Excerpt (from 2005): “The picture we see now in genetics is complex. Variation can occur in a number of ways. DNA sequence is not fate; far from it. The same sequence can yield many different products. Complexes of genes lie behind most discernible traits. Genes can be turned on and off at need. Non-coding DNA is becoming extremely important to understanding how genes do their work. Non-coding RNA, sugars, and lipids–including many cellular components not directly coded for or controlled by the genes–have risen in importance.”
Excerpt (from 2015) “Pseudogenes, for instance, represent a change in functional status from literal DNA to junk DNA, whereas some diseases are caused by either a change from functional DNA to garbage DNA (e.g., Chen et al. 2003) or from junk DNA to garbage DNA (Cho and Brant 2011). Rubbish DNA mutating to functional DNA may be referred to as “Lazarus DNA,” so named after the second most famous resurrected corpse in literature, Lazarus of Bethany (John 11:38–44; 12:1; 12:9; 12:17). Similarly, functional DNA may mutate to garbage DNA, in which case we suggest the term “Hyde DNA” based on the fictional transformation of a benevolent entity into a malicious one (Stevenson 1886). Alternatively, junk DNA may become garbage DNA, for which the term “zombie DNA” has been suggested (Kolata 2010).”
See also: DNA Methylation and organized genomes. Theorists can only add more confusion. They don’t understand anything about the biophysically constrained chemistry of protein folding, which is why they have never linked biologically based cause and effect to biodiversity. Until recently, theorists made claims about mutations and evolution despite what has been learned about RNA-mediated amino acid substitutions during the past few decades. See: CRISPR adaptation biases explain preference for acquisition of foreign DNA, which was reported as: CRISPR Shows How A Bacterial Cell Can Recognize Its Own DNA.
Excerpt: “Solving the riddle of self versus non-self for the bacterial immune system and deciphering the exact mechanism of this step in the CRISPR process gives us important insight into the unseen confrontation that is taking place everywhere, all around us, all the time.”
My comment: The unseen confrontation occurs in the context of viruses and nutrition that link RNA-mediated events to the chemistry of amino acids.
Excerpt: “It is critical that all students of the life sciences know well the structure and chemistry of the amino acids and other building blocks of biological molecules. Otherwise, it is impossible to think or talk sensibly about proteins and enzymes, or the nucleic acids.”
My comment: Dobzhansky tried to make sense of links between amino acids and biodiversity, but theorists accepted only what he claimed about mutations and evolution.
Dobzhansky (1973) Nothing in Biology Makes Any Sense Except in the Light of Evolution
1) “I am a creationist and an evolutionist.”
2) “…the so-called alpha chains of hemoglobin have identical sequences of amino acids in man and the chimpanzee, but they differ in a single amino acid (out of 141) in the gorilla” (p. 127).
Theorists refuse to accept the facts about RNA-mediated amino acid substitutions and cell type differentiation. See: Atheist Matt Dillahunty Goes After Intelligent Design — and Stumbles
Excerpt: “One estimate of the minimum number of amino acids necessary for the stabilization of a folded protein structure is seventy (see p. 346 of Jack Kyte’s Structure in Protein Chemistry, second edition, 2007).
Another point that may be noted is that the amino acids that contribute to the active site are typically scattered throughout the sequence. If modern proteins evolved from shorter polypeptides (in which the crucial amino acids are necessarily close together), this observation that the crucial amino acids in modern proteins are frequently not grouped together is surprising. Why? Because moving them about during their later evolution would require restructuring of the protein — a feat that I would suggest is also prohibitively improbable.”
My comment: Creationists continue to portray the RNA-mediated chemistry of protein folding in the context of biophysical constraints that link ecological variation to ecological adaptation via the physiology of reproduction in all genera. Evolutionists ignore all that and make claims like these:
1) “The reality is that biologists know so little about how the RNAi system works that it is premature to speculate at all about its origins.”
2) “…genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world.”
Until evolutionists address what is currently known by creationists about links from physics and chemistry to the conserved molecular mechanisms of RNA-mediated amino acid substitutions and cell type differentiation, others may want to read the creationist literature. It helps to explain what’s wrong with evolutionary theory. It also explains why serious scientists are now “Combating Evolution to Fight Disease.” The ammunition that serious scientists use to shoot-down the ridiculous theories of pseudoscientists includes published articles like this:
Epigenetic transitions leading to heritable, RNA-mediated de novo silencing in Arabidopsis thaliana
Excerpt: Virus-derived small (s)RNAs link virus-induced gene silencing (VIGS) in plants from DNA methylation to cell type differentiation. The sRNAs are 21/-22 nt in length but they are not referred to as microRNAs (miRNAs) except in a citation that claims “miRNAs trigger widespread epigenetically activated siRNAs from transposons” without indicating what siRNAs are before adding the additional terms “secondary epigenetically activated siRNAs (easiRNAs)” and “tasiRNAs” in the context of transacting-siRNA (tasiRNA) loci that guide RNA-mediated cell type differentiation.
My comment: Attempts to link viral microRNAs in plants to the balance of viral microRNAs and nutrient-dependent microRNAs that link RNA-mediated amino acid substitutions to cell type differentiation in all genera may fail because the term microRNA is not consistently used. “A microRNA (abbreviated miRNA) is a small non-coding RNA molecule (containing about 22 nucleotides) found in plants, animals, and some viruses, which functions in RNA silencing and post-transcriptional regulation of gene expression.”
It is clear that sRNAs are viral microRNAs that link entropic elasticity and the anti-entropic epigenetic effects of nutrient energy to the stability of organized genomes via the biophysically constrained chemistry of protein folding. But that clarity can be achieved only among those who understand the integration of physics, chemistry, and molecular biology of cell type differentiation. See for example: Life is physics and chemistry and communication.
Excerpt: “Most noncoding RNAs operate in complex with proteins as ribonucleoprotein particles such as ribosomal subunits, spliceosomes, editosomes, small nuclear and nucleolarRNPs, microRNAs, long noncoding RNAs, and the ancient and fascinating world of reverse transcriptases.36–39 Many noncoding RNAs are able to base pair to other nucleic acids, especially the non–base-pairing loops of the RNA stemloops, which are rather active in interacting processes.”
My comment: The role of noncoding RNAs is placed into the context of “…the virus-first perspective in that viruses are the first RNA stem loop group–derived agents that predated cellular DNA-based life.” Alternatively, the molecular biologist and biochemist Peter Borger noted in 2009 that “The most parsimonious answer is: the RNA viruses got their genes from their hosts.”
Whether or not RNA viruses predated cellular DNA-based life or got their genes from their hosts may be the concern of theologians and theorists. It is not likely to be of concern to serious scientists who are Combating Evolution to Fight Disease. Serious scientists are armed with information about RNA-directed DNA methylation and RNA-mediated amino acid substitutions that differentiate cell types of all genera. They are fighting against the pseudoscientific nonsense that theorists claim links mutations to the evolution of biodiversity. The fight can be placed into the context of what is known about links from viruses to pathology.
For examples, see: The protein LEM promotes CD8+ T cell immunity through effects on mitochondrial respiration, which was reported as: Scientists find key to ‘turbo-charging’ immune system to kill all cancers
See also: Fruit fly studies shed light on adaptability of nerve cells
Excerpt: “…a feedback mechanism was responsible for these changes and that it relied on the signalling protein Wnt.”
My comment: Nutrient-dependent pheromone-controlled feedback loops linked to chromatin loops also are linked from top-down causation to RNA-directed DNA methylation and RNA-mediated amino acid substitutions that differentiate the cell types of all invertebrates and vertebrates. The honeybee is a model organism of cause and effect. See: Nutrient-dependent/pheromone-controlled adaptive evolution: a model.
Excerpt: The honeybee already serves as a model organism for studying human immunity, disease resistance, allergic reaction, circadian rhythms, antibiotic resistance, the development of the brain and behavior, mental health, longevity, diseases of the X chromosome, learning and memory, as well as conditioned responses to sensory stimuli (Kohl, 2012).
For the vertebrate ecological link see: Wnt signalling underlies the evolution of new phenotypes and craniofacial variability in Lake Malawi cichlids
My comment: Everything currently known about nutrient-dependent RNA-directed DNA metabolism and RNA-mediated amino acids that differentiation cell types in invertebrates and vertebrates can be traced to differences in the metabolism of food by gut bacteria. See: Microbiome Marvels: Tribes’ Gut Bacteria Reveal Biological Surprises
Excerpt: “…bacteria may possess an ancient but complex set of defense mechanisms that swing into action whenever they come across new threats.”
Sabatini’s group has just linked “Nutrient-Sensing Mechanisms across Evolution” and via similarities and differences in nutrient inputs and amino acids that drive mTORC1/TORC1 signaling in diverse organisms. See also: SHMT2 drives glioma cell survival in ischaemia but imposes a dependence on glycine clearance.
Glycine is the only achiral amino acid, and its substitution in the gonadotropin releasing hormone (GnRH) decapeptide, links the nutrient-dependent pheromone-controlled physiology of reproduction in all vertebrates without the pseudoscientific nonsense about mutations and evolution that is touted by theoriests.
See also: “The Darwin Code: Intelligent Design without God”
Excerpt: “In 1996, I proposed to my publishers a novel about the coming changes in biology and evolutionary theory. The novel would describe an evolutionary event happening in real-time–the formation of a new sub-species of human being. What I needed, I thought, was some analog to what happens in bacteria. And so I would have to invent ancient viruses lying dormant in our genome, suddenly reactivated to ferry genes and genetic instructions between humans.
To my surprise, I quickly discovered I did not have to invent anything. Human endogenous retroviruses are real…”
My comment: The retroviruses in gut microbes link ecological variation to ecological adaptation in the context of viral microRNAs and nutrient-dependent microRNAs. The viral microRNAs contribute to entropic elasticity. The nutrient-dependent microRNAs link the anti-entropic epigenetic effects of nutrient uptake to RNA-directed DNA methylation and RNA-mediated amino acid substitutions that stabilize the organized genomes of all genera via their physiology of reproduction.
The physiology of human reproduction is nutrient-dependent. It is pheromone-controlled via the conserved molecular mechanisms of feedback loops linked to chromatin loops and biodiversity in species from microbes to man. Theorists who believe in pseudoscientific nonsense about mutations and evolution have limited discussion of human pheromones and nutrient-dependent RNA-mediated cell type differentiation for that same reason.
The nutrient-dependent control of biodiversity via the metabolism of nutrients is linked from thermodynamic cycles of protein biosynthesis and degradation to cell type differentiation in all genera. Mutations that perturb the thermodynamic cycles are linked to physiopathology, but the theorists have taught people to believe that mutations can be beneficial. If you believe that glioma cell survival in ischaemia is beneficial, you will probably continue to believe that mutations are beneficial.
Mutations are not beneficial. For contrast, differences in gut microbes can be beneficial because they link the production of amino acids from the nutrient-dependent pheromone-controlled physiology of reproduction to amino acid substitutions that differentiate the to cell types of all animals. Gut microbes link ecological variation to ecological adaptation via ecological processes. See: The Gut Microbiota of Rural Papua New Guineans: Composition, Diversity Patterns, and Ecological Processes
Gut microbes link ecological variation to ecological adaptation via nutrient-dependent RNA-directed DNA methlyation and RNA-mediated amino acid substitutions. The substitutions are fixed in the organized genomes humans and other vertebrates and in invertebrates via the metabolism of nutrients by gut microbes to species-specific pheromones that control the physiology of reproduction. No matter how many more times I attest to that fact, evolutionary theorists seem willing to ignore it. No matter how many times others accurately represent biologically-based cause and effect, they will also be ignored by theorists.
See: Tracking niche variation over millennial timescales in sympatric killer whale lineages
Excerpt: “Ecological variation is the raw material by which natural selection can drive evolutionary divergence [1–4].”
See for examples: Nutrient-dependent/pheromone-controlled adaptive evolution: a model.
Conclusion: “Minimally, this model can be compared to any other factual representations of epigenesis and epistasis for determination of the best scientific ‘fit’.”
My comment: Theorists may try to make their theories fit the model, but by doing so they are admitting to decades of foolish claims that have prevented scientific progress.
Excerpt: “This lipid is produced by an enzyme called PfPI3K.”
My comment: The diagram links the enzyme to cell signaling and survival. That suggests that the molecular mechanisms linked to the enzyme and production of the lipid are nutrient-dependent and that production arises via RNA-directed DNA methylation and RNA-mediated amino acid substitutions that stabilize the organized genomes of all genera via fixation in the context of their physiology of reproduction. Any claims that mutations link biologically-based cause and effect to drug resistance must be re-evaluated in the context of what is known about how metabolic networks and genetic networks are linked in all genera.
Excerpt: “Understanding the proximate and ultimate factors that affect the distribution of genetic variation in the genome is a central and enduring goal of population genetics and it carries important implications for a number of evolutionary processes. One implication of this work is that in species with large Nc, such as D. melanogaster, selection plays a dominant role in shaping the distribution of molecular variation in the genome.”
My comment: The authors suggest that Lewontin’s paradox is resolved via empirical evidence that selection on novel mutations offers a potential reconciliation. In a feeble attempt to continue to link mutations to the evolution of biodiversity, they fail to include what is currently known about nutrient-dependent RNA-directed DNA methylation, RNA-mediated amino acid substitutions, and the differentiation of all cell types in all genera via fixation of the amino acid substitutions that occurs only in the context of the physiology of reproduction.
In D. melanogaster, their model organism, they claim that “…selection plays a dominant role in shaping the distribution of molecular variation in the genome.”
It is true that selection of food links the epigenetic landscape to the physical landscape of DNA in organized genomes of species from microbes to mammals via the biophysically constrained RNA-mediated chemistry of protein folding and their physiology of reproduction. All other claims about mutations and evolution seem to be based on the pseudoscientific nonsense of theories that attempt to link selection on mutations to something besides physiopathology, as if serious scientists knew nothing about “Combating Evolution to Fight Disease”
See also: Defining a minimal cell: essentiality of small ORFs and ncRNAs in a genome‐reduced bacterium
Excerpt: “Small open reading frames, of less than 100 residues, made up slightly more than half of the essential components, and they appeared to encode components of larger protein, DNA, or RNA complexes. Protein domains, rather than complete proteins, were often the essential elements of larger proteins, whereas regulatory elements—5′ untranslated regions and noncoding RNAs—were also fundamental components.”
My comment: This was reported in What are the genomic requirements for life? The “residues” that appear to encode components of larger proteins, like the DNA or RNA complexes appear to be amino acids. Amino acid substitutions link nutrient uptake to the physiology of reproduction in all genera via changes in the microRNA/messenger RNA balance that typically lead to DNA repair and organism-level thermoregulation when viral microRNAs are contained by the nutrient-dependent immune system.
In species from microbes to mammals, the nutrient-dependent physiology of reproduction is controlled by exposure to food odors and the metabolism of nutrients to species-specific pheromones via receptor-mediated RNA-directed DNA methylation and RNA-mediated feedback loops linked to chromatin loops and nutrient-dependent biodiversity.
This suggests to me that life involves much more of the biophysically constrained chemistry and conserved molecular mechanisms of cell type differentiation than what is typically considered in the ideas of theorists about the “origin of life.”
Excerpt: “…evolution proceeds firstly via pathways subject to negative regulation, then via promoter mutations and gene fusions, and finally via activation by intragenic gain-of-function mutations.”
My comment: Evidently they did not hear about the re-evolution of the flagellum that occurred over-the-weekend. It was, of course, nutrient-dependent and pheromone-controlled — like all ecological adaptations. See: Bacteria ‘hotwire their genes’ to fix a faulty motor
See also: Oncogene regulated by nutrients identified
Nutrient regulation of mTORC1 signaling is functionally conserved across eukaryotes. That fact appears to link nutrient-dependent RNA-mediated amino acid substitutions to the stability of organized genomes via the physiology of reproduction via works by Sabatini’s groups (mentioned above).
It also helps to link nutrient excess to physiopathology that includes cancer and neurodegenerative diseases such as Alzheimer’s.
See also: How to Build a Worm and Biologists link sexual selection and placenta formation [in a fish] Until serious scientists take the lead and begin to teach what is known about the conserved molecular mechanisms of nutrient-dependent cell type differentiation, few people will learn about the balance of viral microRNAs and nutrient-dependent microRNAs that leads to the RNA-directed DNA methylation and RNA-mediated amino acid substitutions to cell type differentiation in all genera via their physiology of reproduction.