Chimps are not our relatives

The genomic similarity between humans and chimps is only 29.8% - Modern science doesn't support the theory of Evolution

For decades, people are fed with information that we are genetically more than 98 percent similar to chimpanzees. This weak argument has been used to convince people of evolution. Does modern science support this idea? Let us examine.

The comparison of genetic similarity is based on the so-called "protein coding genes", which are only about 1.5% of total DNA. But even if genetic equation would be 100%, we would not become apes, or apes wouldn't be humans. Human genes encoding proteins are very similar to kangaroos, mice, pigs, bats and many other animals due to the way the cell uses dna sections.

Serious science has investigated mechanisms that regulate and guide the morphological features of animals, ie bone size and shape, and other factors affecting appearance. Gene sequences, even protein encoding genes, do not regulate morphology. The shape and size of skull and skeleton are governed by epigenetic markers of histones, in particular acetylation / deacetylation and methylation markers. Histones are DNA compression proteins around which DNA is interwoven, enabling massive information to be compressed into a minimal small space. Epigenetic markers can be attached to the histones that function as if they were a biological database and an addressing system. They control and regulate eg. Protein production machines to select the correct DNA stretches for pre-mRNA and also control the alternative splicing mechanism.

The insertion of histones is associated with long non-coding RNA molecules during embryonic and fetal development. So if we really want to compare the similarity of chimpanzees and humans, we need to compare the similarity of lncRNA molecules. This is where the truth is revealed: the similarity of human and chimpanzee lncRNA molecules is ONLY 29.8% !!! So we have nothing to do with apes. This explains why organ transplants or blood transfusions do not work from chimpanzees to humans. As a whole, human epigenome differs from chimpanzees by more than 30%. According to evolutionary biology studies, our Y chromosome is "horrendously" different compared to chimps. Science does not know the kind of mechanism that could make an ape develop into a human being. Evolutionists need evidence of useful genetic mutations. But they can not be found. Instead, science can show us 203,885 disease-causing genomic mutations as evidence of rapid human genetic degradation. 73% of mutations in the human genome have occurred in the last 5,000 years. Evolutionary theory is the most pernicious heresy of our time. Do not get lost, good people.

Keywords:

skull morphogenesis histone deacetylase
skeletal morphology histone
human chimp lncrna differences

There really is no meaningful peer review at all

There really is no meaningful peer review at all

https://www.sciencealert.com/a-neuroscientist-just-tricked-4-journals-into-accepting-a-fake-paper-on-midi-chlorians

Excerpt: "If we ever needed a timely reminder that in the world of academic publishing not all scientific journals are created equal, we now have it.

To test just how low the quality bar is for exploitative predatory journals, a prominent neuroscientist has tricked four publications into accepting a totally fake paper about midi-chlorians – the entirely fictional life forms in Star Wars that make 'the force' possible.

Neuroskeptic, a working neuroscientist who anonymously blogs about science for Discover, set up the sting, submitting the nonsensical study to nine scientific journals – only to have four of them accept it.

The journals approached are among those sometimes described as predatory in science circles because they exploit researchers into paying fees to have their papers published in them.

But in this case, three of the publications just went ahead and published the fake paper straight up – clearly not having read or checked it first – even without requiring payment of a fee.

Another, the American Journal of Medical and Biological Research, also accepted the paper, but demanded a $360 fee before publishing it.

The absurd thing, as Neuroskeptic explains, is the average human being would only need about five minutes (or less) with the paper to see that it's entirely bogus and riddled with inexplicable Star Wars references.
 

For a start, it's written by none other than the decidedly fishy-looking Dr Lucas McGeorgeand Dr Annette Kin, and while at a very quick scan it might pass for a chemistry discussion, that's only because Neuroskeptic scraped the content of the Wikipedia page on mitochondrion (real) and reworded it, changing references to midi-chlorian/midichlorian (not so real).

To further make things obvious – just in case any 'peer-reviewers' working for the publications were actually paying attention – Neuroskeptic dropped in entire passages ripped off wholesale from Star Wars, inserting them not-so-subtly into the text.

"Midichlorians-mediated oxidative stress causes cardio-myopathy in Type 2 diabetics. As more fatty acids are delivered to the heart, and into cardiomyocytes, the oxidation of fatty acids in these cells increases," the paper reads, sounding kind of legit and science-y, but then suddenly:

"Did you ever hear the tragedy of Darth Plagueis the Wise? I thought not. It is not a story the Jedi would tell you. It was a Sith legend. Darth Plagueis was a Dark Lord of the sith, so powerful and so wise he could use the Force to influence the midichloria to create life."

If that wasn't enough to twig the peer-reviewers, an admission in the study that the "majority of the text in the current paper" was in fact stolen from Wikipedia surely should have let them know something was up?

But again, nothing – at least not on the part of the journals that accepted the paper.

Some of the other journals who didn't accept the paper did pick up on the Star Wars references, but puzzlingly Neuroskeptic was asked to simply revise the text and resubmit it – including suggestions to revert the spelling of "midichlorians" back to "mitochondria". Really?

As funny as it is to see this dysfunctional peer review process laid bare by such overt fakery, it also highlights a serious breach that hurts science – because the existence of this kind of publishing scam exploits real researchers who are trying to get their work noticed – and brings the whole notion of peer review into disrepute.

"It's just a reminder that at some 'peer reviewed' journals, there really is no meaningful peer review at all," Neuroskeptic explains.

"This matters because scientific publishers are companies selling a product, and the product is peer review."

The 'findings' – such as they are – are reported in the International Journal of Molecular Biology: Open Access, the Austin Journal of Pharmacology and Therapeutics (PDF), and the American Research Journal of Biosciences."

My comment: What does this tell about quality of science and peer reviewing?
By the way, do you want to be a scientist? You can do your own research by using this generator that creates papers that sound science.

https://pdos.csail.mit.edu/archive/scigen/

'Evolution' has a direction - Inevitable Degradation

Changes in organisms are based on epigenetic mechanisms or loss of biological information

Textbooks say that evolution is an inevitable natural process that has no direction. According to the theory of evolution, small random changes are naturally selected in a population for better survival fitness. Does this theory have anything to do with observed science? Absolutely not. Let's find out the most significant reasons, why the theory of evolution is a pseudoscientific theory.

1. Human genome is rapidly deteriorating. There are 203,885 disease-causing genomic mutations in the human genome at population level. The number is rapidly getting higher. About 10% of people are living with a genetic disease. One in five 'healthy' adults may carry disease-related genetic mutations. Scientists are in a hurry to develop gene editing architectures, like CRISPR etc. Human Y-chromosome is rapidly losing genetic material. The number of SNPs is correlated with a loss of genes. For example, the Icelanders have lost 1,171 genes. There are over 20 million SNPs in their genome. Modern science is not aware of beneficial random mutations.

2. Rapid genetic degradation is a scientific fact within other mammals too. A good example is the Canidae lineage. The more adaptation and variation, the more organisms experience genetic degradation. The Red Fox has 1,500 protein coding genes less than the Bat Eared Fox or a dog. The lifespan of the Red Fox is only 2-4 years in the wild. It's susceptible to several diseases. The decreasing number of chromosomes within mammals is associated with faulty and lost genes.

Bat-eared fox          72 chromosomes  lifespan 13-15 years

Gray Fox                 66 chromosomes  lifespan 6-8 years 

Fennec Fox             64 chromosomes  lifespan 8-10 years

Bengal Fox              60 chromosomes  lifespan 6-8 years

Kit Fox                     50 chromosomes  lifespan 5.5 years

Tibetan sand fox      36 chromosomes  lifespan 6-10 years

Red Fox                   34 chromosomes  lifespan 2-4 years

3. Bacteria are also rapidly losing genetic material despite their ability to transfer genes between each other.  Gene loss results in robust parasitic or pathogenic bacteria or highly specialized harmful bacteria. This same phenomenon can be observed all over nature. Loss of biological information leads to negative consequences within organisms.

 4. Changes in organisms are based on epigenetic mechanisms directed by diet type, climate, stress, toxicants etc. Traits are not determined by gene sequences. Genes are no drivers or controllers. Alterations in epigenetic information patterns typically result in genetic errors. Aberrant methylation patterns are the most significant reason for genetic degradation. We can slow down the genetic degradation but we can't stop it from happening. It's an inevitable fact that there is only one direction in nature. A dead end. Evolution has never been observed because there are no mechanisms that could increase biological information leading to increase in functional or structural complexity. That's why creation and design. Don't get lost.

Deletional bias shapes bacterial genomes - No evolution observed

Deletional bias shapes bacterial genomes - loss of information leads to robust parasites

https://www.researchgate.net/publication/11763350_Mira_A_Ochman_H_Moran_NA_Deletional_bias_and_the_evolution_of_bacterial_genomes_Trends_Genet_17_589-596

Excerpt from the abstract: "Although bacteria increase their DNA content through horizontal transfer and gene duplication, their genomes remain small and, in particular, lack nonfunctional sequences. This pattern is most readily explained by a pervasive bias towards higher numbers of deletions than insertions. When selection is not strong enough to maintain them, genes are lost in large deletions or inactivated and subsequently eroded. Gene inactivation and loss are particularly apparent in obligate parasites and symbionts, in which dramatic reductions in genome size can result not from selection to lose DNA, but from decreased selection to maintain gene functionality. Here we discuss the evidence showing that deletional bias is a major force that shapes bacterial genomes."

Mira, A., Ochman, H. & Moran, N.A. Deletional bias and the evolution of bacterial genomes. Trends Genet. 17, 589−596.

https://en.wikipedia.org/wiki/Bacterial_genome

Excerpt: "Genome sequences show that parasitic bacteria have 500-1200 genes, free-living bacteria have 1500-7500 genes, and archaea have 1500-2700 genes."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3060909/

Excerpt: "In contrast, comparative genomic studies have revealed that in some cases, the genomes of bacteria, such as Rickettsia or Mycobacteriaspp. , are reduced. For example, the genomes of Mycobacterium leprae, Yersinia pestis and Salmonella Typhi contain hundreds of degraded genes. The evolution of specialized bacteria, including pathogenic bacteria, consists mainly of gene losses. Moreover, extreme genome decay is often accompanied by a low GC% content. Furthermore, genes that encode “virulence factors” are also found in the genomes of non-pathogenic bacteria, such as free-living bacteria, which may carry more “virulence factors” than do pathogenic bacteria. By counting the number of genes involved in transcription, host-dependent bacteria (including pathogens) were found to have significantly fewer transcriptional regulators than free-living bacteria."

https://infogalactic.com/info/Bacterial_genome_size

Excerpt: "These results indicate that genome size reduction can occur relatively rapidly and loss of certain genes can speed up the process of bacterial genome compaction."
 

http://creation.com/images/pdfs/tj/j29_2/j29_2_110-118.pdf

Excerpt: "What makes the M. leprae genome interesting is its small genomic variance; leprosy genomes are >99.9% similar, and have only 807 polymorphic sites, and only 4–5 subtypes. They have found that ancient leprosy genomes are very similar to modern ones. Thus, due to this similarity if they can replicate factors and conditions that halted the spread of leprosy in the 14th century, then this could possibly put an end to the modern leprosy epidemic.14,15 The leprae genome is very stable,16 and is thus at the end stage of the genome reduction process."

My comment: Horizontal gene transfer (HGT) occurs between bacteria. According to newest research, eukaryotic-to-bacteria HGT can only be demonstrated under optimized laboratory conditions. This means bacteria might get new genetic material only from other bacteria or archaea, that are also experiencing rapid genome degradation. That's why bacteria could never evolve into something other than bacteria. Interesting is that gene loss results in robust parasitic or pathogenic bacteria or highly specialized harmful bacteria. This same phenomenon can be observed all over nature. Loss of biological information leads to negative consequences within organisms. This is far from evolution.

We have fewer protein-coding genes than an earthworm

Genes don't make us who we are

Humans have fewer protein-coding genes (~19,600) than an earthworm (~20,470). This means that the genes we thought made us who we are, don't.

Genes are no controllers. Genes are not your destiny.

For building over one million different human proteins, our cells need epigenetic information layers that regulate a mechanism called alternative splicing. Thousands of different protein isoforms can be built based on a 'gene' (a dna section or several sections that are chosen by the RNA) without changing its sequence. The entire concept of a 'gene' should be redefined.

Life is not driven by gene sequences. Genes are driven by lifestyle.
 

Source: http://schoolbag.info/biology/living/living.files/image350.jpg

The Epigenetics Behind Unique Human Faces

Gene sequences don't determine traits

https://www.whatisepigenetics.com/epigenetics-behind-unique-human-faces/

Excerpt: "Here’s a strange question many people probably have not given much thought to: why are our faces shaped the way they are? We know that no two faces are perfectly alike, but why exactly might one person have a long nose and another a small forehead? How is it that our earlobes are attached to our ears and not our chins? Researchers from Switzerland and France have wondered this, and published a study in Science that suggests epigenetics might be a key player.

Filippo Rijli from Friedrich Miescher Institute for Biomedical Research, along with his team, discovered that epigenetic mechanisms known as histone modifications are involved in regulating face morphogenesis, or the biological process that creates the shape of one’s face. Even though genes controlling facial shape are nearly identical for every person, each face is interestingly unique.

When an embryo is in the early stages of development, the structure that consists of DNA wrapped around proteins, known as chromatin, maintains its plasticity in specialized cells. These particular cells are called neural crest cells, which go on to form different facial structures and give rise to most of the bones and cartilage of the face and skull.

Genes, at this point, are ready to respond to local cues. When particular environmental signals reach the neural crest, a switch occurs from a poised state to an active chromatin state. This begins position specific transcriptional programs that form the face.

Neural crest cells obtain a “positional” identity that is connected to their location in the face as it develops. As the cells migrate from the neural tube to the various areas of the head, the position identity is acquired. This identity is dependent on the interactions with the environment and the path which the cells take. Interestingly, the positional identity is not permanent even after migration, as neural crest cells are able to maintain some plasticity.
 

Rijli and his team, with the help of Michael Stadler, FMI computational biologist, have uncovered the details of how neural crest cells are able to maintain plasticity through migration, while also being ready to respond to environmental cues and begin the position-specific transcriptional programs which form the face. Ultimately, they found that this process is enabled by epigenetic regulation of chromatin organization.

“This is a novel conceptual framework for understanding how different facial features arise,” Rijli said about the team’s study. “Epigenetic poising may allow cranial neural crest cells to rapidly adapt their response to local variations in environmental signaling, thus potentially explaining differences in facial shape between individuals.”

Specifically, they looked at different chromatin profiles of neural crest cells in various positions prior to and after migration. First author Maryline Minoux said, “in the postmigratory neural crest cells, the promoters of the differentially silenced genes – i.e. genes not expressed in some populations, but expressed in others – were maintained in a bivalent configuration marked by both repressive H3K27me3 and activating H3K4me2 epigenetic histone modifications.”

The histone modifications poised the genes for activation. Interestingly, this configuration was already found in the neural crest cells before they had even begun migration. As soon as the cells are exposed to particular environmental cues, they get rid of the repressive H3K27 trimethylation mark (H3K27me3) and begin to form various facial features.

Additionally, the authors also discovered that the Ezh2 (Enhancer of zeste homolog 2) component of the PRC2 (Polycomb Repressive Complex 2) had a hand in regulating the poised chromatin state. PRC2 is an established chromatin remodeler during the embryo’s development. 

Even if the genes responsible for these craniofacial structures are almost the same in each person, epigenetics could contribute to the reason why some people have a more pronounced forehead, high cheekbones, a button nose, or almond-shaped eyes. Although additional research is needed, the study offers novel insights into the epigenetic regulation of the formation of our facial features."

My comment: Unique human facial features are not result of sequence variation. Traits are determined by epigenetic control of gene expression and transcription. This also explains why genetically identical twins might have different colors of skin, eyes or hair. There is no such thing as different human races. We're all the same humankind, created by God.

Drinking alcohol while pregnant could have transgenerational effects

Epigenetics - Drinking alcohol while pregnant could have transgenerational effects

https://scienmag.com/drinking-alcohol-while-pregnant-could-have-transgenerational-effects/

Excerpt: "RIVERSIDE, Calif. – Soon-to-be mothers have heard the warning – don't drink while pregnant. The Centers for Disease Control and Prevention (CDC) has issued numerous statements about the dangers of alcohol consumption during pregnancy, as it can lead to Fetal Alcohol Spectrum Disorders (FASD) in newborns.

Despite this, many women drink during pregnancy, a choice that scientists have known for years could hurt these mothers' children. Today, there is a new reason why an expectant mother should put down that glass of wine – drinking alcohol during pregnancy will not only affect her unborn child, but may also impact brain development and lead to adverse outcomes in her future grand- and even great-grandchildren.

The new study by Kelly Huffman, psychology professor at the University of California, Riverside, titled "Prenatal Ethanol Exposure and Neocortical Development: A Transgenerational Model of FASD," was published in the journal Cerebral Cortex.

"Traditionally, prenatal ethanol exposure (PrEE) from maternal consumption of alcohol, was thought to solely impact directly exposed offspring, the embryo or fetus in the womb. However, we now have evidence that the effects of prenatal alcohol exposure could persist transgenerationally and negatively impact the next-generations of offspring who were never exposed to alcohol," Huffman said.
 

Previous work from the Huffman Laboratory at UCR has shown that PrEE impacts the anatomy of the neocortex, the part of the brain responsible for complex behavior and cognition in humans, and that PrEE can lead to abnormal motor behavior and increased anxiety in the exposed offspring. Huffman and a group of UCR students have extended this research by providing strong evidence that in utero ethanol exposure generates neurobiological and behavioral effects in subsequent generations of mice that had no ethanol exposure.

To determine whether the abnormalities in brain and behavior from prenatal ethanol exposure would pass transgenerationally, Huffman generated a mouse model of FASD and tested many aspects of brain and behavioral development across three generations. As expected, the first generation, the directly exposed offspring, showed atypical gene expression, abnormal development of the neural network within the neocortex and behavioral deficits. However, the main discovery of the research lies in the subsequent, non-exposed generations of mice. These animals had neurodevelopmental and behavioral problems similar to the those of the first, directly exposed generation.

"We found that body weight and brain size were significantly reduced in all generations of PrEE animals when compared to controls; all generations of PrEE mice showed increased anxiety-like, depressive-like behaviors and sensory-motor deficits. By demonstrating the strong transgenerational effects of prenatal ethanol exposure in a mouse model of FASD, we suggest that FASD may be a heritable condition in humans," Huffman said.

The multi-level analyses in this study suggest that alcohol consumption while pregnant leads to a cascade of nervous system changes that ultimately impact behavior, via mechanisms that can produce transgenerational effects. By gaining an understanding of the neurodevelopmental and behavioral effects of prenatal ethanol exposure that persist across generations, scientists and researchers can begin to create novel therapies and methods of prevention."

My comment: Drinking alcohol during pregnancy will not only affect mother's unborn child, but may also impact brain development and lead to adverse outcomes in her future grand- and even great-grandchildren. Alcohol results in modifications in epigenetic patterns of a developing embryo and these alterations are passed down for future generations.

GENETIC DEGRADATION - Parents might choose from a range of embryos created in a lab with their DNA

Genetic degradation leads to a need of creating modified embryos

http://www.independent.co.uk/news/science/sex-procreation-hank-greely-stanford-professor-prediction-humans-no-longer-reproduce-a7821676.html

Excerpt: "Within three decades people will no longer be having sex to procreate, a professor from Stanford University has said.

Hank Greely, the director of Stanford’s Law School’s Center for Law and the Biosciences, believes the reproductive process will begin with parents choosing from a range of embryos created in a lab with their DNA.

Although this can already take place, Mr Greely believes it will become far cheaper to do so and couples will opt for this method to prevent diseases.

The process involves taking a female skin sample to create stem cells, which is then used to create eggs. 

 

These eggs are then fertilised with sperm cells, resulting in a selection of embryos.

Screening of the embryos would highlight any potential diseases and the Stanford professor believes the process will get to a point where parents can also potentially have the ability to choose eye or hair colour.

“I think one of the hardest things about this will be all the divorces that come about when she wants embryo number 15 and he wants embryo number 64,” Mr Greely said at Aspen Ideas Festive, Tribune reported.

“I think the decision making will be a real challenge for people. How do you weigh a slightly higher chance of diabetes with slightly lower risk of schizophrenia against better musical ability and a much lower risk of colon cancer? Good luck.”

My comment: Rapid human DNA degradation is resulting in serious efforts to avoid genetic diseases. This can be done by editing the dna sequences or by letting parents to choose from a range of the less damaged embryos. This method works within genetic diseases but not in traits, like height, morphology, musicality, hair or skin color etc. because they are determined by epigenetic mechanisms during embryonic development.

However, these plans prove how serious problems the theory of evolution has. But will ideas like this open people's eyes to see that evolution is not happening?

High fat Diet During Pregnancy Increases Breast Cancer Risk in the Future

Epigenetic modifications passed down through generations

https://www.labroots.com/trending/cell-and-molecular-biology/6355/fat-diet-pregnancy-increases-breast-cancer-risk-future?utm_content=bufferdb386&utm_medium=social&utm_source=facebook.com&utm_campaign=buffer

Excerpt: "Researchers have learned that slight modifications to the genome - epigenetic changes - can be caused by environmental influences, and can be passed down through generations. Pursuing this line of thinking, researchers at Georgetown Lombardi Comprehensive Cancer Center analyzed mice over generations, finding that when pregnant females consume a diet high in fat derived from common corn oil, there is a significant increase in the risk of breast cancer for three generations of offspring.

The senior author of the report, Leena Hilakivi-Clarke, PhD, a Professor of Oncology at Georgetown Lombardi suggests it’s worth pursuing this research in pregnant women. "It is believed that environmental and life-style factors, such as diet, plays a critical role in increasing human breast cancer risk, and so we use animal models to reveal the biological mechanisms responsible for the increase in risk in women and their female progeny," Hilakivi-Clarke explained.

High-fat diets have already been connected to an increase in inflammation, and epidemiological studies have determined that inflammation is linked to an increased risk of cancer, she said. Hilakivi-Clarke has previously found that pregnant mice consuming a high fat diet have female pups that experience increased cancer risk. In this work, when pregnant mice changed to a high fat diet during their second trimester, which is when the germ line transmitting genetic material between generations, there is also an increased breast cancer risk in the second generation.
 

A genetic analysis showed that between the first and third generations after a high fat diet, there were several genetic modifications. Some of those modifications occurred in genes linked to increased breast cancer risk, increased resistance to cancer treatment, impaired anti-cancer immunity, and poor cancer prognosis in women. The scientists found three times as many genetic alterations in the mammary tissue of the third generation over the first when comparing high-fat diet and control progeny.

"The soil in the breast, so to speak, remained fertile for breast cancer development in our high-fat experimental mice," Hilakivi-Clarke said.

In this study, the fat consumed by the ice was designed to mimic what a human would eat, said Hilakivi-Clarke. The mice in this study also had the same caloric intake overall. "But our experimental mice got 40 percent of their energy from fat, and the control mice got a normal diet that provided 18 percent of their energy from fat. The typical human diet now consists of 33 percent fat,” she said.

"Studies have shown that pregnant women consume more fats than non-pregnant women, and the increase takes place between the first and second trimester. Of the 1.7 million new cases of breast cancer diagnosed in 2012, 90 percent have no known causes. Putting these facts, and our finding, together really does give food for thought,” she concluded."

My comment: Genetic changes are typically results of epigenetic modifications. Aberrant methylation patterns expose the genome to instability which might lead to sequence alterations. Cancer is a lifestyle disease. Poor diet is the most significant factor contributing risk of having cancer. Because different epigenetic modifications are inherited by several mechanisms, that acquired risk of having cancer is passed down through generations.

Life is not driven by gene sequences. Genome is driven by lifestyle. There is no such thing as mutation driven evolution. Don't get misled.

The entire concept of “gene” has to be reconsidered

New discoveries change our understanding of genes and their purposes

http://jonlieffmd.com/blog/new-complexity-in-dna-regulation

Highlights:

"But, now multiple vast networks of regulation have been found that include more than forty different types of tags placed on both DNA and the protective histone proteins that allow access to DNA strands. All of these tags alter genetic function and are based on the actions of protein enzymes."

Another type of regulation involves the shape of the DNA both in small loops and large placement inside of highly structured nucleus scaffolds with dramatic influence on genetic functions.

The very complex editing of messenger RNA can make up to 500 different proteins from a single strand of DNA—what used to be called a gene, but now is hard to define. Genes can overlap and triggers of regulation can happen in the gene or in the regulatory strand.

What is equally amazing is that mental events—thought—almost instantly triggers large networks of many genes at the same time. How does this happen?
  

Now entirely new sets of factors have appeared that are based on physical properties of the coding of RNA and the liquid phase transitions that separate active and inactive sections of the chromosomes. The first unusual new physical properties occur when there are repeated patterns of code. The regions of regulatory code where there are large amounts of repeats have been correlated with multiple different degenerative diseases such as Huntington’s and ALS. The second is the way that active and inactive sections of the DNA are in different regions of the nucleus.

It is not known how many overlapping layers of regulation there are:

Some include:

• Histones protect DNA and must be opened to be used. There are now forty different tags that determine whether histones can be opened or not to utilize DNA.
• There are many newly discovered tags on DNA itself that alter function.
• Thousands of proteins called promoters and enhancers start and stop DNA function.
• Promoters work in many different places for each gene and in different places for each type of human cell. Also, for even more complexity, multiple promoters combine into larger machines, some touching the DNA and some only combining with the other promoters. Multiple structures exist for each gene in different places.
• There are multiple different places where transcription starts for each “gene”, again undermining the notion of the simple “gene.”
• Thousands of large and small RNAs interact in multiple ways to regulate what pieces of DNA are used.
• Many different mechanisms are used to repair DNA errors without obvious direction.
• Eight million factors affect the RNA particles that are made from at least 20% of all DNA (maybe up to 50%). Messenger RNA somehow determines multiple different edits from the same pieces of DNA.
• Pieces of DNA and RNA are taken from multiple places, strands are cut out and others sewn together without clear direction.
• In some DNA there are two superimposed codes at once in one section of DNA. These are related to new messenger RNA folding, and multi-use codons called “duons.” The first purpose is to transcribe DNA code to RNA code to make proteins. The second purpose is to bind regulatory factors, as the regulatory regions do to trigger other genes.
• Transcription factors bind inside at least 13% of “genes” themselves, not just the regulatory regions nearby. This finding was truly shocking since the DNA in the gene, then, must code for two meanings at once for two entirely different purposes.
• RNA splicing, can make up to 500 different proteins from the same pieces of DNA. The RNA cuts out sections and sews others together. Recently, it has been demonstrated that the pieces that are sewn together by the messenger RNA may come from multiple different areas that used to be called individual genes.
• Four million different switches are active, often operating in multiple places at once; 18,000 places where active RNA is made; and 8 million different particles interacting to regulate these RNAs.
• The entire concept of “gene” has to be reconsidered because messenger RNA takes pieces from different regions to make one RNA edit for a protein.
• The 3D shape of the DNA chromosome is correlated with the activity of the genes inside.
• The links exist at multiple levels.
• Loops of chromatin make space for enhancers to land. A larger relationship exists for specific places in the nucleus to impact on particular active DNA sites.
• Special protein structures alter polymerase activity.
• Chromosomes with fewer active genes are placed at the edge of the nucleus while the active ones are near the center.
• Less active sections are placed near the nuclear lamina, which is close to membrane.
• The location can suppress the genetic machinery.
• If the chromatin is opened but not used, the entire section is moved to a different location.
• The exact location of the gene in space in the nucleus influences its activity.
• To fit 2 yards of DNA into a tiny nucleus is a monumental engineering feat. DNA is highly compacted yet has to be instantly available to rapidly make proteins in neurons with a momentary change of thought."

My comment: Messenger RNA takes pieces of genes from different locations to make one RNA edit for a required protein. Where is the regulation for this? Certainly not in gene sequences. These epigenetic mechanisms, 3D genome, overlapping genes and codon duons tell us about an extremely complex language that points to perfect design. There is no such a thing as mutation driven evolution. Gene centric population genetics and the theory of evolution have seriously failed. Again.

Life is not driven by gene sequences. Genes are driven by lifestyle. Don't get lost.