Is the age of the gene finally over?

To understand the challenge to the “superwatch” model by the erosion of the gene-centric view of nature, it is necessary to recall August Weismann’s seminal insight more than a century ago regarding the need for genetic determinants to specify organic form. As Weismann saw so clearly, in order to account for the unerring transmission through time with precise reduplication, for each generation of “complex contingent assemblages of matter” (superwatches), it is necessary to propose the existence of stable abstract genetic blueprints or programs in the genes- he called them “determinants”- sequestered safely in the germ plasm, away from the ever varying and destabilizing influences of the extra-genetic environment. Such carefully isolated determinants would theoretically be capable of reliably transmitting contingent order through time and specifying it reliably each generation. Thus, the modern “gene-centric” view of life was born, and with it the heroic twentieth century effort to identify Weismann’s determinants, supposed to be capable of reliably specifying in precise detail all the contingent order of the phenotype. Weismann was correct in this: the contingent view of form and indeed the entire mechanistic conception of life- the superwatch model- is critically dependent on showing that all or at least the vast majority of organic form is specified in precise detail in the genes. Yet by the late 1980s it was becoming obvious to most genetic researchers, including myself, since my own main research interest in the ‘80s and ‘90s was human genetics, that the heroic effort to find information specifying life’s order in the genes had failed. There was no longer the slightest justification for believing there exists anything in the genome remotely resembling a program capable of specifying in detail all the complex order of the phenotype. The emerging picture made it increasingly difficult to see genes as Weismann’s “unambiguous bearers of information” or view them as the sole source of the durability and stability of organic form. It is true that genes influence every aspect of development, but influencing something is not the same as determining it. Only a small fraction of all known genes, such as the developmental fate switching genes, can be imputed to have any sort of directing or controlling influence on form generation. From being “isolated directors” of a one-way game of life, genes are now considered to be interactive players in a dynamic two-way dance of almost unfathomable complexity, as described by Keller in The Century of The Gene- Michael Denton “An Anti-Darwinian Intellectual Journey”, Uncommon Dissent (2004), pages 171-2

ET

January 6, 2019

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Seversky, contrary to your materialistic "bottom up" Darwinian hopes, according to empirical science the gene, as envisioned by Darwinists, has actually died,,,, not just mistakenly assumed to be dead as with Twain.

The Gene Myth, Part II - August 2010 Excerpt: “It was long believed that a protein molecule’s three-dimensional shape, on which its function depends, is uniquely determined by its amino acid sequence. But we now know that this is not always true – the rate at which a protein is synthesized, which depends on factors internal and external to the cell, affects the order in which its different portions fold. So even with the same sequence a given protein can have different shapes and functions. Furthermore, many proteins have no intrinsic shape, (intrinsically disordered proteins), taking on different roles in different molecular contexts. So even though genes specify protein sequences they have only a tenuous (very weak or slight) influence over their functions. ,,,,So, to reiterate, the genes do not uniquely determine what is in the cell, but what is in the cell determines how the genes get used. Only if the pie were to rise up, take hold of the recipe book and rewrite the instructions for its own production, would this popular analogy for the role of genes be pertinent. Stuart A. Newman, Ph.D. – Professor of Cell Biology and Anatomy http://darwins-god.blogspot.com/2010/08/gene-myth-part-ii.html Ask an Embryologist: Genomic Mosaicism - Jonathan Wells - February 23, 2015 Excerpt: humans have a "few thousand" different cell types. Here is my simple question: Does the DNA sequence in one cell type differ from the sequence in another cell type in the same person?,,, The simple answer is: We now know that there is considerable variation in DNA sequences among tissues, and even among cells in the same tissue. It's called genomic mosaicism. In the early days of developmental genetics, some people thought that parts of the embryo became different from each other because they acquired different pieces of the DNA from the fertilized egg. That theory was abandoned,,, ,,,(then) "genomic equivalence" -- the idea that all the cells of an organism (with a few exceptions, such as cells of the immune system) contain the same DNA -- became the accepted view. I taught genomic equivalence for many years. A few years ago, however, everything changed. With the development of more sophisticated techniques and the sampling of more tissues and cells, it became clear that genetic mosaicism is common. I now know as an embryologist,,,Tissues and cells, as they differentiate, modify their DNA to suit their needs. It's the organism controlling the DNA, not the DNA controlling the organism. http://www.evolutionnews.org/2015/02/ask_an_embryolo093851.html Genes and Organisms: Improvising the Dance of Life - Stephen L. Talbott - Nov. 10, 2015 Excerpt: The performances of countless cells in your body are redirected and coordinated as part of a global narrative for which no localized controller exists. This redirection and coordination includes a unique choreography of gene expression in each individual cell. Hundreds or thousands of DNA sequences move (or are moved) within vast numbers of cell nuclei, and are subjected to extraordinarily nuanced, locally modulated chemical activity so as to contribute appropriately to bodily requirements that are nowhere codified — least of all in those DNA sequences.,,, DNA in its larger matrix You may recall from my earlier article, “Getting Over the Code Delusion” (Talbott 2010), that packing DNA into a typical cell nucleus is like packing about 24 miles of very thin, double-stranded string into a tennis ball, with the string cut up (in the normal human case) into 46 pieces, corresponding to our 46 chromosomes. To locate a protein-coding gene of typical size within all that DNA is like homing in on a one-half-inch stretch within those 24 miles. Or, rather, two relevant half-inch stretches located on different pieces of string, since we typically have two copies of any given gene. Except that sometimes one copy differs from the other and one version is not supposed to be expressed, or one version needs to be expressed more than the other, or the product of one needs to be modified relative to the other. So part of the job may be to distinguish one of those half-inch stretches from the other. “Decisions” everywhere, it seems. But no such decisions are made in a vacuum. As it happens, the chromosome does not consist of a naked DNA double helix. Our DNA, rather, is bound up with a massive, intricate, and dynamic protein-RNA-small molecule complex (called chromatin) that is as fully “informative” for the cell as the DNA sequence itself — and, you might say, much more active and directive.,,, the cell, by managing the shifting patterns of the chromatin infrastructure within which DNA is embedded, brings our chromosomes into movement on widely varying scales. These include large looping movements that put particular genes into connection with essential regulatory sequences and with other, related genes (that is, with other one-half inch stretches of our “24 miles of string in a tennis ball”).,,, A gene is not in any case the kind of rigidly defined entity one might hope to calculate with. As a functional unit appropriate to current circumstances, it must be cobbled together by the cell according to the needs of the moment. There is no neatly predefined path to follow once the cell has located the “right” half inch or so of string, or once it has done whatever is necessary to bring that locus into proper relation with other chromosomal loci participating in the same “dance”. ,,, A decisive problem for the classical view of DNA is that “as cells differentiate and respond to stimuli in the human body, over one million different proteins are likely to be produced from less than 25,000 genes”.30 Functionally, in other words, you might say that we have over a million genes.,,, http://www.natureinstitute.org/txt/st/org/comm/ar/2015/genes_29.htm What If (Almost) Every Gene Affects (Almost) Everything? – JUN 16, 2017 Excerpt: If you told a modern geneticist that a complex trait—whether a physical characteristic like height or weight, or the risk of a disease like cancer or schizophrenia—was the work of just 15 genes, they’d probably laugh. It’s now thought that such traits are the work of thousands of genetic variants, working in concert. The vast majority of them have only tiny effects, but together, they can dramatically shape our bodies and our health. They’re weak individually, but powerful en masse. https://www.theatlantic.com/science/archive/2017/06/its-like-all-connected-man/530532/ Theory Suggests That All Genes Affect Every Complex Trait – June 20, 2018 Excerpt: Mutations of a single gene are behind sickle cell anemia, for instance, and mutations in another are behind cystic fibrosis. But unfortunately for those who like things simple, these conditions are the exceptions. The roots of many traits, from how tall you are to your susceptibility to schizophrenia, are far more tangled. In fact, they may be so complex that almost the entire genome may be involved in some way,,, One very early genetic mapping study in 1999 suggested that “a large number of loci (perhaps > than 15)” might contribute to autism risk, recalled Jonathan Pritchard, now a geneticist at Stanford University. “That’s a lot!” he remembered thinking when the paper came out. Over the years, however, what scientists might consider “a lot” in this context has quietly inflated. Last June, Pritchard and his Stanford colleagues Evan Boyle and Yang Li (now at the University of Chicago) published a paper about this in Cell that immediately sparked controversy, although it also had many people nodding in cautious agreement. The authors described what they called the “omnigenic” model of complex traits. Drawing on GWAS analyses of three diseases, they concluded that in the cell types that are relevant to a disease, it appears that not 15, not 100, but essentially all genes contribute to the condition. The authors suggested that for some traits, “multiple” loci could mean more than 100,000. https://www.quantamagazine.org/omnigenic-model-suggests-that-all-genes-affect-every-complex-trait-20180620/ Gene Pleiotropy Roadblocks Evolution by Jeffrey P. Tomkins, Ph.D. – Dec. 8, 2016 Excerpt: Before the advent of modern molecular biology, scientists defined a gene as a single unit of inheritance. If a gene was found to influence multiple externally visible traits, it was said to be pleiotropic—a term first used in 1910.2 During this early period of genetic discovery, pleiotropy was considered to be quite rare because scientists assumed most genes only possessed a single function—a simplistic idea that remained popular throughout most of the 20th century. However, as our understanding of genetics grew through DNA science, it became clear that genes operate in complex interconnected networks. Furthermore, individual genes produce multiple variants of end products with different effects through a variety of intricate mechanisms.2,3 Taken together, these discoveries show that pleiotropy is a common feature of nearly every gene.,,, The pleiotropy evolution problem is widely known among secular geneticists, but rarely discussed in the popular media. In this new research report, the authors state, “Many studies have provided evidence for the ability of pleiotropy to constrain gene evolution.”,,, “Our study provided supportive evidence that pleiotropy constraints the evolution of transcription factors (Tfs).”,,, The authors state, “We showed that highly pleiotropic genes are more likely to be associated with a disease phenotype.”,,, http://www.icr.org/article/9747 Darwinism vs Biological Form – video https://www.youtube.com/watch?v=JyNzNPgjM4w

bornagain77

January 5, 2019

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Is The Age Of The Gene Finally Over?

Since it appears we still have much to learn, I'd say it's more like - to paraphrase Mark Twain - that reports of its demise are greatly exaggerated. It's still a work-in-progressSeversky

January 5, 2019

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I come here seldom anymore but today I was searching the archives for something I posted 10 years ago and found this video that I once posted . http://bit.ly/2RvgQtA It is relevant to the topic Also I saw one thread was deleted from 10 years ago and I am not sure why. It was available in the Wayback time machine but not in the archives. Are there others?jerry

January 5, 2019

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People of Evolutionistan are finally catching on. But let's not forget that DNA and "the gene" have been artificially hyped for a reason - to justify "evolution". It has always been clear to anyone willing to see, that the information carried by the 3 billion base pairs of DNA nucleotides - each containing 2 bits of information (ACGT) - in the human genome amounts to only 6 G-bit of data which is less than 1 G-Byte (fits easily on a thumb drive). This is hardly enough to capture the complete manufacturing specifications for the simplest products around us like a pencil or a tire, let alone anything alive: http://nonlin.org/dna-not-essence-of-life/Nonlin.org

January 5, 2019

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