Epigenetic inheritance through non-coding RNAs

Sperm non-coding RNAs mediate transgenerational epigenetic inheritance of traits


Excerpt: "There is strong evidence that suggests certain environmental or lifestyle factors may lead to increased risk of developing chronic diseases. These factors such as diet, behavior, stress, exposure to pollutants, and physical activity have been known to cause epigenetic changes which may be passed down from one generation to the next. It is believed that a father’s exposure to environmental factors can play a role in an offspring’s epigenetic patterns and health.

Recent evidence suggests that sperm epigenetic modifications can survive reprogramming following fertilization and be inherited by the embryo. Three types of epigenetic modifications that can be paternally inherited are DNA methylation, histone modifications and noncoding RNAs (ncRNAs).

DNA methylation is the process by which methyl groups are added to cytosine or adenine and inhibit transcription. DNA methylation patterns are erased and reestablished during gametogenesis and embryogenesis. These two points provide susceptible windows for environmental exposures to alter methylation patterns. Changes in DNA methylation can induce abnormalities in chromatin structure and gene expression.

Studies have shown that certain DNA methylation marks can survive genome-wide reprogramming and be inherited. For example, paternal pre-diabetes has been demonstrated to increase the susceptibility of diabetes in an offspring due to altered sperm DNA methylation patterns. A father’s exposure to phthalates has been shown to impact epigenetic marks on sperm DNA and can have an impact on a couples’ ability to have children. Even stressed fathers might epigenetically pass on high blood sugar to their kids.

Noncoding RNAs are RNA fragments, such as miRNA, siRNA, piRNA and IncRNA, which regulate gene expression levels at the transcriptional and post-transcriptional level. During the sperm maturation process, sperm cells are able to uptake novel miRNAs. For example, miR-34c, which is the most abundant sperm miRNA, has been shown to be necessary for early embryonic cell division. This provides a mechanism in which ncRNA may be inherited and can have an impact on embryonic development and offspring health. miRNA-375 which is associated with paternal stress has been linked to depressive behavior and compromised glucose metabolism in offspring.

Another study found that obese males exhibited abnormal expression of several miRNAs in their sperm. The miRNAs are believed to pass on insulin resistance to offspring, which can cause diabetes. These results demonstrate the potential impact the ncRNA can have on embryonic development and induced epigenetic inheritance."
My comment: Human sperm contains thousands of RNA transcripts. The number of different long non-coding RNAs is more than 25,000 and different microRNAs are also counted in several thousands. Non coding RNAs are essential in stem cell programming. After the fertilization, embryonic cells are stem cells, which means they are lacking information structures required for cellular differentiation. Traits and characteristics of the developing embryo are established by these non-coding RNA transcripts in a process called epigenetic reprogramming. They transmit necessary epigenetic markers for DNA methylation patterns, histone markers and chromatin folding. Several studies confirm this scientific fact:


These crucial non-coding RNA molecules refute the Darwinian tree of life. By comparing non-coding RNA transcripts, we can find huge differences between organisms. For example, the similarity between human/chimp lncRNA transcripts is only under 30%. The more we understand about cellular mechanisms and regulatory factors, the weaker is the position of the pseudoscientific theory of evolution.


Epigenetic mechanisms behind flower coloration

DNA methylation patterns regulate flower coloration


Excerpt: "Lotus (Nelumbo nucifera), among the top ten famous Chinese traditional flowers, is well known for its prominent beautiful flowers. Flower coloration, affected by three types of pigments (anthocyanin, betalains and carotenoids), has been one of the hotspots in biological studies and appealed interests of many researchers. However, there is hardly any study on lotus flower.

Under the supervision of Prof. YANG Pingfang from Wuhan Botanical Garden, PhD student DENG Jiao conducted gel-based comperative proteomic analysis of petals between red and white lotus cultivars to uncover the flower coloration mechanism.

Pigments analysis of petals of red and white lotus cultivars revealed that the anthocyanins could only be detected in red cultivar. 88 differentially expressed protein spots (36 more-abundant and 52 less- abundant) were successfully identified through the comparative proteomic analysis between these two cultivars. With the Kyoto encyclopedia of genes and genomes (KEGG) pathway analysis, 4 enzymes (flavonoid 3-hydroxylase, anthocyanidin synthase,anthocyanidin 3-O-glucosyltransferase and glutathione S-transferase) were identified to be involved in anthocyanin pathway.

Analysis on the differentially accumulated proteins indicated that anthocyanindin synthase (ANS) gene might be the key factor that controlled the differential biosynthesis and accumulation of anthocyanins in these two lotus cultivars.

Based on the proteomic data, DNA methylation was analyzed on the promoter sequences of ANS gene in both cultivars, revealing different methylation intensity could lead to the varied flower coloration in red and white lotus flowers.

This research enlightens the mechanism of flower coloration, and the further understanding of flower coloration regulation at epigenetic level in lotus."

My comment: Pigment, coat, fur, skin or flower coloration is regulated by epigenetic mechanisms. DNA doesn't determine traits. Genetically identical cats might have different colors of furs. Genetically identical mice with different colored coats also point out how the epigenetic factors regulate the traits. Genetically identical human twins might have different colors of skin, hair and eyes. Human skin color is also regulated by inheritable epigenetic mechanisms and factors. Life is not driven by gene sequences. Genes are driven by lifestyle. Don't get lost.


Scientists start to realize that mutations don't drive evolution

Natural selection is not able to weed out harmful mutations - Scientists try to revert genetic alterations


Excerpt: "NEW YORK (GenomeWeb) – Broad Institute researchers David Liu and Feng Zhang have both developed new CRISPR-based systems, one for editing point mutations in the genome and the other for editing RNA, they revealed today in separate studies.

Liu's work, published in Nature, uses a guide RNA and catalytically impaired CRISPR-Cas9 to convert A-T base pairs to G-C base pairs in the genome, enabling the editing of single point mutations without the induction of double-stranded DNA breaks (DSBs).

The study builds on previous work done in Liu's lab in which researchers developed third-generation base editors called BE3s that consist of a catalytically impaired CRISPR-Cas9 mutant that cannot make DSBs, a single-strand-specific cytidine deaminase that converts C to uracil in the single-stranded DNA bubble created by Cas9, a uracil glycosylase inhibitor that impedes uracil excision and downstream processes that decrease base editing efficiency and product purity, and nickase activity to nick the non-edited DNA strand, directing cellular mismatch repair to replace the G-containing DNA strand.

In a press conference call about the study, Liu said this kind of editing enables the efficient and permanent conversion of C-G base pairs to T-A base pairs, and addresses point mutations found in roughly 15 percent of genetic diseases."

My comment: Actually more than 50% of disease-causing genetic mutations are missense/nonsense point mutations. (http://www.hgmd.cf.ac.uk/ac/index.php)

"However, the spontaneous deamination of cytosine and 5-methylcytosine in DNA is a major source of de novomutations, and about half of known pathogenic SNPs are C-G to T-A transitions, Liu and his coauthors at the Broad and Harvard University wrote in their paper. Therefore, converting A-T base pairs to G-C bases could help treat many more genetic diseases.

The deamination of adenine results in inosine, which is treated as guanine by DNA and RNA polymerases. However, there are no naturally occurring enzymes that deaminate adenine in DNA, so the researchers' first task was to directly engineer such an enzyme. They engineered E. coli TadA tRNA adenosine deaminase (TadA) through seven rounds of bacterial evolution to accept DNA as a substrate when fused to a catalytically impaired CRISPR-Cas9.

What resulted was an Adenine Base Editor (ABE). It transforms A to inosine, which is read as G. Similar to the BE3 base editor, the ABE also contains a nickase which causes the non-edited DNA strand to replace the T with a C. The CRISPR-Cas9 contained in the system binds to the guide RNA, and guides the ABE to the editing site — however, it has been impaired so that it can no longer induce DSBs.

REPAIRing RNA nucleotides

Meanwhile in Science, Zhang and his coauthors at the Massachusetts Institute of Technology and Harvard Medical School described their new CRISPR-based RNA editing system, called RNA Editing for Programmable A to I Replacement (REPAIR), which allows for the temporary repair of single RNA nucleotides in mammalian cells without permanently altering the genome.

While DNA editing holds promise for treating genetic disease, temporary editing of RNA has potential for treating diseases caused by temporary changes in cell state. In their study, the researchers profiled Type VI CRISPR systems to engineer a Cas13 ortholog capable of robust knockdown, and used catalytically-inactive Cas13 (dCas13) to direct adenosine-to-inosine deaminase activity by ADAR2 to transcripts in mammalian cells.

To demonstrate the broad applicability of the REPAIR system for RNA editing in mammalian cells, the team designed guides against two disease-relevant mutations: 878G>A in X-linked nephrogenic diabetes insipidus and 1517G>A in Fanconi anemia. They transfected expression constructs for cDNA of genes carrying these mutations into HEK293FT cells and tested whether REPAIR could correct the mutations, and found that they were able to achieve 35 percent correction in the first and 23 percent correction in the second.

They then tested the ability of REPAIR to correct 34 different disease-relevant G-to-A mutations and found that they were able to achieve significant editing at 33 sites with up to 28 percent editing efficiency. "The mutations we chose are only a fraction of the pathogenic G-to-A mutations (5,739) in the ClinVar database, which also includes an additional 11,943 G-to-A variants," the authors wrote. "Because there are no sequence constraints, REPAIRv1 is capable of potentially editing all these disease-relevant mutations, especially given that we observed editing regardless of the target motif."

In the press conference for his Nature paper, Liu called Zhang's work "an impressive and exciting development," and said that he's hopeful that DNA base editing and RNA base editing can be used together as complementary tools to address a broad range of research and therapeutic applications."

My comment: The cell is able to edit sequences of RNA-molecules. This complex mechanism is called RNA editing. Scientists try use this designed mechanism for reverting pathogenic point mutations.

A few years ago SNP's were thought to be the main reason for different human traits. Today we know that methylated cytosines are prone to turn into thymines in deamination caused by oxidative stress and other factors contributed by diet or life habits. Today scientists are understanding that the DNA is not determining traits of organisms. They are also realizing that mutations result in genetic degradation and loss of biological information. Serious scientists also understand that the cell uses the DNA as a passive information library for building RNA-products, that mediate the necessary information for cellular differentiation, metabolism, immunity and transmission of environmental signals. That's why it's a good idea to edit RNA-molecules. Editing DNA might not be successful because the DNA is never used directly in cellular processes. A functional RNA is not a direct copy of a DNA strand. It needs modification and it is regulated by several epigenetic factors, such as chromatin shape, CpG methylation and histone markers.

There is no natural selection that could eliminate these pathogenic mutations. Genetic diseases are in an explosive growth and scientists are in a hurry to develop efficient methods for repairing human genome. The theory of evolution is the most serious heresy of our time. Don't get lost.


Evolution has no mechanism

Epigenetic alterations and the genomic instability

The methylation structures of DNA and histones stabilize the genome. In order for the cell to function properly along to the program written for it, many epigenetic information structures will need to be in the right place. Even a small disturbance or imbalance in the methylation profiles may lead to genomic instability and hence to errors i.e. mutations in DNA, the cellular passive information library.

A stem cell has its DNA complete but the stem cell does nothing because it lacks epigenetic programming. It has no function or purpose. It needs epigenetic information structures to get the task and identity. Just DNA does not give the cell a function or identity.

Organisms experience ecological adaptation driven by food, climate, various stressors, environmental toxicants, sensory stimuli, etc. Adaptation to changing conditions always leads to changes in epigenetic information structures. Methylation profiles that experience changes will expose DNA to harmful mutations. This scientific fact can be examined by keywords:

epigenetic alterations genomic instability mutation

Recent significant observations of the ecological adaptation of organisms have been rapid and significant changes in the beak sizes and shapes of the Darwin's Finches. Scientists have already admitted that the changed dietary type led to changes in epigenetic information structures and variations in bird morphology. Other researchers have reported some changes in those birds' DNA. This is mainly about SNPs, ie point mutations and CNVs, that is, copy number variations. Point mutations can also be found in tens of millions in the human genome at the population level. Their number correlates with disease-causing genetic mutations that are already 220,270 at an annual rate of more than 20,000. The large number of SNPs in the dog genome correlates with the prevalence of hereditary diseases in dogs. In nature, the Red Fox has less than 1500 protein DNA encoding sequences less than, for example, a Bat-Eared Fox that has not undergone so many adaptation steps as the Red Fox. The disappearance of information is also evident in the fusion of  chromosomes and the decrease in their number.

It is therefore perfectly clear that changing epigenetic information structures are contributing to genetic degradation, although there are, of course, other causes. Viruses have been found to cause genomic instability. Viruses also need methyl groups for their own gene expression but lack mechanisms for methyl production. Therefore, they take it from its host cell whose genome becomes unstable due to the imbalance in the methylation profiles. The more genomes degenerate, the weaker the DNA repair mechanisms work and the faster the degradation phenomenon.

There is no mechanism for evolution because any change in organisms is due to the epigenetic regulation of existing biological information OR the gradual but inevitable corruption of information.


DNA has no control in cellular processes

Alternative splicing points to Intelligent Design

Alternative splicing is a complex mechanism that helps us understand that DNA does not control cellular mechanisms. Many people still think that one gene encodes one protein. Actually, the whole idea of ​​DNA genes encoding something is completely incorrect, at least within eukaryotes. 

It is important to understand the principles of alternative splicing. Without going into deep scientific terminology, I will briefly explain how alternative splicing works.

The cell reads certain DNA sections from which it builds a so-called pre-mRNA. The cell modifies this RNA transcript using a complex protein complex called a spliseosome. The spliseosome will carefully cut off that pre-mRNA from certain sequences to construct exactly the RNA sequence required by the cell for the required protein production. From one and the same DNA sequence, the cell is thus capable of manufacturing up to thousands of different proteins using this technology. For example, using the fruit fly Dscam gene the cell can produce as many as 38,016 different proteins. Without changing the DNA sequence! In the human genome there are only about 19,600 DNA sequences used to protein production, that is, less than that of a roundworm, but the number of different proteins in our body is up to two million according to some estimates. The ingenious alternative splicing mechanism makes this possible. In recent years, it has also been found that even most long non-coding RNA molecules go through alternative splicing procedure.
Alternative splicing is guided and controlled by several epigenetic factors such as DNA methylation profiles, histone epigenetic markers, and epigenetic markers of non-coding RNA molecules known in more than 140 different types.

More than 90% of human DNA-genes are read into an alternative splicing procedure. The number has risen from year to year as the research progresses. It is a clever and complex  mechanism that allows the implementation of alternative programs in the cell and hence the whole organism morphology and other features. Knowing the alternative splicing mechanism will help us understand that DNA is a kind of library information in the cell that it needs to produce the necessary proteins and to transmit epigenetic information about the environment to the organism's cells. DNA is passive information that does not control anything. DNA genes may overlap or embed with each other. The cell chooses different  strands of the DNA and constructs complex RNAs. Organisms may actually modify their own genome with many different mechanisms. This is done by nutrition, climate, stress factors, sensory stimulus etc. It has also been found that even our thoughts and attitudes can modify our DNA.

The alternative splicing mechanism points out that all changes in organisms are based on the alternative epigenetic regulation of existing biological information OR for gradual but unavoidable information corruption, ie genetic degeneration (whereby the alternatives are reduced). Therefore there is no mechanism for evolution. So do not be lost, good people.


January 2018: More Real World Evidence of Genetic Degeneration

January 2018: More Real World Evidence of Genetic Degeneration


Excerpt: "The newest edition of Genetic Entropy (2014), has shown that genetic degeneration is not just a theoretical concern, but is observed in numerous real-life situations. Genetic Entropy has reviewed research that shows: a) the ubiquitous genetic degeneration of the somatic cells of all human beings; and b) the genetic germline degeneration of the whole human population. Likewise Genetic Entropy has reviewed research that shows rapid genetic degeneration in the H1N1 influenza virus. Genetic Entropy also documents “evolution in reverse” in the famous LLEE bacterial experiment (article available here).
  • A new paper (Lynch, 2016) written by a leading population geneticist, shows that human genetic degeneration is a very serious problem. He affirms that the human germline mutation rate is roughly 100 new mutations per person per generation, while the somatic mutation rate is roughly 3 new mutations per cell division. Lynch estimates human fitness is declining 1-5% per generation, and he adds; “most mutations have minor effects, very few have lethal consequences, and even fewer are beneficial.”
  • Our new book “Contested Bones” (available at ContestedBones.org) cites evidence showing that the early human population referred to as Neanderthal (Homo neanderthalensis) was highly inbred, and had a very high genetic load (40% less fit than modern humans) (Harris and Nielsen, 2016; Roebroeks and Soressi, 2016). See pages pages 315-316. This severe genetic degeneration probably contributed to the disappearance of that population (PrÜfer et al., 2014; Sankararaman et al., 2014).
  • Similarly, the new book Contested Bones (pages 86-89), cites evidence that the early human population referred to as “Hobbit” (Homo floresiensis), was also inbred and apparently suffered from a special type of genetic degeneration called “reductive evolution” (insular dwarfing) (Berger et al., 2008; Morwood et al., 2004). This results in reduced body size, reduced brain volume, and various pathologies (Henneberg et al., 2014).
  • Contested Bones (pages 179-210) also cites evidence that the early human population referred to as Naledi (Homo naledi), was likewise inbred and suffered from “reductive evolution”, again resulting in reduced body size, reduced brain volume, and various pathologies.
  • Contested Bones (pages 53-75) also cites evidence that many other early human populations, broadly referred to as Erectus (Homo erectus), were inbred and suffered from “reductive evolution” (Anton, 2003). However, it seems the genetic degeneration of Erectus was less advanced—generally resulting in more moderate reductions in body size, brain size, and pathologies. Indeed, many paleoanthropologists would fold both Hobbit and Naledi into the more diverse Erectus category. 
  • An important but overlooked paper, written by leading population geneticists (Keightley et al., 2005), reported that the two hypothetical populations that gave rise to modern man and modern chimpanzee both must have experienced continuous genetic degeneration during the last 6 million years. The problems associated with this claim should be obvious. Their title is: Evidence for Widespread Degradation of Gene Control Regions in Hominid Genomes, and they state that there has been the“accumulation of a large number of deleterious mutations in sequences containing gene control elements and hence awidespread degradation of the genome during the evolution of humans and chimpanzees.” (emphasis added).
  • A new paper (Gaur, 2017), shows that if a substantial fraction of the human genome is functional (is not junk DNA), then the evolution of man would not be possible (due to genetic degeneration). Gaur states that human evolution would be very problematic even if the genome was 10% functional, but would be completely impossible if 25% or more was functional. Yet the ENCODE project shows that at least 60% of the genome is functional.
  • A new paper (Rogers and Slatkin, 2017), shows that mammoth populations were highly inbred and carried an elevated genetic load (likely contributing to their extinction due to “mutational meltdown”).
  • A paper (Kumar and Subramanian, 2002) shows that mutation rates are similar for all mammals, when based on mutation rate per year (not per generation). This means that mammals (both mice and men) should degenerate similarly in the same amount of time. This suggests that the major mutation mechanisms are not tightly correlated to cell divisions.
  • A new paper (Ramu et al., 2017), shows that the tropical crop, cassava, has been accumulating many deleterious mutations, resulting a seriously increasing genetic load, and a distinct decline in fitness.
  • Another paper (Mattila et al. 2012), shows high genetic load in an old isolated butterfly population. “This population exemplifies the increasingly common situation in fragmented landscapes, in which small and completely isolated populations are vulnerable to extinction due to high genetic load.”
  • Another paper (Holmes, E. C. 2003), shows that all RNA viruses must be young—less than 50,000 years. This is consistent with our H1N1 influenza study that show that RNA virus strains degenerate very rapidly."
My comment: Time will not rescue the theory of evolution. Time means degeneration. We can only observe rapid change in nature caused by epigenetic regulation of existing biological information OR gradual but inevitable disppearance of information. 


Daily cycle of gene expression is regulated by 3D genome folding

3D genome folding regulated by clock proteins makes gradual gene expression possible


Excerpt: "It's well known that the human body functions on a 24-hour, or circadian, schedule. The up-and-down daily cycles of a long-studied clock protein called Rev-erb coordinates the ebb and flow of gene expression by tightening and loosening loops in chromosomes, according to new research from the Perelman School of Medicine at the University of Pennsylvania. The findings appear online this week in Science.

Over the last 15-plus years, a team led by the new study's senior author Mitchell A. Lazar, MD, Ph.D., director of Penn's Institute for Diabetes, Obesity, and Metabolism, has been teasing out the versatile role of Rev-erb in maintaining daily cycles of the body's molecular clock, metabolism, and even brain health.

"Many studies, including this one, point to a link between the human internal clock and such metabolic disorders as obesity and diabetes," Lazar said. "Proteins such as Rev-erb are the gears of the clock and understanding their role is important for investigating these and many other diseases."

Human physiology works on a 24-hour cycle of gene expression (when the chromosome coding region is translated by RNA and then transcribed to make protein) and is controlled by the body's molecular clock. Core clock proteins activate or repress protein complexes that physically loop one part of a chromosome to become adjacent to a distant part of the same chromosome.
The Penn team showed that daily oscillations of Rev-erb control gene expression in the mouse liver via interactions between on-and-off regions on the same chromosome. Previous work from the team demonstrated that by 5 p.m., Rev-erb increases to its highest concentration in mouse liver, where it turns off certain genes and therefore protein transcription. But as the day turns to night, its concentration steadily decreases and nearly vanishes from the liver by 5 a.m.

Without Rev-erb around, expression of its target genes returns. And this process repeats normally, day after day. Other researchers have established that activator proteins drive the formation of chromosome loops to turn on genes; however, how repressor proteins such as Rev-erb regulate their part in turning off gene expression has remained unanswered, until now.

In this study, the team demonstrated that Rev-erb represses transcription by loosening chromosome loops. Rev-erb kicks out the protein complexes that bridge the distant regions of the chromosome, thereby destabilizing the loop and turning off the gene.

"The mechanisms by which Rev-erb loosens loops in DNA, leading to circadian repression of transcription, are likely to apply to other clock proteins," Lazar said. Recent studies have tied Rev-erb to cancer and cardiovascular disease. The team aims to look at new drugs that affect chromosome looping to see how it may affect gene expression in cancer cells and tissues other than the liver. "

My comment: Here we can see an incredible, sophisticated mechanism controlling gradual gene expression. This is also an example of how analogue information is used in the cell. This points to Intelligent Design and Creation.


Single-cell analysis reveals dramatic changes in the brain's gene expression patterns after visual stimulation

Bursts of neuronal activity that last only milliseconds trigger lasting changes in the brain


Excerpt: "Using novel technologies developed at HMS, the team looked at how a single sensory experience affects gene expression in the brain by analyzing more than 114,000 individual cells in the mouse visual cortex before and after exposure to light.

Their findings revealed a dramatic and diverse landscape of gene expression changes across all cell types, involving 611 different genes, many linked to neural connectivity and the brain’s ability to rewire itself to learn and adapt.

The results offer insights into how bursts of neuronal activity that last only milliseconds trigger lasting changes in the brain, and open new fields of exploration for efforts to understand how the brain works.
“What we found is, in a sense, amazing. In response to visual stimulation, virtually every cell in the visual cortex is responding in a different way,” said co-senior author Michael Greenberg, the Nathan Marsh Pusey Professor of Neurobiology and chair of the Department of Neurobiology at HMS.

“This in essence addresses the long-asked question about nature and nurture: Is it genes or environment? It’s both, and this is how they come together,” he said.

Neuroscientists have known that stimuli—sensory experiences such as touch or sound, metabolic changes, injury and other environmental experiences—can trigger the activation of genetic programs within the brain.

They then exposed the mice to light and studied how it affected genes within the brain. Using technology developed by the Klein lab known as inDrops, they tracked which genes got turned on or off in tens of thousands of individual cells before and after light exposure.

The team found significant changes in gene expression after light exposure in all cell types in the visual cortex—both neurons and, unexpectedly, non-neuronal cells such as astrocytes, macrophages and muscle cells that line blood vessels in the brain.

Roughly 50 to 70 percent of excitatory neurons, for example, exhibited changes regardless of their location or function. Remarkably, the authors said, a large proportion of non-neuronal cells—almost half of all astrocytes, for example—also exhibited changes.

The team identified thousands of genes with altered expression patterns after light exposure, and 611 genes that had at least two-fold increases or decreases.

These findings open a wide range of avenues for further study, the authors said. For example, how genetic programs affect the function of specific cell types, how they vary early or later in life and how dysfunction in these programs might contribute to disease, all of which could help scientists learn more about the fundamental workings of the brain.

“Experience and environmental stimuli appear to almost constantly affect gene expression and function throughout the brain. This may help us to understand how processes such as learning and memory formation, which require long-term changes in the brain, arise from the short bursts of electrical activity through which neurons signal to each other,” Greenberg said.One especially interesting area of inquiry, according to Greenberg, includes the regulatory elements that control the expression of genes in response to sensory experience. In a paper published earlier this year in Molecular Cell, he and his team explored the activity of the FOS/JUN protein complex, which is expressed across many different cell types in the brain but appears to regulate unique programs in each different cell type."

My comment: Sensory experiences affect gene expression patterns in the brain that controls gene expression patterns and epigenetic information layers in other parts of the body. This is why a fish in a dark environment is able to rapidly alter its gene expression patterns and become blind. Nothing to do with random mutations or selection. All kind of visual stimulation affects the brain and after that, overall inheritable epigenetic information layers in the body. Any change in organisms is based on epigenetic regulation of existing biological information OR loss of it.


DNA is not your destiny

DNA genes don't determine traits - Why mapping your DNA may be less reliable than you think


Excerpt: "Yet, the more genomes researchers study, the more evidence mounts that using DNA to predict health risks is anything but precise – for now, at least. These days, nature's longest thread comes off a like a trickster, shape-shifting from person to person, written in a wily language no one fully understands, with at least three billion ways to misread it.

Launched publicly in Canada in 2012, the PGP aims to build an open, online database of Canadian genomes for use by researchers anywhere and more than 1,100 Canadians have signed up so far. But by unravelling the entire codes of just the inaugural participants, what the project leaders have found is both promising and perplexing: medically relevant information in each volunteer, but also a vast trove of mysterious quirks and dramatic glitches that none of them expected to see in a cohort of healthy people.

Surprising, too, is that many of the volunteers carry mutated genes that suggest they should be sick, diseased or even near death – but aren't.

Take Participant No. 16, whose genes seem to tell the grim story of an aortic stenosis. The potentially lethal heart defect develops before birth, narrowing the body's main artery just above the valve that connects it to the heart, forcing it to work harder, which can lead to chest pains, heart failure and the risk of sudden death. On paper, No. 16 looks like a time bomb. In real life, he is a healthy 67-year-old who works long hours, skis, trains with CrossFit three times a week and, according to a CT scan, has a normal heart.
Participant No. 27 is another jolt. Missing from about 70 per cent of her blood cells is an entire chromosome, the X sex chromosome, of which women usually have two copies. On paper, No. 27 has mosaic Turner syndrome, a rare disorder that only affects females and can lead to impaired sexual development, short stature, a webbed neck and heart problems. In reality, she is a healthy 54-year-old who had no inkling her DNA harboured such a twist.

The report, compiled by 53 researchers at the Hospital for Sick Children and the University of Toronto, captures the staggering breadth of how much is left to learn before science can properly interpret humanity's operating code. It offers proof that most research to date has overlooked the different types of genetic glitches that can lead to health problems, while adding to the growing realization that many genes once thought to cause disease probably don't.

Just ask Participant No. 16 about the heart abnormalities his genes suggest.

You can imagine someone getting this report back and saying, 'Oh my God, I'm gonna die of this! How do I check it out?' Then there will be echocardiograms and all these things being done on people who are perfectly healthy," says Doug Mowbray, who wasn't troubled by his vexing results because the participants had a genetic counsellor walk them through the fog. But also because he's a doctor himself – a radiologist, in fact, in Southwestern Ontario. He knew his heart was normal because he took a good look at it while calibrating a new imaging scanner a few years ago.

All of which implies that in these foggy days of the so-called genomic revolution, people can easily be led astray by test results that may bring false comfort, or needless stress and treatment – especially now, when the largely unregulated market of direct-to-consumer DNA tests is booming."

My comment: The DNA genes don't determine traits. There are no skin color, height, intelligence, obesity or any other trait that is directly connected to a certain gene. The ‘grammar’ of the human genetic code is more complex than that of even the most intricately constructed spoken languages in the world. There are only ~19,600 DNA genes used for protein encoding machineries in our DNA, but the number of different protein isoforms in our bodies might be up to one million. Mutations in these overlapping and embedded genes are typically very harmful. The DNA is a library that cells use for managing their tasks.

Traits are determined by our epigenome. This covers the DNA methylation profiles, a huge diversity of histone chemical tags (a biological database) and different types of coding and non-coding RNA-molecules that function as epigenetic information carriers between cells.

Life is not driven by the DNA genes. Genes are driven by your lifestyle. Genes are followers, not leaders. That's why the theory of evolution is the most serious heresy of our time. Don't get lost.


Reasons why epigenetics will not rescue the theory of evolution

Reasons why epigenetics will not rescue the theory of evolution

Evolutionists think that epigenetics would somehow support the theory of evolution. They use, for example, terms like phenotypic plasticity, which means rapid adaptation of an organism to environmental changes without changes in DNA. They argue that evolution takes place slowly so that gradual changes will accumulate into permanent changes in the organism's genome. It is time to expose the evolutionists' delusions.

1. Epigenetic mechanisms do not produce new biological information. The most important epigenetic mechanisms and factors influencing them in the cell are DNA methylation, histone epigenetic markers, and over 140 of different types of epigenetic markers mediated by RNA molecules. Epigenetic information may be of a digital nature (histone markers), analogue (e.g., methylation profiles of the CpG islands, 3D genome and its folding) or metadata, i.e. information on the way information is processed.

Almost all epigenetic information is reset during the embryonic development. However, the epigenetic information structures associated with the immune system are not reset so that offspring will be able to survive against viruses and other pathogens.
2. DNA methylation profiles stabilize the genome and their balance significantly affect the ability of DNA repair mechanisms to function correctly. Epigenetic mechanisms are often said to have no effect on changes in DNA, but this is not really the case. In many studies, medical scientists have found that abnormalities or disruptions in DNA methylation profiles result in erroneous gene expression and harmful sequence changes in the DNA. The most significant mechanism of harmful mutations is the conversion of methylated cytosine (5mC) to thymine, which is not corrected by the repair enzyme glycosylase. It has also been found that hydroxymethylated cytosines tend to change to guanine.

There may be a number of reasons for changes and disturbances in the DNA methylation profiles. The most significant are oxidative stress and changed dietary habits especially within animals in nature. Smoking and alcohol consumption have also been found to cause imbalance in the methylation profiles, which therefore triggers sequence alterations in the DNA. There are already 220,270 disease-causing genetic mutations in the human DNA at population level with an annual growth of over 20,000 !!

Modern science therefore does not know any mechanism that would lead to an increase in biological information that would result in an growth of functional or structural complexity, which can be considered as an evolutionary requirement. Contemporary observations show that any change in organisms is based on epigenetic regulation of existing biological information, or the gradual but inevitable disappearance of information. That is why the evolutionary theory is the most serious heresy of our time. Don't get lost.

Studies confirming the above information:



Trying to fit groups of people into races is biologically inaccurate

DNA genes don't define 'race'


Excerpt: "Many scientists have criticized the idea of using genomic data to talk about ancestry.
..."You cannot look at an individual's DNA and read it like a book or a map of a journey," the group concluded.

By the same token, and perhaps more importantly, Dermitzakis dismissed the idea of using genetics to define "race."

There's a dark history of using genetics to talk about race. As Adam Rutherford (a former geneticist and now a writer) points out at The Guardian, one of the pioneers of the study of human genetics, Francis Galton, was also one of the creators of the eugenics movement. But since then, the study of genetics has exposed exactly why "race" is not a biological concept.
One Redditor asked Dermitzakis if the presence of certain genetic traits in certain parts of the world — traits that make fast-twitch muscle fibers common in a population in West Africa, or traits that made it easier for people in Nepal to adapt to high altitudes — defined "races" of people. The questioner wanted to know if there were racist implications in genetics that led to potential stereotyping of groups of people.

Dermitzakis said that trying to fit groups of people into "races" was biologically inaccurate in the first place.

"There are no races but individuals that sometimes are more related to each other than to others," he said. "If you see it that way then all data will make more sense."

The fact that certain characteristics exist in a certain area just means that those traits have been passed on frequently in that area. Because of those markers, genetic differences can be used to track the movements of populations around the globe, but there's no one genetic signal that makes anyone a different race.

As population geneticist John Novembre explained it in a later Reddit AMA: "There simply hasn’t been enough time since we spread across the globe for extensive differences to have accumulated across the genome."

(My comment: Time will not result in accumulation across the genome, time means degradation.)

Novembre says that "race to me, as I see it used in the world today and in US census categories, is something much more driven by historical legacy than biological understanding — it stems from a legacy based on judging a small number of external characteristics that hide the great amount of genetic similarity that exists under the surface."

The great irony of genetics, Rutherford writes, is that it is the very field that disproved the beliefs of some of its racially-prejudiced early practitioners. Instead of showing how different we are, we've learned that from a biological standpoint, we're 99.9% the same."

My comment: The DNA genes are no drivers or controllers. They are followers. Life is not driven by gene sequences, but genes are driven by lifestyle and geographical place of living. Skin color is not determined by gene sequences but epigenetic control of gene expression. Genetically identical monozygotic twins might have different colors of skin, eyes and hair. Traits are not determined by DNA gene sequences, instead, they will be set on places during embryonic development by non coding RNA molecules, such as lncRNAs and miRNAs. The number of functioning lncRNA molecules in human sperm exceeds the number of protein encoding genes in our DNA. The theory of evolution is the most serious heresy of our time. Don't be deceived.