nfollowing articles will expand upon other important molecular structures. But\nfirst:<\/p>\n\n\n\n GLOSSARY<\/p>\n\n\n\n Chromatin\u2014a\ncomplex of DNA, RNA and proteins from which chromosomes condense during cell\ndivision.<\/p>\n\n\n\n Epigenetic\u2014changes\nin an organism caused by modification of gene expression rather than alteration\nof the genetic code.<\/p>\n\n\n\n Inner\nCell Mass\u2014the mass of cells in an embryo, which eventually become the fetus.<\/p>\n\n\n\n Primitive\nendoderm\u2014the layer of cells, which develop into the digestive tract.<\/p>\n\n\n\n Trophectoderm\u2014the\nmembrane of cells that forms the wall of the early embryo, which provides\nnutrients to the embryo and later becomes the placenta.<\/p>\n\n\n\n ARTICLE\n I <\/p>\n\n\n\n \u201cChromatin\nRemodelling Proteins and Cell Fate Decisions in Mammalian Preimplantation\nDevelopment,\u201d Anzy Miller and Brian Hendrich.<\/p>\n\n\n\n The authors begin with a good review\nof the embryologic process. The very first cell divisions produce a ball of\ncells, each cell having the potential to form any cell in the developing embryo\nor placenta. As more and more cells are produced, some are located on the\noutside of the embryo and some are completely surrounded by other cells. It is\nhere that cells undergo the very first lineage commitment event. The outer\ncells form the trophectoderm (TE) and lose the potential to form embryonic\nlineages. The inner cells form the Inner Cell Mass (ICM), which retain\nembryonic potential.[6]<\/a><\/p>\n\n\n\n The second cell-fate commitment\noccurs as the ICM transforms into extraembryonic primitive endoderm (PrE) and\nwhat is called a pluripotent epiblast (where pluripotent means each cell has\nthe potential to become many different cell types; and epiblast is the ball of\nrapidly growing cells.)[7]<\/a>\nThis enlarging embryo goes through several identifiable stages including\npreimplantation, implantation, placentation and gastrulation (the gastrula is\nthe stage where the embryo consists of three layers\u2014ectoderm, mesoderm and\nendoderm). Growth from one stage to the next is controlled by many different\nfactors which, \u201cmodulate embryonic chromatin structure, impose cellular\npolarity and direct distinct gene expression programs in the first cell\nlineages.\u201d[8]<\/a>\nCell growth is defined by gene expression patterns, and gene expression is\ncontrolled by how the DNA is packaged into chromatin.[9]<\/a>\nAnd here lies an unavoidable reality; all of the information and programming\nneeded for the embryo to grow into an adult is present at the beginning of\nfirst cell division. No further information is gained. A second fact with which\nNeo-Darwinists must deal is that a simple one-to-one relationship of\nDNA-to-morphology as Darwin\u2019s theory implies, cannot exist. (For a medical\nexample involving vision see my book The\nCollapse of Darwinism, <\/em>chapter 9 Genetics, p. 184.)<\/p>\n\n\n\n From the beginning of cell division we\nare already dealing with complex \u201cgene expression patterns,\u201d \u201cgene expression\nprograms,\u201d and \u201cmolecular mechanisms through which chromatin remodelers\nfacilitate the successful completion of the first cell fate decisions.\u201d[10]<\/a>\nWe are also dealing with vague and poorly understood processes naively referred\nto as \u201ccontrolled,\u201d \u201cimpose\u201d and \u201cdirect.\u201d All of these patterns, programs and\nmolecular mechanisms along with their control, imposition and direction must be\nencoded within DNA and ready to go at fertilization. Darwinists are incapable\nof describing the accumulation of random mutations that led to this arrangement\nand function of DNA. <\/p>\n\n\n\n Now the authors delve into the\ncomplex genetics, which I have very briefly and superficially summarized.\nBriefly, Chromatin remodelling complexes are divided into four classes\n(SWI\/SNF, ISWI, IN080 and CHD families). Each chromatin remodeler controls\ndistinct aspects of chromatin biology.[11]<\/a>\nThe complexity of chromatin remodelling is impressive. There are many complexes\nthat belong to each family some of which contain as least 15 different\nsubunits. And loss of subunits is incompatible with successful development.[12]<\/a>\nThe authors suggest this when they state, \u201cThis work highlights two important\npoints: that the essential targets of a chromatin remodeler may vary depending\non the tissue and\/or developmental stage and that, while the developing embryo\nis fairly robust, only small changes in gene expression can be enough to\nculminate in developmental failure.\u201d[13]<\/a>\nHere we see that not only is chromatin complex, it is delicate. And this is\nmerely the tip of the iceberg.<\/p>\n\n\n\n In summary, chromatin remodelling\nproteins ensure that cell fate decisions occur correctly throughout\ndevelopment, and importantly, very specific proteins are necessary for these\ncell fate decisions.[14]<\/a><\/p>\n\n\n\n ARTICLE\nII<\/p>\n\n\n\n \u201cCHDI\nControls Cell Lineage Specification through Zygotic Genome Activation,\u201d Shinnosuke\nSuzuki and Naojiro Minami.<\/p>\n\n\n\n In this article the authors focus on\ncell lineage specification (the process of cell division and differentiation). Cell\nlineage specification is dependent on epigenetic factors (factors that regulate\ngene expression) and chromatin remodeling factor CHD1. Together, epigenetic factors\nand CHD1 are involved in gene expression networks.[15]<\/a>\nImmediately after fertilization, the zygote becomes a totipotent cell (a cell\nthat can differentiate into every type of cell needed). This totipotent cell\ninitiates a developmental program that eventually results in the production of\na new organism, which consists of a myriad of differentiated cells after\nextensive reconfiguration.[16]<\/a>\nThis reconfiguration process is dependent on transcripts and proteins that\nremodel maternal and paternal genomes. <\/p>\n\n\n\n The authors go into great detail\ndescribing the chemical structure, function and interdependency of numerous\ntranscription factors involved in cell lineage specification. And of course\nthese are only the factors about which we know anything. Although the authors\ngo into excruciating detail discussing how some factors operate, and illuminate\nthe incredible complexity of fetal development, they make it clear that this is\nmerely the tip of the iceberg, \u201cHowever, it is still far from clear how the\ngene expression required for each developmental stage is controlled.\u201d[17]<\/a>\n<\/p>\n\n\n\n For our purposes\u2014applying embryology\nto Darwin\u2019s theory\u2014this article clearly demonstrates the astronomically complex\nstate of DNA controlled fetal development. This development requires highly\ncontrolled genetic networks that interact and are interdependent on poorly\nunderstood epigenetic factors and proteins. The likelihood of these dynamically\nfunctioning genetic networks having been created by Darwin\u2019s numerous\nsuccessive slight modifications becomes increasingly remote with the discovery\nof every new molecule. <\/p>\n\n\n\n ARTICLE\nIII<\/p>\n\n\n\n \u201cTranscriptional\nRegulation and Genes Involved in First Lineage Specification During\nPreimplantation Development,\u201d Wei Cui and Jesse Mager.<\/p>\n\n\n\n The authors investigate how successful\ndevelopment from a single-cell zygote into a complex multicellular organism\nrequires precise coordination of various cell-fate decisions. They note that\nmultiple transcription factors are enriched and others are upregulated. This\narticle reviews transcriptional control mechanisms and the genes responsible for\nthe distinct differences in first cell lineage specification, which are\ncategorized into three separate major events. <\/p>\n\n\n\n The first major event to occur is the\nmaternal-to-zygotic transition (MZT), which includes degradation of maternal\nmRNA\u2019s and replacement with zygotic transcripts.[18]<\/a>\nThis requires \u201cdramatic reprogramming of gene expression.\u201d[19]<\/a>\nA second major event that must occur early is embryo compaction and\npolarization, which occurs in the eight-cell stage.[20]<\/a>\nCompaction must occur in a precise manner so that cell polarization and thus\ncell division-dependent repositioning may occur properly. A third critical\nevent that must occur is blastomere allocation into two distinct types of cell\ndivisions during the 8-16-cell transition, which requires \u201cappropriate regulation\nand mutually exclusive localization\u201d of transcription factors.[21]<\/a>\nThe authors go on to explain in great detail how these transcription factors\nand genes interact and what can go wrong when any one of 53 genes do not\ninteract appropriately.[22]<\/a><\/p>\n\n\n\n To illustrate the astronomically complex\nnature of early implantation the authors state, \u201cOur screen selected genes to\ntarget based solely on expression during preimplantation and resulted in 7.4%\nof genes (53\/712) with phenotypes. If there are ~11,000 genes expressed during\npreimplantation (Stanton and Green 2001), our results suggest that ~800 genes\nare required for lineage development and\/or specification during\npreimplantation-the majority of which have yet to be discovered.\u201d[23]<\/a>\nThe authors conclude that first cell lineage decision is determined by many\ndistinct mechanisms some of which act in parallel and some that act in\nnetworks.[24]<\/a>\nDespite everything described here, the authors conclude that, \u201cunderstanding of\nthe genes required for the first lineage specification remains elusive.\u201d[25]<\/a>\nIt seems quite unbelievable that Darwin\u2019s random mutations could produce such\nincredibly complex networks of genetic interaction. The sheer number of genes\nalone (not to mention the complexity of information) is pushing the likelihood\nof Darwin\u2019s mechanism to the point of infinity. <\/p>\n\n\n\n ARTICLE\nIV<\/p>\n\n\n\n \u201cROCK\nand RHO Playlist for Preimplantation Development: Streaming to HIPPO Pathway\nand Apicobasal Polarity in the First Cell Differentiation\u201d Vernadeth Alarcon\nand Yusuke Marikawa.<\/p>\n\n\n\n The authors begin by describing a\nmere embryologic observation that is misused by Neo-Darwinists as a mechanism,\n\u201cIn placental mammalian development, the first cell differentiation produces\ntwo distinct lineages that emerge according to their position within the embryo:\nthe trophectoderm (TE, placenta precursor) differentiates in the surface while\nthe inner cell mass (ICM, fetal body precursor) forms inside.\u201d[26]<\/a>\nThey ask the question, \u201cWhat kinds of mechanisms would allow each cell to\ninterpret its position within the embryo and to execute specific\ndifferentiation programs?\u201d[27]<\/a>\nWhen reading Neo-Darwinists explanation of embryology, one will all too\nfrequently encounter statements that claim organs develop as a result of the\nthree dimensional position cells take in a growing embryo (topography). A quick\ninternet search provides numerous examples of this oversimplification including\nthis from Scientific American, \u201cThus the position\n<\/strong>(location) of a cell in the early embryo largely determines <\/strong>what cell type it will become in the end of the process\nof the embryonic development [bold not mine].\u201d[28]<\/a>\nThis feeble attempt to simplify embryology is also an attempt to avoid the\nextreme complexity inherent within embryology and antithetical to Darwin\u2019s\ntheory. The authors state, \u201cActivities of RHO\/ROCK are required to promote TE\ndifferentiation and to concomitantly suppress ICM formation. RHO\/ROCK operate\nthrough the HIPPO signaling pathway, whose cell position-specific modulation is\ncentral to establishing unique gene expression profiles that confer cell fate\u201d[29]<\/a>\n<\/p>\n\n\n\n When discussing the regulation of\nlineage-specific gene expressions, signaling both upstream and downstream, the\nauthors state, \u201cThe genome content is equivalent among most cell types in the\nembryo, so that cell differentiation mainly occurs through differential gene\nexpressions by transcriptional regulations of distinct sets of genes in a\nlineage-specific manner.\u201d[30]<\/a>\nThe important concepts here are the phrases \u201cdifferential gene expression\u201d by\n\u201cdistinct sets of genes.\u201d There is no simple position-to-cell-type relationship\nas Neo-Darwinists would have it. There is in reality a massively complex set of\ninteracting genetic programs. The authors describe over 30 genes and other\ngenetic factors involved in just this study of preimplantation development during\nfirst cell division. <\/p>\n\n\n\n CONCLUSION:<\/p>\n\n\n\n This\nbook presents complex information that is ignored by Neo-Darwinists. The\ncreation of species through the natural selection of random mutations must\noccur in the DNA, and that DNA must direct development of an embryo, fetus,\ninfant, child and finally an adult. As an example healthy, disease free vision\nrequires input from every chromosome demonstrating there is no simple\none-to-one relationship of DNA to functioning anatomy and physiology; and no\ncomputer model exists that can demonstrate which nucleotides mutated to what\nnucleotides to produce any organ, system or network in the human being. No\nNobel Laureate, professor or politician can prove this last statement wrong,\nand by Darwin\u2019s own words his theory absolutely breaks down. [1]<\/a> Anzy\nMiller and Brian Hendrich, \u201cChromation Remodelling Proteins and Cell Fate\nDecisions in Mammalian Preimplantation Development,\u201d Chromatin Regulatioin of Early Embryonic Lineage Specificaiton <\/em>(Cham:\nSpringer, 2018), 4.<\/p>\n\n\n\n [2]<\/a>\nId.<\/p>\n\n\n\n [3]<\/a>\nId.<\/p>\n\n\n\n [4]<\/a>\nId.<\/p>\n\n\n\n [5]<\/a>\nId.<\/p>\n\n\n\n [6]<\/a> I.,\n3.<\/p>\n\n\n\n [7]<\/a>\nId.<\/p>\n\n\n\n [8]<\/a>\nId., 1.<\/p>\n\n\n\n [9]<\/a>\nId., 3.<\/p>\n\n\n\n [10]<\/a>\nId.<\/p>\n\n\n\n [11]<\/a>\nId., 6.<\/p>\n\n\n\n [12]<\/a>\nId., 8.<\/p>\n\n\n\n [13]<\/a>\nId.<\/p>\n\n\n\n [14]<\/a>\nId., 10. <\/p>\n\n\n\n [15]<\/a>\nShinnosuke Suzuki and Naojiro Minami, \u201cCHD1 Controls Cell Lineage Specification\nThrough Zygotic Genome Activation,\u201d Chromatin\nRegulation of Early Embryonic Lineage Specification <\/em>(Cham: Springer, 2018),\n15.<\/p>\n\n\n\n [16]<\/a>\nId.<\/p>\n\n\n\n [17]<\/a>\nId., 25.<\/p>\n\n\n\n [18]<\/a>\nWei Cui and Jesse Mager, \u201cTranscriptional Regulation and Genes Involved in\nFirst Lineage Specification During Preimplantation Development,\u201d Chromatin Regulation of Early Embryonic\nLineage Specification <\/em>(Cham: Springer, 2018), 31.<\/p>\n\n\n\n [19]<\/a>\nId., 33.<\/p>\n\n\n\n [20]<\/a>\nId.<\/p>\n\n\n\n [21]<\/a>\nId., 34.<\/p>\n\n\n\n [22]<\/a>\nId., 39. <\/p>\n\n\n\n [23]<\/a>\nId., 41. <\/p>\n\n\n\n [24]<\/a>\nId.<\/p>\n\n\n\n [25]<\/a> <\/p>\n\n\n\n [26]<\/a>\nVernadeth Alarcon and Yusuke Marikawa, \u201cROCK and RHO Playlist for\nPreimplantation Development: Streaming to HIPPO Pathway and Apicobasal Polarity\nin the First Cell Differentiation,\u201d Chromatin\nRegulation of Early Embryonic Lineage Specification <\/em>(Cham: Springer, 2018),\n47.<\/p>\n\n\n\n [27]<\/a>\nId., 49.<\/p>\n\n\n\n [28]<\/a>\nBora Zivkovic, \u201cBIO101-From Two Cells to Many: Cell Differentiation and\nEmbryonic Development,\u201d Scientific\nAmerican, <\/em>September 10, 2001. Accessed online at\nblogs.scientificamerican.com July 4, 2019.<\/p>\n\n\n\n
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