Population genetics can't solve the 'Missing Heritability' problem

Do we really want to squander our time and resources chasing ghosts?

Excerpt: "By Evan Charney, Duke Institute for Brain Science, Duke University:
One of the hopes and promises of the Human Genome Sequencing Project was that it would revolutionize the understanding, diagnosis, and treatment of most human disorders. It would do this by uncovering the supposed “genetic bases” of human behavior. With a few exceptions, however, the search for common gene variants -“polymorphisms” – associated with common diseases has borne little fruit. And when such associations have been found the polymorphisms seem to have little predictive value and do little to advance our understanding of the causes of disease. 

And to date, not a single polymorphism has been reliably associated with any psychiatric disorders nor any aspect of human behavior within the “normal” range (e.g., differences in “intelligence”).

To some researchers this state of affairs has given rise to a conundrum known as the “problem of missing heritability.” If traits such as intelligence are reported to be 50% heritable, goes the theory, why have no genes associated with intelligence been identified?

...GCTA studies, however, just like their twin study predecessors, suffer from serious methodological problems that call into doubt the legitimacy of their findings. They, too, are likely to generate spurious associations and faulty estimates of genetic contributions to variation in traits.

One well-known example of a false association between a polymorphism and a trait was the link between the dopamine receptor gene DRD2 and alcoholism. Initial studies suggested a strong association, but subsequent investigations found none when more effective controls for population stratification were imposed.

Advocates of GCTA, however, tell us that in order to find the multitude of polymorphisms of tiny effect underlying heritability estimates we must undertake ever larger studies involving hundreds of thousands of persons. These polymorphisms of tiny effect, however, are so many ghosts and the search for them is the last gasp of a failed paradigm. Do we really want to squander our time and resources chasing ghosts?"

My comment: Population genetics is the most significant field of pseudosience that maintains the heretical darwinian theory of evolution. There are over 900,000 SNPs identified in the human genome but not a single polymorphism has reliably associated with any psychiatric disorder or trait linked to human intelligence. Only few SNPs are confirmed to be associated with adaptation and those changes in genome are contributed by mechanisms involved in the immune system (for example lactose tolerance and high altitude adaptation). The conclusion is obvious: GENES ARE NOT DRIVERS. The missing heritability problem is solved by deep understanding of how epigenome is regulated. Within this concept, there are several factors influencing the orchestra: non coding RNA molecules, RNA methylation, exosomes, extracellular vesicles, DNA methylation, histone methylation/acetylation, prions, flanking binding sites and several other mechanisms that affect transgenerational epigenetic inheritance. Changes organisms experience are not based on random errors but Intelligently designed and created mechanisms. These mechanisms are not designed to cause large scale evolution, but only rapid and effective adaptation that prepares the offspring for changing environment. Don't get lost.


Seven ion flow motors synchronized with a planetary gearbox

This hi-speed organism has more parts than a jumbojet - But it is able to replicate


Excerpt: "In November, 2012, two scientific groups from Osaka University in Japan and Aix-Marseille Université in France made a startling discovery.

They set out to uncover the power behind the tiny tails (flagella) that allowed the MO-1 marine bacterium to swim. Using electron cryotomography—an electron microscope and very cold temperatures — they found this “simple” creature’s tails are powered by seven motors, arranged in a hexagonal array, with all gears interacting with 24 smaller gears between them.

“The seven tails (flagella) rotate one way, and the smaller gears rotate the opposite way to maximize torque while minimizing friction,” Rose notes.

These gears or bearings enable the flagella to spin very fast—so the MO-1 can swim ten times faster than E. coli and Salmonella. Some have referred to this as “the Ferrari of flagella,” due to its speed and advanced design.

“This discovery baffled the microbiological world with it’s uncanny complexity,” Rose notes. “Think of it, not one but seven proton synchronized motors interconnected with a planetary gearbox.”

“The seven flagella propellers are inter-linked for minimum drag profile and maximum thrust by using 24 gears and a sheath, similar to modern aircraft and mufti-engine helicopters!”

“It actually has gears and it keeps all seven motors synchronized,” he notes. “Typically, any geared engines have no more than two motors. The best we could do in a helicopter is three engines and a multiple gear box to sync the engines.”

“The motors can drive the MO-1 bacteria at relative speeds of 100 body lengths/second. A Cheetah achieves a land speed of only 25 body lengths/second in comparison and that’s in air, not fluid!” he says.

This “simple” bacterium has nearly the same number of parts as a Boeing 747 — six million — which like the aircraft, work together perfectly. But these parts allow the bacterium to do something the 747 can’t do – multiply itself. Note, the MO-1 bacterium has three more motors than the Boeing model."


My comment: Synchronizing two motors is a very challenging job for engineers. Making three motors to produce simultaneous power requires extremely accurate and careful design. But seven ion flow motors synchronized by a planetary gearbox, that's really challenging. And that super complex organism is able to replicate. Rapidly. These MO-1 bacteria are able to reverse their direction after hitting an obstacle. And they can follow and sense the magnetic field.

These tiny hi-speed perfectly designed organisms point to Creation and Design. The evolutionary theory is a major lie. 


Pig-human hybrids are just evolutionary story-telling

Human cells integrated into pig and cow embryos

Excerpt: "Those scientists experimented with several different chimeras, including rat cells injected into mouse embryos, rat cells injected into pig embryos, and human cells injected into pig embryos with varying levels of success. The mouse chimeras developed gall bladders made entire of rat cells, even though evolution took rat gall bladders away. The rat-pig chimeras didn’t work at all.

But let’s focus on the pig-human chimeras for now. Last year, we reported that these same scientists were injecting human stem cells, the “blank” cells that can turn into other cell types, into 1500 developing pigs when they were just proto-embryo balls of cells called blastocysts. This new research reports the results of the implantations. Initially, the human cells seemed to attach and grow, but once the pig fetuses had implanted into the uterine walls of the mother pigs and grown for four weeks, the researchers only measured a few traces of human cells."

My comment: Integrating human stem cells into pig embryos has nothing to do with assumed evolutionary relationship between them. Only 0.001% of human stem cells managed to survive in pig embryos during this short petri dish experiment. Why?

1. Stem cells lack epigenetic markers that are needed for cellular differentiation. These pluripotent stem cells are at open state ready for differentiating into any kind of tissue type.
You can read about how removing the epigenetic markers from cells affect their state from here.

2. The experiment was made using petri dishes as platforms for pig embryos. This means they were not affected by the most significant regulatory mechanism, microRNAs. These non coding RNA molecules are crucial elements in the cellular differentiation. You can read about their function from here

3. Several mechanisms during pig reproduction will make the embryo to develop into a pig. Too much of foreign stem cells in the embryo will cause the pregnancy to fail. This is ensured by this kind of mechanisms.

Human-pig hybrids are just funny fairy tales. However, I will not read them to my kids. Don't get misled.


Mutations cause genetic disorders - Evolution not observed

Mutations make genomes weaker - Evolution not observed

Excerpt: "The largest ever genetic study of children with previously undiagnosed rare developmental disorders has discovered 14 new developmental disorders. Published today in Nature, the research led by scientists at the Wellcome Trust Sanger Institute also provided diagnoses of rare conditions for over a thousand children and their families.

These diagnoses allow families with the same genetic conditions to connect and access support, and help inform better clinical management. The study also accelerates research into disease mechanisms and possible therapies.

Each year, thousands of babies are born who do not develop normally because of errors in their genetic makeup. This can lead to conditions such as intellectual disability, epilepsy, autism or heart defects. There are over 1,000 recognised genetic causes, however many individual developmental disorders are so rare that the genetic causes are not known. The Deciphering Developmental Disorders (DDD) study aims to find diagnoses for children with as yet unknown developmental diseases, and demonstrate that new genomic technologies can provide improved diagnostic tests.

Working with 200 NHS clinical geneticists, the researchers screened all 20,000 human genes from more than 4,000 families, from across the UK and Republic of Ireland, with at least one child affected by a developmental disorder. The DDD team focused on spontaneous new mutations that arise as DNA is passed on from parents to children. The children's conditions were also clinically assessed and the team combined the results to match up children with similar disorders to provide diagnoses.

The study team was able to diagnose children who had new mutations in genes already linked to developmental disorders—approximately one quarter of the patients in the study. In addition, they identified 14 new developmental disorders, all caused by spontaneous mutations not found in either parent.

Overall, the researchers estimated that for 42 per cent of the children in the study, a new mutation in a gene important for healthy development is likely to be the underlying cause of their condition. The DDD study also estimated that, on average, 1 in 300 children born in the UK have a rare developmental disorder caused by a new mutation. This adds up to 2,000 children a year in the UK.

They also demonstrated that older parents have a higher risk of having a child with a developmental disorder caused by a new mutation. The chances rose from 1 in 450 for 20-year old parents having a child with a rare developmental disorder to 1 in 210 for 45 year-old parents.

From this, the researchers calculated that nearly 400,000 of the 140 million annual births across the world will have a developmental disorder caused by a spontaneous new mutation that is not carried by either parent."

My comment: Unfortunately human genome is rapidly getting degraded. Mutations are not able to increase the amount of biological information. Mutations are genetic errors that are not causing any kind of evolution or even adaptation. WHO has recognized over 10,000 monogenic diseases due to mutations. Mutation rate is so fast that without genome editing techniques mankind has only 150-200 generations left. Rapid mutation rate also points out that mankind is not so old as we've been taught. The evolutionary theory is the biggest lie ever. Don't get misled.


The field of epigenetics may have been literally scratching the surface

Genes are not drivers - cellular mechanisms control which stretches of DNA are accessible to be read out and translated into proteins

Excerpt: "Epigenetics—the study of genome modifications that control cell fate, some of which are thought to reflect environmental influences on the genetics of health and disease—is one of the key frontiers of modern genomics. At the heart of epigenetics is the question of how cells control which stretches of DNA are accessible to be read out and translated into proteins, and which sequences are spooled away and archived on nucleosomes.

The dominant model in the field portrays nucleosomes as passive spindles, themselves 'octamers' made up of eight blocks of rigid histone proteins that snap together like Lego pieces when wrapped in DNA, and which must break apart or slide out of the way to allow their archived DNA to become active again. But Sinha, Gross and Narlikar's new study promises to change this paradigm, demonstrating that nucleosomes are capable of shifting like putty in response to as-yet unknown signals.

"The field of epigenetics may have been literally scratching the surface," Narlikar said, referring to the field's focus on the function of epigenetic "marks," such as the chemical tags called methyl groups, on the exposed surfaces of histone proteins. "Altering the shape of the nucleosome, a fundamental building block of the chromosome, could in principle have large effects on processes ranging from genome organization to epigenetic inheritance."

In particular, according to Narlikar, a malleable nucleosome would make it possible for cells to read out segments of DNA without completely disassembling the nucleosome. This offers a potential explanation for mysterious histone modifications that would be buried uselessly deep inside the nucleosome according to the traditional model, and suggests a new mechanism for the extreme compaction chromosomes undergo during cell division, and offers potential answers to the chicken-and-egg problem of how cells know how to pull specific DNA sequences out of the archives without being first able to "see" them.

"If you look at crystal structures of the conventional model of the nucleosome, there's no slack, no room for the DNA to be pulled out. To read the DNA, you would have to move the whole histone octamer out of the way," Narlikar said. "What we're seeing is that you can keep them in place and still expose the DNA by changing the shape of the nucleosome."

The new discovery was made possible by a new and technically challenging nuclear magnetic resonance (NMR) method, which discerns features of chromatin dynamics that are invisible to other commonly used approaches. The technique revealed changes in how histones contact one another, demonstrating convincingly that nucleosomes are dynamic, rather than rigid.

In describing the work, Narlikar quoted Proust, who wrote, "The only true voyage of discovery, … would be not to visit strange lands but to possess other eyes, to behold the universe through the eyes of another…."

"The new NMR approach literally allowed us to look with 'other eyes,' and in doing so allowed us to discover a fundamental new property of chromatin," Narlikar said.

Much is still unknown, Narlikar said, about the details of nucleosomes' shape-shifting abilities, as well as what types of cellular biochemical signals regulate their dynamics, and exactly what effects these changes have on DNA regulation. "All of these ideas are speculative at this point. But we wouldn't have had the conceptual framework to think of any of these hypotheses until there was reason to think of the nucleosome as dynamic rather than rigid. The number of questions this opens up is incredibly exciting."

My comment: Genes are just raw material for clever cellular mechanisms that are regulated by several factors and influenced by diet, stress, climate and other environmental factors. Seeing this kind of complexity, 3D shape shifting and its affect to the regulation of how genes are used for protein production or hided from transcription machineries, points to Intelligent design and creation. There are only mechanisms that affect the protein production and randomness has no role within these clever processes. That's why the evolutionary theory and natural selection are the biggest lies ever.


Rapid Evolution Observed?

Rapid Evolution Observed?

Katie bought an Anole Lizard. But she didn't follow recommendations on how to feed her new pet. The lizard turned dark brown. She has just observed rapid 'evolution' to occur. The reason for this rapid change is obvious; she gave only mealworms for the lizard instead of nutrient rich crickets and cockroaches. Here's the story:


The same phenomenon is happening in nature. All the time and everywhere. But it will never lead to evolution. Rapid changes within Darwin's Finches happen for the same reasons. Diet changes the epitranscriptome which alters gene expression patterns. You can read about this scientific fact from here:



Evolutionary biology is using rapid changes within Florida Anole Lizards as a model example of evolution:

This is false science. Organisms experience changes due to intelligent mechanisms coded in their cells, not by random mutations or genetic errors. Sometimes changes occur very rapidly, just in days:


"Forty days in, those vegetarian iguanas managed to keep the same weight as iguanas given a balanced diet. Dissections revealed a possible reason: Vegetarians’ small intestines had grown 17% longer. Plus, their guts harbored a more diverse community of microbes than lizards on the typical diet, including higher numbers of a few microbe groups suspected to break down fiber, the team reports today in the Journal of Experimental Biology.

This kind of rapid adaptation is not possible without Intelligent Design and Creation. Don't get misled.


Genetic variation will not lead to evolution

Scientists Make Connection Between Genetic Variation and Immune System in Risk for Neurodegenerative and Other Diseases

Excerpt: "The researchers recruited a subset of 461 volunteers from the PhenoGenetic Project of African American, East Asian American, or European American ancestry. Two different types of immune cells — T cells and monocytes — were purified from each individual's blood, representing the adaptive and innate arms of immunity, respectively. The researchers profiled these cells to measure the expression of 19,114 genes in each cell type. They then examined genetic variants throughout the human genome for their effects on gene expression in these two representative populations of immune cells.

They discovered that genetic variation influencing a person's risk for multiple sclerosis, rheumatoid arthritis, and type 1 diabetes is more likely to control gene activity in T cells than in monocytes. In contrast, genetic variation that increases one's risk for neurodegenerative diseases, such as Alzheimer's and Parkinson's disease, shows a striking enrichment of functional effects in monocytes."

My comment: Gene sequence alterations occur, that's true. But random base pair substitutions, genetic errors and mistakes never lead to evolution. However, base pairs can sometimes change due to mechanisms involved typically in the immune system. These one nucleotide level alterations never lead to evolution. For assumed large scale evolution you need new genes that are introduced for complex gene regulatory networks. You also need information how these genes are to be expressed and how several complex regulatory factors interact with them. Large scale evolution has never been observed because it is not possible to happen. Genetic variation is associated with genomic degradation and this is something we can observe:


"Monogenic diseases result from modifications in a single gene occurring in all cells of the body. Though relatively rare, they affect millions of people worldwide. Scientists currently estimate that over 10,000 of human diseases are known to be monogenic. Pure genetic diseases are caused by a single error in a single gene in the human DNA."

Over 10,000 genetic diseases point out the impossibility of evolution. Don't get misled.

Bringing extinct species back to life - is it possible?

Bringing extinct species back to life - is it possible?

Excerpt: "If the DNA inside the nucleus is well preserved enough to take control of the egg, it just might start dividing into a mammoth embryo. If the scientists can get past that hurdle, they still have the formidable task of transplanting the embryo into an elephant’s womb. Then, as Zimov cautions, they will need patience. If all goes well, it will still be almost two years before they can see if the elephant will give birth to a healthy mammoth.

“The thing that I always say is, if you don’t try, how would you know that it’s impossible?” says Hwang."

My comment: Bringing extinct species back to life is not possible. Why? Here's because:

1. The necessary information needed for embryonic development is not written in the DNA only. You need information of how genes need to be expressed. You need information of correct histone methylation patterns and several other regulatory factors.

2. Using cells of dead animals, even if they were properly preserved, that means in conditions at least -20 C degrees, doesn't quarantee the correct gene expression to find its status in embryonic development. Markers needed for gene expression are wiped out after the fertilization. 

3. The most significant reason for why cloning will not be successful is that non coding RNAs, microRNAs etc. play the most significant role in embryonic development. Traits are not determined by gene sequences. Instead, programmable maternal and paternal microRNAs direct the embryonic development after the fertilization and during pregnancy.

This is why we have not seen a single successful de-extinction example. But 'scientists' want to maintain an illusion of de-extinction and that's why they are telling imaginary stories of how we could and should bring some species back to life. These are only evolutionary stories and they have nothing to do with modern, serious science.


New finding reveals the importance of non-coding RNAs in stem cell fate

Traits are not determined by gene sequences

Excerpt: "MicroRNAs are small, non-coding RNAs that do not translate into proteins, yet have a profound impact on gene expression regulation. He and her colleagues found that a microRNA called miR-34a appears to be a brake preventing both ES and iPS cells from producing extra-embryonic tissues. When this microRNA was genetically removed, both ES and iPS cells were able to expand their developmental decisions to generate embryo cell types as well as placenta and yolk sac linages. In their experiments, about 20 percent of embryonic stem cells lacking the microRNA exhibited expanded fate potential. Furthermore, this effect could be maintained for up to a month in cell culture.

"What is quite amazing is that manipulating just a single microRNA was able to greatly expand cell fate decisions of embryonic stem cells," He said. "This finding not only identifies a new mechanism that regulates totipotent stem cells, but also reveals the importance of non-coding RNAs in stem cell fate."

Additionally, in this study, He's group discovered an unexpected link between miR-34a and a specific class of mouse retrotransposons. Long regarded as "junk DNA," retrotransposons are pieces of ancient foreign DNA (my comment: this is an assumption) that make up a large fraction of the mammalian genome. For decades, biologists assumed that these retrotransposons serve no purpose during normal development, but He's findings suggest they may be closely tied to the decision-making of early embryos."

My comment: Programming of stem cells is done by microRNAs. Every somatic cell in your body has the exact same gene sequences. The DNA in the cells need to be expressed by epigenetic control of gene expression in order to achieve required cell specific differentiation status. This complex programming is made by microRNAs.

MicroRNAs can be found in human sperm for example. They cause epigenetic alterations to be inheritable through several, even hundreds of generations. MicroRNAs are the master regulators of gene expression. Skin, hair and eye color are inherited by microRNAs and other non-coding DNA. That's why genetically identical twins can differ with skin, hair and eye color. That's why this kind of phenomenon is possible:


Excerpt: "But, as it now turns out, scientists have claimed that traces of our EX PARTNER could also appear in our little one’s genetic makeup.

Yup, even if it’s not their baby - weird, huh?

Scientists at the University of South Wales observed an instance of telegony (physical traits of previous sexual partners being passed down to future children) during a study on fruit flies.

Apparently the offspring of the flies matched the size of the first male the mother mated with, rather than its biological father.

“Males contribute DNA to fertilise an egg, but we believe there is something more complex going on.”

It is thought that molecules of the semen produced by the mother’s first sexual partner had been absorbed into her immature eggs."

My comment: MicroRNAs of the semen produced by the mother's ex sexual partners affect the gene expression of the embryonic cells. This points out that gene sequences don't determine traits of the child. Doctrines of population genetics are totally wrong. The evolutionary theory is a dangerous heresy.


The Simplest Living Organism Ever Has 437 Genes

You need at least 500,000 perfectly organized base pairs in order to have a living cell


Excerpt: "If synthetic biology has a rockstar, it’s Craig Venter, and he’s back with a new hit. Venter and his team say they’ve created one of the simplest organisms theoretically possible using a combination of genetic engineering techniques, in-lab DNA-synthesis, and trial-and-error.

The work, published Thursday in Science, describes a self-replicating bacterium invented by Venter and his team that contains just 437 genes, a “genome smaller than that of any autonomously replicating cell found in nature,” according to the paper. The work sheds light on the function of the individual genes necessary to have life, and it also shows us just how little we actually know about specific gene functions."

My comment: The number of base pairs in a gene varies a lot. You need about 1,000 base pairs for having a 'simple' protein coding gene. But in some genes there are even 100,000 base pairs in ONE gene. And you need at least hundreds of genes for creating a living cell. This means that in order to have a living cell you need at least 500,000 base pairs that need to be perfectly organized in their places. But genes by themselves are not able to form a living cell. You need much much more. Craig Venter's team tried to design a synthetic living cell by using complex computer software alone, but their every effort failed. The only way for creating a minimal living cell was to knock down genes one by one in a living organism, with trial-and error, and find the final working combination of genes by which the cell was able to live and reproduce.

The message of this experiment is crystal clear: Random undirected processes are not able to create life. Life arises only from LIFE itself. Life is much more than a cocktail of chemical elements. The simplest living cell seems to be a super complex organism and it doesn't start to live without perfect design. Abiogenesis is a false theory.


It's time to forget false ideas about junk-dna

'Mysterious' non-protein-coding RNAs play important roles in gene expression

Excerpt: "
In cells, DNA is transcribed into RNAs that provide the molecular recipe for cells to make proteins. Most of the genome is transcribed into RNA, but only a small proportion of RNAs are actually from the protein-coding regions of the genome.

"Why are the non-coding regions transcribed at all? Their function has been mysterious," said Shelley Berger, PhD, a professor of Cell and Developmental Biology and director of the Penn Epigenetics Institute in the Perelman School of Medicine at the University of Pennsylvania.

Berger and Daniel Bose, PhD, a postdoctoral fellow in her lab, study the regulation of gene expression from enhancers, non-coding regions of the genome more distant from protein-coding regions. Enhancers boost the rate of gene expression from nearby protein-coding genes so a cell can pump out more of a needed protein molecule. A mysterious subset of non-coding RNAs called enhancer RNAs (eRNAs) are transcribed from enhancer sequences. While these are important for boosting gene expression, how they achieve this has been completely unknown.

Shedding new light on these elusive eRNAs, they showed that CBP, an enzyme that activates transcription from enhancers, binds directly to eRNAs. This simple act controls patterns of gene expression in organisms by regulating acetylation, a chemical mark that directs DNA tightly packed in the nucleus of cells to loosen to promote transcription. Their findings are published this week in Cell.

"The cells in our bodies share the same genes and DNA sequences, and differ only in how these genes are expressed," Bose said. "Enhancers and eRNAs are critical for this process. Our work shows an exciting new way that eRNAs produce these different patterns of gene expression. We asked if eRNAs work directly with CBP, and found that they do."
Using biochemical assays, they showed that the region of CBP that binds to RNA also can regulate the ability of CBP to work with chemical mark. By binding to this region, eRNAs can directly stimulate CBPs' acetylation activity.

"There is increased interest in enhancers and eRNAs in the cancer biology world because defective enhancers can cause too much or too little of a protein to be made, or can cause the coding region to be turned off or on, or can make a protein at the wrong time," Berger said. Knowing more about how enhancers and eRNAs function will help oncologists, since recent DNA sequencing of tumors from humans show that numerous mutations associated with cancers and other diseases occur in enhancer regions of the genome—not in protein-coding regions.

"Fundamentally, this is important science because we show that enhancer RNAs have a key role throughout the genome and body to guide protein production," Berger said. "We identified, across the genome, that enhancer RNAs were the most common type of RNA that bound to CBP, and that by making this interaction, eRNAs play a crucial role in regulating CBP activity and gene expression."

My comment: Every cell in an eukaryotic organism has virtually the exact same genetic sequences. So how is it possible for the cell to produce a specialized protein? How is it possible for the cell to get differentiated for its task? Why does a muscle cell function as a muscle cell and why does a neuronal cell function as it does?

The necessary instructions for the task of the cell are written on top of genes and histones. These markers are called inheritable epigenetic markers and they determine how genes are expressed, what kind of protein genes produce and for which tasks the cells get specialized. Non coding RNAs play an important role within gene expression and protein production.

Protein production is accuratedly controlled by several sophisticated mechanisms. You can read it from here: 
These noncoding RNAs are able to override genetic errors and faulty genes. That's why mutations, that are errors and mistakes in gene sequences don't play a role in biodiversity. 
There is no junk in the DNA. Comparing only similarities of protein coding genes and making assumptions of evolutionary relationships is really bad science. The evolutionary theory is a big lie. 


Direct communication between cell's surveillance and protein synthesizing machinery eliminates genetic errors

Direct communication between cell's surveillance and protein synthesizing machinery eliminates genetic errors

Excerpt: "Consider a car maker," said Baker. "If a faulty brake pedal sneaks past quality control and gets installed into a new car, the primary result is an improperly functioning car, which, in itself, is bad. However, failure to remove the car from the road could have grave secondary consequences if it leads to the damage of other cars, drivers or roads. Efficient quality control processes are therefore necessary, and ones that identify and remove faulty genetic intermediates from the cell are absolutely critical for avoiding downstream consequences that could negatively impact the function of the entire cell."

New research out of Case Western Reserve University School of Medicine describes a mechanism by which an essential quality control system in cells identifies and destroys faulty genetic material. The findings were published online December 23 in Nature Communications.

Kristian Baker PhD, associate professor in the Center for RNA Molecular Biology at Case Western Reserve University School of Medicine led the study that provided evidence for direct communication between the cell's protein synthesis machinery – the ribosome – and the protein complex that recognizes and destroys defective genetic intermediates called messenger RNAs (mRNAs).

"We aimed to understand how cells are able to recognize mRNA that is defective and distinguish it from normal mRNA. For most cells this process is critical for survival, but we didn't yet understand how it works, especially when the difference between the two is very subtle," said Baker. "Our findings clearly show that surveillance machinery involved in identifying faulty mRNA functionally interacts with the ribosome, the apparatus responsible for synthesizing proteins in the cell. It is now clear that these two elements communicate and work closely together to recognize and eliminate aberrant mRNA from the cell."

Cells convert sections of DNA encoding genes into mRNA that serves as a blueprint for the synthesis of a protein. In some cases, the DNA template has suffered damage or errors occur when copying the information such that the mRNA contains a "premature stop codon." Premature stop codons cause the ribosome to halt synthesis early, before the entire protein is made, resulting in a truncated protein that often lacks function, or worse, can wreak havoc on other normal processes in the cell. Baker's research focused on how cells identify when an mRNA has a premature stop codon and then target the faulty genetic intermediate for rapid disposal to avoid the harmful effects of truncated proteins.

In the new study, Baker and her team of researchers uncovered that ribosomes were stalled on mRNA at premature stop codons. This observation led to the discovery that one of proteins in the surveillance complex, UPF1, was important for interacting with the stalled ribosome and assisting with its release from the mRNA. The inability of UPF1 to properly communicate with the ribosome results in the failure of the mRNA to be targeted to rapid elimination and inactivates the whole surveillance system. Moreover, Baker's findings indicated that UPF1 harnesses energy found in adenosine triphosphate – a reserve for energy storage in the cell – to influence the function of the ribosome, and that this step in the cellular checkpoint is necessary for recognizing and destroying mRNA with premature stop codons.

Baker's efforts could potentially be leveraged for the future treatment of genetic diseases. "About one-third of all genetic diseases involve a gene mutation that introduces a premature stop codon into the corresponding mRNA. In some cases, a therapeutic strategy that either instructs the ribosome to bypass this stop or that interferes with the recognition or elimination of the mRNA could restore some level of functional protein and lessen disease symptoms in patients," said Baker. "What is most exciting is that once developed, such a strategy could be applied not just to a single genetic disease, but to any that occur as a consequence of these particular mutations."

My comment: This great discovery points out that DNA and genes are just raw material for sophisticated cellular mechanisms. Genes are not your destiny. Genes are not drivers or leaders, they are followers. This discovery destroys false ideas of genetic mutations that are assumed to lead to evolution. Population genetics with its gene centricism  is a major field of pseudoscience. This remarkable finding points to design and creation and helps us understand why mutations have no role in biodiversity. The cell has several surveillance and repair mechanisms for maintaing genomic integrity. mRNA is not just copied from the DNA. Instead, it undergoes several stages of quality control and fine-tuning. These mechanisms require intelligence. Theories of random mutations leading to evolution are FALSE SCIENCE!


A shocking DNA test result!

A white American girl has the greatest gene resemblance to Somalia and Sudan!

Excerpt: "I’ve recently received some shocking, life-altering news. My whole world has changed. I’ve lost all sense of identity and have so many questions. I took a DNA test and discovered I’m not who I thought I was.

The test, which I purchased through Living Social at a deep discount, is designed to tell you the top areas of the world whose current people have genes similar to yours. It doesn’t necessarily mean that your family is originally from that location, but it can be reasoned that if you have similar DNA, then you could possibly have ancestral connections to that place. That’s what the company’s website says anyway.

I received the test in the mail and after a few quick swabs of the mouth, I sent the sample back and waited. About 8 days later, the results were accessible online. They tell you the top 10 countries you’re connected to, along with some scientific gobbly gook that means nothing to the average person.

Before I give you the results, first let me tell you what I was expecting. As a white girl with known ties to England and Germany, I was expecting mostly European countries to pop up. In fact, I thought for sure there would be nothing new to learn or anything to gain from taking the test. I just thought the whole thing was interesting and that it would be cool to verify what I already knew.

Without further ado, I give you the results. Here are the countries that I have the greatest gene resemblance to:

1. Somalia
2. Sudan
3. Spain
4. Brazil
5. Morocco
6. Qatar
7. Afghanistan
8. Venezuela
9. Turkey
10. Columbia"

My comment: Gene sequences don't determine skin, hair or eye color. Gene sequences don't determine traits. Traits are inherited and determined by epigenetic control of gene expression. Here's an interesting video showing reactions of people who realize that all human beings are kind of cousins, the one and the same human kind created by God.


If you are not sure about your genetic relationships, or even if you were, it's worth considering the DNA test. You will be surprised. After the test you will realize the fabrification of the evolutionary theory. You have surprising relatives!


Inuit live in very cold climates, why do they have dark skin?

Inuit dark skin determined by vitamin D rich diet

Excerpt 1: "But Inuit vitamin D intake wasn’t dependent upon the sun. They get all that they need from their diet, heavy on types of fatty fish that are naturally rich in vitamin D. The plentiful amounts of the vitamin kept them from developing less melanin. In fact, before milk was fortified with D, people living outside of Northern Canada and Alaska loaded their diets with fishy products, such as cod liver oil, to get their daily supplement. So despite their chilly climate and lack of sun exposure, it’s the Inuit diet that has kept them in their natural glow."


Excerpt 2:"The MC1R gene provides instructions for making a protein called the melanocortin 1 receptor. This receptor plays an important role in normal pigmentation. The receptor is primarily located on the surface of melanocytes, which are specialized cells that produce a pigment called melanin. Melanin is the substance that gives skin, hair, and eyes their color. Melanin is also found in the light-sensitive tissue at the back of the eye (the retina), where it plays a role in normal vision.

Melanocytes make two forms of melanin, eumelanin and pheomelanin. The relative amounts of these two pigments help determine the color of a person's hair and skin. People who produce mostly eumelanin tend to have brown or black hair and dark skin that tans easily. Eumelanin also protects skin from damage caused by ultraviolet (UV) radiation in sunlight. People who produce mostly pheomelanin tend to have red or blond hair, freckles, and light-colored skin that tans poorly. Because pheomelanin does not protect skin from UV radiation, people with more pheomelanin have an increased risk of skin damage caused by sun exposure.

The melanocortin 1 receptor controls which type of melanin is produced by melanocytes. When the receptor is activated, it triggers a series of chemical reactions inside melanocytes that stimulate these cells to make eumelanin. If the receptor is not activated or is blocked, melanocytes make pheomelanin instead of eumelanin."

My comment: The skin color is determined by epigenetic control of gene expression. Factors influencing the skin color are vitamin D levels in diet and vitamin D production induced by exposure to sunlight. Mutations are not the reason for human skin color variation. We all are the same kind of human beings. There is not such a thing as a human race.

Identical twins can have very different skin, hair or eye colours. Gene sequences don't determine these traits. Population genetics and the evolutionary theory tell serious lies. Don't get misled.



Most immune responses are genetic, very personalised and finely tuned

Immune system associated genes don't change due to random mutations

Excerpt: "Nearly three quarters of immune traits are influenced by genes, new research from King's College London reveals.

The study published today in Nature Communications, adds to a growing body of evidence that the genetic influence on our immune system is significantly higher than previously thought.

Researchers from King's, supported by the NIHR Biomedical Research Centre at Guy's and St Thomas' Foundation Trust and King's College London, analysed 23,000 immune traits in 497 adult female twins from the TwinsUK cohort. They found that adaptive immune traits - the more complex responses that develop after exposure to a specific pathogen, such as chickenpox - are mostly influenced by genetics.

They also highlight the importance of environmental influences such as our diet, on shaping the innate immunity (the simple core immune response found in all animals) in adult life.

The findings could help to improve understanding of the immune system and the interaction of environmental factors. It could also form the basis of further research into treatments for various diseases, including rheumatoid arthritis and psoriasis.

Dr Massimo Mangino, lead researcher from King's College London said: 'Our genetic analysis resulted in some unusual findings, where adaptive immune responses, which are far more complex in nature, appear to be more influenced by variations in the genome than we had previously thought. In contrast, variation in innate responses (the simple non specific immune response) more often arose from environmental differences. This discovery could have a significant impact in treating a number of autoimmune diseases.'

Professor Tim Spector, Director of the TwinsUK Registry at King's College London said: 'Our results surprisingly showed how most immune responses are genetic, very personalised and finely tuned. What this means is that we are likely to respond in a very individualised way to an infection such as a virus - or an allergen such as a house dust mite causing asthma. This may have big implications for future personalised therapy.'

My comment: Yes, genes can be changed. But genes are changed if there is a need for the change. Immune system uses several complex mechanisms where epigenetic factors are tightly linked with genetic factors. They function at individual level and are influenced by environmental elements, typically diet. That's why twins may have very different shapes of innate immune system.

CpG island methylation can be mentioned as an example of an epigenetic mechanism within immune system.

RNA-mediated cellular mechanisms can cause gene sequence alterations by using the following mechanisms in CpG island rich genes, for example:

a. Hypermethylated cytosine turns to thymine.
b. Hydroxymethylated cytosine turns to guanine.

However, these substitutions at single nucleotide level don't increase genomic information. They don't lead to increase of functional or structural complexity. Large scale evolution has no mechanism. There is not such a thing as mutation driven evolution. Genes are not drivers, they are followers. Gene centric evolutionary theory is a dangerous heresy.


We can fight several types of cancer by eating healthy food

Unbalance of epigenetic factors is the most significant reason for cancers - Healthy diets help us prevent cancers

A 3,000-year-old medical claim surprises modern scientists.

Excerpt: "UT Southwestern Medical Center scientists have uncovered the chemical process behind anti-cancer properties of a spicy Indian pepper plant called the long pepper, whose suspected medicinal properties date back thousands of years.

The secret lies in a chemical called Piperlongumine (PL), which has shown activity against many cancers including prostate, breast, lung, colon, lymphoma, leukemia, primary brain tumors, and gastric cancer.
Using x-ray crystallography, researchers were able to create molecular structures that show how the chemical is transformed after being ingested. PL converts to hPL, an active drug that silences a gene called GSTP1. The GSTP1 gene produces a detoxification enzyme that is often overly abundant in tumors.

"We are hopeful that our structure will enable additional drug development efforts to improve the potency of PL for use in a wide range of cancer therapies," said Dr. Kenneth Westover, Assistant Professor of Biochemistry and Radiation Oncology. "This research is a spectacular demonstration of the power of x-ray crystallography."

The long pepper, a plant native to India, is found in southern India and southeast Asia. Although rare in European fare, it is commonly found in Indian stores and used as a spice or seasoning in stews and other dishes. It dates back thousands of years in the Indian subcontinent tied to Ayurveda, one of the world's oldest medical systems, and was referred to by Hippocrates, the ancient Greek physician known as the father of medicine.

"This study illustrates the importance of examining and re-examining our theories. In this case we learned something fundamentally new about a 3,000-year-old medical claim using modern science," said Dr. Westover." "

My comment: This finding points out the importance of healthy diet helping prevent cancers and diseases. Good quality food helps balancing our epigenome, especially correct methylation levels of the DNA. Mutations are not the true reason for cancers, they are consequences followed by unbalanced epigenome. Because epigenetic factors are in response of cellular differentiation and specialization, it's by logic that 
unbalanced methylation levels and patterns of the DNA and histones lead to erroneous cellular differentiation.

Diet changes the genome. Lack of vitamins, minerals and other important dietary elements also change the genome, sometimes into wrong direction. These epigenetic mechanisms are not able to create new genomic information or new genes for gene regulatory networks. That's why the evolutionary theory is a major lie.


MicroRNA expression is regulated by DNA methylation

MicroRNA expression is regulated by DNA methylation: a complex cascade of gene regulation events


Excerpt: "MicroRNAs (miRNAs) are non-coding RNAs, roughly 22 nucleotides in size that are central and negative regulators of gene expression. They exert their functions through base-pairing with the 3’UTR of mRNAs and block expression at the transcriptional and post-transcriptional levels, depending on the perfect or imperfect match in sequences between miRNAs and their target genes. miRNAs are central nodes in a variety of biological processes like cell proliferation, apoptosis, migration and differentiation, and are considered to be “epigenetic controllers” because they influence gene expression without altering the genomic sequence. Altered expression of miRNAs is a commonly observed in various pathological conditions, including cancer, where they can act as tumor suppressor genes or oncogenes. Similar to protein-coding genes, miRNAs are also subject to epigenetic regulation by DNA methylation in their promoter regions. DNA methylation of miRNAs indirectly influences the regulation of the miRNA target genes, silencing or overexpressing them in case of hypo- or hypermethylation of miRNAs respectively.

DNA methylation patterns are also altered in cancer. Usually aberrant methylation is not restricted to few genes, but instead changes are widespread throughout the genome. The functional result of DNA methylation is highly context dependent and can have opposite effects on gene expression depending if it occurs in the promoter of a coding gene or a miRNA. Presence of DNA methylation at a gene promoter often results in downregulation of the gene. However, DNA methylation of miRNAs leads to an overexpression of their target genes. Moreover, miRNAs can influence the expression of many targets and their gene targets can be regulated by multiple miRNAs at the same time, creating a network of miRNAs-targets which vastly increases the complexity of gene regulation.

In effort to provide clarification on how DNA methylation and miRNAs work together to regulate gene expression, our group analysed the effects of miRNA DNA methylation on several genes involved in Neuroblastoma, a tumor of infancy. We identified four miRNAs (miR34b, miR34c, miR149 and miR124-2) subjected to DNA methylation in their regulatory regions. Interestingly, these miRNAs share several targets (CDK6, CDK4, E2F1, E2F3, CCND1, CCNE2, BCL2 and MYCN) which are known central actors in cell cycle and apoptosis pathways and are involved in the pathogenesis of Neuroblastoma. We demonstrated that despite differences between cell lines at the gene expression level, the miRNAs-gene network is invariably disrupted in these pathways. Treatment with 5’Azacytidine, an epigenetic drug which induces global demethylation of the genome, revealed an inverse correlation between methylation status of these miRNAs and the expression of their gene targets. 5’Azacytidine treatment resulted in a down regulation of miRNA-regulated genes. Furthermore, introducing these miRNAs into neuroblastoma cells by miRNA-mimic transfections is able to partially block the cell cycle switch towards an apoptotic fate.

Overall these data reveal a complex, multi-level interaction of epigenetically altered miRNAs which fail to properly regulate the cell cycle, leading to diminished effectiveness of the apoptotic process. This suggests that DNA methylation regulates gene expression on multiple levels to regulate cell homeostasis and cancer progression. These data are not exhaustive but we consider them to be crucial pieces of a larger puzzle: additional miRNAs could be under control of DNA methylation, influencing cell cycle and apoptosis. Conversely, the miRNAs analysed here could also target other genes and pathways in addition to those we have considered. Additionally, scientific literature has disclosed several genes that are directly silenced by methylation rather than miRNAs. Because of the multiple levels of epigenetic regulation, we strongly believe that a detailed “map” of epigenetic alterations would define a more complete interaction between DNA methylation, miRNAs, and gene expression. This map could then help predict the effectiveness of epigenetic therapies in the treatment of neuroblastoma as well as other epigenetic diseases."

My comment: We can observe an incredible piece of design with microRNAs:

1. They are programmed by very specific way where several factors influence the final product. Because the DNA methylation affects the regulation of microRNA expression, it confirms previous observations that diet is the most significant factor causing changes in genomes of organisms.

2. The cell has several mechanisms for regulating gene expression; the DNA methylation normally suppresses and silences genes but with microRNA regulation the cell is able to both silence and overexpress their target genes along to 
levels of hyper- or hypomethylation of the DNA.

3. One gene is used for coding for several proteins by cellular mechanisms. One microRNA can have even hundreds of target genes. Gene regulatory networks constitute a complex orchestra and microRNA regulatory networks multiply this complexity by a significant factor.