Intense breeding has eroded genetic diversity - No evolution observed

Intense breeding has eroded genetic diversity


Excerpt: "Broadening crop phenotypic diversity is a key issue facing the challenge of sustainable food security and crop adaptation to ongoing climate changes.

Chromatin marks and epigenetic regulatory mechanisms are essential to the control of plant developmental processes and in shaping plant phenotypic plasticity, including adaptive responses to environmental stresses.

Stability and heritability features of epigenetic marks and knowledge of epigenetic regulatory mechanisms are crucial for breeding applications.

Modeling epigenetic variations requires understanding epigenetic regulatory mechanisms to further predict their impact on plant performances.
Modeling epigenetic variations with a process-based approach could help to assess and quantify their impacts on plant performances and then to guide the decision to either induce or repress them. This modeling feedback is central to model-driven breeding strategies.

Crop modelers are urged to take epigenetic variations into account to assist breeding strategies.

Epigenetic variations are involved in the control of plant developmental processes and participate in shaping phenotypic plasticity to the environment. Intense breeding has eroded genetic diversity, and epigenetic diversity now emerge as a new source of phenotypic variations to improve adaptation to changing environments and ensure the yield and quality of crops. Here, we review how the characterization of the stability and heritability of epigenetic variations is required to drive breeding strategies, which can be assisted by process-based models. We propose future directions to hasten the elucidation of complex epigenetic regulatory networks that should help crop modelers to take epigenetic modifications into account and assist breeding strategies for specific agronomical traits."

My comment: Breeding means epigenetic intensification or debilitation of desired traits. Shifting with epigenetic information profiles, in an artificial or adaptational way, results in erosion of genetic information layers. Any change in organisms occurs due to epigenetic regulation of existing biological information OR gradual but inevitable corruption of information. That's why there's no mechanism for evolution. Don't get lost.


Organisms need genetic rescue because evolution is not happening

Adaptation results in a weakened gene pool - There is no mechanism for evolution


Excerpt: "Wildlife populations are most threatened when their numbers become reduced to the point that their genetic diversity is lost. Their narrowing gene pool can accelerate into what is called an “extinction vortex.” With ever fewer gene variants (alleles), the ability to adapt and evolve declines. As inbreeding increases, deleterious genes accumulate, and fitness plummets. The creatures typically have fewer offspring, many of them physically or behaviorally impaired, susceptible to disease, increasingly incapable of thriving. Most people assume they are doomed, but that no longer has to be what happens.

“Genetic rescue” restores genetic diversity. Conservation biologists are warming to its use with growing proof of its effectiveness. One study of 156 cases of genetic rescue showed that 93% had remarkable success. The most famous case was a dramatic turnaround for the nearly extinct Florida panther. By the mid-1990s only 26 were left, and they were in bad shape. In desperation, conservationists brought in 8 female Texas cougars (which are closely related to the Florida cats). Five of the females reproduced. The result of the outcrossing was a rapid increase in litter success—424 panther kittens born in the next 12 years. The previous population decline of 5% a year reversed to population growth of 4% a year. Signs of inbreeding went away, and signs of increasing fitness grew. Scientists noticed, among other things, that the genetically enriched panthers were becoming harder to capture.
Often genetic diversity can be restored by means as straightforward as connecting isolated populations with wildlife corridors or larger protected areas, but new technological capabilities are broadening the options for genetic rescue. Advanced reproductive technology offers an alternative to transporting whole genetically-distinct parents—artificial insemination has brought genetic refreshment to cheetahs, pandas, elephants, whooping cranes, and black-footed ferrets. With the cost of genome sequencing and analysis coming down, it is becoming possible to examine each stage of genetic rescue at the gene level instead of having to wait for external traits to show improvement. This has already been done with Rocky Mountain bighorn sheep.

Another strategy being considered is “facilitated adaptation.” Different populations of a species face different local challenges. When a particular population can’t adapt fast enough to keep up with climate change, for example, it may be desirable to import the alleles from a population that has already adapted. With gene editing becoming so efficient (CRISPR etc.), the desired genes could be introduced to the gene pool directly. If necessary, the needed genes could even come from a different species entirely. That is exactly what has been done to save the American chestnut from the fungus blight that killed four billion trees early in the 20th century and reduced the species to functional extinction. Two fungus-resistant genes were added from wheat, and the trees were made blight-proof. They are now gradually in the process of being returned to their keystone role in America’s great eastern forest.

One further reservoir of genetic variability has yet to be employed. In museums throughout the world there are vast collections of specimens of species that have been reduced to genetically-impoverished remnant populations in the wild or in captive breeding programs. Those museum specimens are replete with “extinct alleles” in their preserved (though fragmented) DNA. Ancient-DNA sequencing and analysis is becoming so precise, the needed alleles can be identified, reproduced, and reintroduced to the gene pool of the current population, restoring its original genetic diversity. The long-dead can help rescue the needful living."

My comment: A gene pool of an organism stays about the same or it experiences gradual but inevitable weakening due to adaptation to changing conditions. At molecular biological level, adaptation always occurs due to epigenetic mechanisms and factors and it typically results in alterations in DNA sequence. But as we can see, sequence modifications don't lead to evolution but accumulation of harmful mutations, loss of diversity, loss of functions and genetic degradation. In the future, thousands of species will need genetic rescue, including human populations. It's interesting to see when people realize that evolution is not happening.



Biological forward-planning and epigenetic memory point to Design

Biological forward-planning and epigenetic memory point to Design


Excerpt: "To study how long the environment can leave a mark on genetic expression, a team led by scientists from the European Molecular Biology Organisation (EMBO) in Spain took genetically engineered nematode worms that carry a transgene for a fluorescent protein. When activated, this gene made the worms glow under ultraviolet light.

Then, they switched things up for the nematodes by changing the temperature of their containers. When the team kept nematodes at 20° Celsius (68° F), they measured low activity of the transgene - which meant the worms hardly glowed at all.

But by moving the worms to a warmer climate of 25° C (77° F), they suddenly lit up like little wormy Christmas trees, which meant the fluorescence gene had become much more active.

Their tropical vacation didn't last long, however. The worms were moved back to cooler temperatures to see what would happen to the activity of the fluorescence gene.

Surprisingly, they continued to glow brightly, suggesting they were retaining an 'environmental memory' of the warmer climate – and that the transgene was still highly active.

Furthermore, that memory was passed onto their offspring for seven brightly-glowing generations, none of whom had experienced the warmer temperatures. The baby worms inherited this epigenetic change through both eggs and sperm.
The team pushed the results even further - when they kept five generations of nematodes at 25° C (77° F) and then banished their offspring to colder temperatures, the worms continued to have higher transgene activity for an unprecedented 14 generations.

That's the longest scientists have ever observed the passing-down of an environmentally induced genetic change (My addition: this is an epigenetic change) . Usually, environmental changes to genetic expression only last a few generations.

"We don't know exactly why this happens, but it might be a form of biological forward-planning," said one of the team, Adam Klosin from EMBO and Pompeu Fabra University, Spain.

"Worms are very short-lived, so perhaps they are transmitting memories of past conditions to help their descendants predict what their environment might be like in the future," added co-researcher Tanya Vavouri from the Josep Carreras Leukaemia Research Institute in Spain.

There's a reason why scientists turn to C. elegans as a model organism - after all, those 14 generations would only take roughly 50 days to develop, but can still give us important clues on how environmental genetic change is passed down in other animals, including humans.

There are many examples of this phenomenon in worms and mice, but the study of environmental epigenetic inheritance in humans is a hotly debated topic, and there's still a lot we don't know.

"Inherited effects in humans are difficult to measure due to the long generation times and difficulty with accurate record keeping," stated one recent review of epigenetic inheritance.

But some research suggests that events in our lives can indeed affect the development of our children and perhaps even grandchildren - all without changing the DNA.

For example, studies have shown that both the children and grandchildren of women who survived the Dutch famine of 1944-45 were found to have increased glucose intolerance in adulthood.

Other researchers have found that the descendants of Holocaust survivors have lower levels of the hormone cortisol, which helps your body bounce back after trauma.
The 2017 study on nematodes is an important step towards understanding more about our own epigenetic inheritance - especially because it serves as a remarkable demonstration of how long-lasting these inter-generational effects may be.

My comment: The inheritance of acquired characteristics is based on epigenetic memory. The fact that the cell has a memory, a changing state of information it can transfer to its offspring, tells about designed mechanisms. Using memory requires extremely complex information management systems:

- What kind of memory format is to be used?
- What is the mechanism that writes the memory?
- Which mechanism chooses what to write about?
- By which media and mechanism is the memory transferred to offspring?
- What mechanism reads the written memory?
- How will the information written in memory be converted to such a form that it leads to the desired outcome, that is, to the correct gene regulation?

Epigenetic memory is controlled by co-operation of histone epigenetic markers and non-coding RNA molecules (lncRNAs, piRNAs, siRNAs, miRNAs) that transmit the necessary information. 

The memory management system must be ready at once. Such complex information management systems don't evolve. Evolution theory is the most serious heresy of our time.


It’s Easy to Be an Atheist if You Ignore Science

Scientists do not have even the slightest clue as to how life could have begun through an unguided naturalistic process


Excerpt: "Although the general public is disconcertingly unaware of it, it is a fact that scientists do not have even the slightest clue as to how life could have begun through an unguided naturalistic process absent the intervention of a conscious creative force.

Here are just a few well-chosen statements on the Origin of Life:

  • (2016) “[There is] collective cluelessness…those who say this is well worked out, they know nothing, nothing about chemical synthesis…Those who think that scientists understand the details of life’s origin are wholly uninformed. Nobody understands…when will the scientific community confess to the world that they are clueless on life’s origin, that the emperor has no clothes?” James Tour — Professor of Chemistry, Rice University (Synthetic chemist and among the top ten most cited chemists in the world)
  • (2011) “The Origin of Life field is a failure.” Eugene Koonin, microbiologist at the National Center for Biotechnology Information
  • (2011) “With respect to the Origin of Life, I find the more we learn about cells, the more complex they seem; they are just incredibly complex things, and to go from what we can see today and try to reason where it came from, I think is really impossible.” Lee Hartwell, Nobel Prize in Medicine, 2001
  • (2007) “How? [did life begin] I have no idea.” George Whitesides, Professor of Chemistry, Harvard University, Winner of the Priestley Medal in Chemistry (second only to the Nobel Prize)
  • (2001) “The origin of life appears to me as incomprehensible as ever, a matter for wonder but not for explication.” Franklin Harold, Professor Emeritus, Department of Biochemistry and Molecular Biology, Colorado State University
  • (1983) “In short, there is not a shred of objective evidence to support the hypothesis that life began in an organic soup here on earth.” Sir Fred Hoyle, distinguished British astronomer, physicist, mathematician (without question one of the greatest scientific minds of the 20th century)
  • (1981) “Since Science does not have the faintest idea how life on earth originated…it would only be honest to confess this to other scientists, to grantors, and to the public at large.” Hubert Yockey, physicist and renowned information theorist

As Biochemist Klaus Dose wrote: “Experimentation on the origin of life…has led to a better perception of the immensity of the problem of the origin of life on Earth rather than to its solution.” Researchers Carl Woese and Gunter Wachtershauser concur: “While we do not have a solution, we now have an inkling of the magnitude of the problem.”

Why are researchers having such difficulties discovering a naturalistic Origin of Life? Let’s let the aforementioned and atheist microbiologist Eugene Koonin answer this question: “Certainly this is not due to a lack of experimental and theoretical effort, but to the extraordinary intrinsic difficulty and complexity of the problem. A succession of exceedingly unlikely steps is essential for the Origin of Life…these make the final outcome seem almost like a miracle.”

Translation for the lay-person: Discovering how unguided naturalistic forces could assemble a living cell — a molecular machine that is more sophisticated and functionally complex than anything human technology has ever produced — is a problem of nightmarish proportions.

When one dispassionately contemplates the enormous difficulties involved in a naturalistic origin of life, it is not surprising at all that one often suggested solution is Intelligent Design or Divine Creation. In fact, any number of world class scientists themselves have brought up the issue:

  • “Abiogenesis [life from non-life] strikes many as virtually miraculous…you might get the impression from what I have written not only that the origin of life is virtually impossible, but that life itself is impossible…So what is the answer? Is life a miracle after all?” (Dr. Paul Davies)
  • “[We have no naturalistic explanation for] the origin of life, which is unknown so far…As long as the origin of life can’t be explained in natural terms, the hypothesis of an instant Divine creation of life cannot objectively be ruled out.” (Dr. Christian DeDuve, Nobel Prize-Medicine, 1974)
  • “There are only two possibilities as to how life arose. One is spontaneous generation arising to evolution; the other is a supernatural creative act of God. There is no third possibility.” (George Wald, Nobel Prize-Medicine, 1967)
  • “Although a biologist, I must confess I do not understand how life came about…I consider that life only starts at the level of a functional cell. The most primitive cells may require at least several hundred different specific biological macro-molecules. How such already quite complex structures may have come together remains a mystery to me. The possibility of the existence of a Creator, of God, represents to me a satisfactory solution to this problem.” (Dr. Werner Arber, Nobel Prize-Medicine, 1978)
  • “From my earliest training as a scientist I was very strongly brainwashed to believe that science cannot be consistent with any kind of deliberate creation. That notion has had to be very painfully shed. I am quite uncomfortable in the situation, the state of mind I now find myself in. But there is no logical way out of it; it is just not possible that life could have originated from a chemical accident.” (Chandra Wickramasinghe, mathematician, astronomer, astrobiologist – longtime collaborator of Sir Fred Hoyle)
  • “Indeed, such a theory [Intelligent Design] is so obvious that one wonders why it is not widely accepted as being self-evident. The reasons are psychological rather than scientific.” “A common sense interpretation of the facts suggests that a super intellect has monkeyed with the laws of physics, as well as with chemistry and biology, and that there are no blind forces worth speaking about in nature.” (Sir Fred Hoyle)
If a rational, truth-seeking individual is asked: “How did life begin; naturalistic, unguided forces or Divine Creation?” There are only two possible answers: (a) Divine Creation or (b) I don’t know, the jury is still out; but atheism – a denial of the existence of a Creator of life — is not possible anymore….unless, of course, as I stated in the title of this article, you are prepared to ignore science and scientists. And if so, you might just as well go and play children’s games and with children’s toys, like…..LEGO blocks."


Science is messy and unpredictable

Genes will no longer be seen as the blueprint for life



- Scientists and philosophers are beginning to doubt the relevance of the gene for understanding biology.
- Despite being central to the subject for over a century, there has never been a universally accepted, constant definition of what genes actually are.
- From the beginning, scientists have tried to link human characteristics to genes, but had limited success in establishing stable connections.
As a consequence, the function of genes is now understood to depend on systems of epigenetic inheritance and environmental signalling. 
- Whether a gene is activated (or not) to produce a protein depends on how it is "packaged" into chromosomes, and information the organism receives from the environment. 
- Genes may consist of separate building blocks that are distributed over the genome and have different functions. They may overlap and be read in a variety of ways. Their products in turn, may be cut into pieces and then spliced together again in a variety of ways. All of these activities depend on a variety of signals – from within the cell, from other cells, or from the environment.
But genes will no longer be seen as the blueprint for life, even if technological and medical applications of gene technology suggest this.Instead, they are increasingly seen as only one of the many resources that organisms make use of in adapting to challenges in their environments.
The history of the gene, once believed to be one of the biggest triumphs of 20th century science, shows how messy and unpredictable science is.

My comment: DNA is just passive information layer the cell uses for building different and complex RNA-products. This process is controlled by epigenetic factors and mechanisms. This is why any change in organisms is based on epigenetic regulation of EXISTING biological information. This regulation often results in degradation of genetic information. That's why there's no mechanism for evolution.


GUARDIN lncRNA protects our genome and maintains DNA integrity

GUARDIN lncRNA protects our genome and maintains DNA integrity


Excerpt: "Batman swoops through Gotham, Supergirl flies over National City, and the Black Panther keeps his keen eyes on Wakanda; every superhero acts as a guardian of the beloved place they call home, protecting from any number of devious and dastardly threats. Now, researchers from the laboratory of Xu Dong Zhang and Mian Wu (Henan Provincial People’s Hospital, Zhengzhou, China) have revealed that a superhero also protects our genome and maintains DNA integrity: the long non-coding RNA (lncRNA) we now know as GUARDIN! 

In brief, the authors set out to identify additional lncRNAs induced by the tumor suppressor and DNA damage repair facilitator p53 that help to maintain genome integrity. p53 plays multiple roles in response to threats to genome integrity, including the promotion of cell cycle arrest to allow DNA damage repair or signaling for the apoptosis of cells with severely damaged DNA. 

So what fantastical deeds by GUARDIN did the authors discover? 
  • Employing p53-null human lung adenocarcinoma cells carrying an inducible wild-type p53 expression system, the authors aimed to uncover new p53-responsive lncRNAs 
    • This approach highlighted the accumulation of the longest isoform of the RP3-510D11.2 lncRNA, which the authors named GUARDIN 
  • Wild-type p53 expression in several cancer cell lines increases GUARDIN expression via direct binding to the GUARDIN promoter 
  • Activation of the DNA damage response leads to GUARDIN upregulation both in cancer and normal human cells 
  • Detailed analysis suggested that GUARDIN promotes survival and proliferation by protecting against the constitutive cellular stresses present in cells, as well as exogenous genotoxic stress, by employing two primary mechanisms: 
    • miRNA Sponge: GUARDIN prevents the activation of the DNA damage response at telomere ends by sequestering microRNA-23a and thereby promoting the accumulation of its target, the telomeric repeat-binding factor 2 (TRF2), a critical component of the shelterin complex that protects telomere ends RNA Scaffold: GUARDIN enhances DNA damage repair by acting as an 
    • RNA scaffold to promote the heterodimerization of breast cancer 1 (BRCA1) and BRCA1-associated RING domain protein 1 (BARD1), thereby promoting BRCA1 stability and function 
  • GUARDIN silencing triggered apoptosis and senescence, but also enhanced the cytotoxicity of exogenous genotoxic stress and inhibited cancer xenograft growth 
    • Small molecules that block the interaction of GUARDIN with miRNA-23a and BRCA1 may represent a means to improve cancer treatment 
What the talented team discovered in this new p53-based study may permit the design of new and more effective anti-cancer therapies, with our new superhero GUARDIN playing the central role.


My comment: What factors drive the cell to build RNA-molecules that help in maintaining genomic integrity? It's clear that random mutations are not able to create this kind of DNA repair and protection mechanism. This finding points to Design and Creation. Don't be deceived.


RNA editing - more reasons why DNA doesn't determine traits

RNA editing - sophisticated mechanisms point to Design


Excerpt: "Occasionally researches encounter a gene with a sequence of nucleotides that does not match exactly that in its RNA product:
  • messenger RNA (mRNA) or
  • ribosomal RNA (rRNA) or
  • transfer RNA (tRNA) and even
  • microRNA (miRNA)
  • long non coding RNA (lncRNA)

If the product is mRNA, some of the codons in the open reading frame (ORF) of the gene specify different amino acids from those in the protein translated from the mRNA of the gene.

The reason is RNA editing: the alteration of the sequence of nucleotides in the RNA
  • after it has been transcribed from DNA but
  • before it is translated into protein

RNA editing occurs by two distinct mechanisms:
  • Substitution Editing: chemical alteration of individual nucleotides.These alterations are catalyzed by enzymes that recognize a specific target sequence of nucleotides (much like restriction enzymes):
    • cytidine deaminases that convert a C in the RNA to uracil (U);
    • adenosine deaminases that convert an A to inosine (I), which the ribosome translates as a G. Thus a CAG codon (for Gln) can be converted to a CGG codon (for Arg).
  • Insertion/Deletion Editing: insertion or deletion of nucleotides in the RNA.These alterations are mediated by guide RNA molecules that
    • base-pair as best they can with the RNA to be edited and
    • serve as a template for the addition (or removal) of nucleotides in the target"

My comment: DNA is just passive information library for the cell that has several clever ways to modify RNA products. RNA editing occurs before alternative splicing. I have collected a few valuable scientific facts about RNA-editing that help us understand the significance of RNA molecules:
  • Animal cells use an editing mechanism that converts adenosine residues to inosine residues (which masquerade as guanosine residues) in messenger RNA. (Masquerading technology points to extreme complexity of information handling.)
  • RNA editing generates post-transcriptional sequence alterations.
  • RNA editing can generate a multitude of transcript isoforms and can potentially be used to optimize protein function in response to varying conditions.
  • This has a biological significance in controlling the amount of functional RNA molecules in the cell, in expanding the functionality of a limited set of transcripts, and in defending the cell against certain RNA viruses.
  • More than half the amino acids of the genetic code can be altered in this fashion.There are at least 100 million adenosine-to-inosine RNA editing sites in human transcripts.
  • More than 140 types of chemical modifications have been found in RNA.
RNA products don't tolerate mutations. Even the slightest epigenetic errors are associated with serious diseases. That's why the theory of mutation driven evolution is the most serious heresy of our time. Don't get lost.


Mutation rate and lack of beneficial mutations destroy the theory of evolution

Mutation rate and lack of beneficial mutations destroy the theory of evolution

Genetically (DNA) all people are 99.9 % similar. The 0.1% difference is strongly related to hereditary diseases. Behind this scientific fact is the NHGRI (The National Human Genome Research Institute).


Every time DNA is passed on to the next generation, 100 to 200 new mutations accumulate in the human genome. This is what Nature's research says.


The human genome has about 3.3 billion base pairs. The 0.1% difference in the genome means about 3.3 million differences in base pair-level at the whole population level.

The rate of mutation in the human genome is likely to be accelerating, but it is possible to estimate in what time genetic errors are accumulated in the human genome. This is Nature's release:

"Of 1.15 million single-nucleotide variants found among more than 15,000 protein-encoding genes, 73% in arose the past 5,000 years, the researchers report."
Beneficial mutations are difficult, if not impossible to discover. Few that have been interpreted to be useful cause some adverse consequences (eg sickle cell anemia). Obviously, most of the mutations are either neutral or harmful and are a major cause of rare diseases.


As genetic editing methods become more common, scientists try to repair CG> TA changes in the human genome. This also tells us that genetic mutations are mostly harmful and have nothing to do with the variation of human traits.

Mechanisms of genetic degradation are already quite well known. On the other hand, no one is able to demonstrate an effective mechanism for evolution. We can only detect epigenetic regulation of existing biological information or corruption of biological information leading to gradual but inevitable degradation of information. All the evidence points to recent Creation and Biblical Truths.


lncRNAs control cell differentiation

lncRNAs control cell differentiation - Mutations don't result in evolution


Excerpt: "Several years ago, biologists discovered a new type of genetic material known as long noncoding RNA. This RNA does not code for proteins and is copied from sections of the genome once believed to be “junk DNA.”

Since then, scientists have found evidence that long noncoding RNA, or lncRNA, plays roles in many cellular processes, including guiding cell fate during embryonic development. However, it has been unknown exactly how lncRNA exerts this influence.

Inspired by historical work showing that structure plays a role in the function of other classes of RNA such as transfer RNA, MIT biologists have now deciphered the structure of one type of lncRNA and used that information to figure out how it interacts with a cellular protein to control the development of heart muscle cells. This is one of first studies to link the structure of lncRNAs to their function.

“Emerging data points to fundamental roles for many of these molecules in development and disease, so we believe that determining the structure of lncRNAs is critical for understanding how they function,” says Laurie Boyer, the Irwin and Helen Sizer Career Development Associate Professor of Biology and Biological Engineering at MIT and the senior author of the study, which appears in the journal Molecular Cell on Sept. 8.

Learning more about how lncRNAs control cell differentiation could offer a new approach to developing drugs for patients whose hearts have been damaged by cardiovascular disease, aging, or cancer.

In the new study, the researchers decided to investigate which regions of the 600-nucleotide RNA molecule are crucial to its function. “We knew Braveheart was critical for heart muscle cell development, but we didn’t know the detailed molecular mechanism of how this lncRNA functioned, so we hypothesized that determining its structure could reveal new clues,” Xue says.

To determine Braveheart’s structure, the researchers used a technique called chemical probing, in which they treated the RNA molecule with a chemical reagent that modifies exposed RNA nucleotides. By analyzing which nucleotides bind to this reagent, the researchers can identify single-stranded regions, double-stranded helices, loops, and other structures.

This analysis revealed that Braveheart has several distinct structural regions, or motifs. The researchers then tested which of these motifs were most important to the molecule’s function. To their surprise, they found that removing 11 nucleotides, composing a loop that represents just 2 percent of the entire molecule, halted normal heart cell development.

The researchers then searched for proteins that the Braveheart loop might interact with to control heart cell development. In a screen of about 10,000 proteins, they discovered that a transcription factor protein called cellular nucleic acid binding protein (CNBP) binds strongly to this region. Previous studies have shown that mutations in CNBP can lead to heart defects in mice and humans.

Further studies revealed that CNBP acts as a potential roadblock for cardiac development, and that Braveheart releases this repressor, allowing cells to become heart muscle.

“This is one of the first studies to relate lncRNA structure to function,” says John Rinn, a professor of stem cell and regenerative biology at Harvard University, who was not involved in the research.
Long non coding RNA molecule - a complex structure built from passive DNA.

“It is critical that we move toward understanding the specific functional domains and their structural elements if we are going to get lncRNAs up to speed with proteins, where we already know how certain parts play certain roles. In fact, you can predict what a protein does nowadays because of the wealth of structure-to-function relationships known for proteins,” Rinn says.

Building a fingerprint

Scientists have not yet identified a human counterpart to the mouse Braveheart lncRNA, in part because human and mouse lncRNA sequences are poorly conserved, even though protein-coding genes of the two species are usually very similar. However, now that the researchers know the structure of the mouse Braveheart lncRNA, they plan to analyze human lncRNA molecules to identify similar structures, which would suggest that they have similar functions.

“We’re taking this motif and we’re using it to build a fingerprint so we can potentially find motifs that resemble that lncRNA across species,” Boyer says. “We also hope to extend this work to identify the modes of action of a catalog of motifs so that we can better predict lncRNAs with important functions.”
The researchers also plan to apply what they have learned about lncRNA toward engineering new therapeutics. “We fully expect that unraveling lncRNA structure-to-function relationships will open up exciting new therapeutic modalities in the near future,” Boyer says."

My comment: Can you see the obvious contradiction in this article? These crucial RNA molecules don't tolerate mutations. Mutating only 2% of lncRNA:s nucleotides results in abnormal heart cell development. Researchers admit that lncRNAs have a very important role in cellular differentiation. This is because they are in response of establishing epigenetic information layers for the developing cell. Especially this means histone epigenetic markers. 'LncRNAs are poorly conserved', as evolutionists say. This means there are huge differences in them between different species. Human/Chimp lncRNAs are very different. Evolutionists claim that human lncRNAs have rapidly evolved. However, mutations in these crucial RNA-molecules are associated with serious diseases. That's why we have nothing to do with apes. The theory of evolution is the most serious heresy of our time. Don't be deceived.


Insane Probability of Evolution

Evolution is not mathematically possible


Excerpt: "Let us assume the "first living cell" had 300 gene complexes, with an average length of 3,000 nucleotides (or nucleotide pairs).  Human gene complexes are far more complicated, and longer, than the gene complexes of the "first living cell" (if such a cell ever existed).

Now let us assume the probability of a random permutation of 3,000 nucleotides, being able to create a gene complex for the "first living cell," was 10‑5.  This number is ridiculously generous to the theory of evolution (i.e. the real probability is much, much less than that).

Thus, we have a probability that an RNA or DNA strand for the "first living cell" would have a viable permutation of nucleotides is: 10(‑5x300) which is equal to 10‑1,500.  The "‑5" is the probability of a single new gene complex forming from a randomly generated permutation of 3,000 nucleotides; and the 300 is the number of gene complexes which must be made.
Using the above example, 50 of the 300 gene complexes would be used to create one protein structure.

But even the above probability of 10‑1,500 ignores a lot of things, such as the viability of different combinations of proteins (remember, proteins must fit together, thus just having a bunch of proteins doesn't help at all, they must be a "set" of proteins which have very specific shapes and have specific amino acids in just the right places), but we will use the above numbers.

Remember, 10‑100 is an impossible probability.  A probability of 10‑500 is an insane probability because it is 10400 times smaller than an impossible probability.

Now we are talking about a number which is 101,000 times smaller than an insane probability (i.e. 10(1,500‑500) equals 101,000)."

My comment: Have a blessed Easter!


G protein-coupled receptors act as little computing devices

G protein-coupled receptors act as little computing devices decoding complex information


Excerpt: "Scientists at the National Institute on Drug Abuse (NIDA) Intramural Research Program (IRP) have uncovered evidence that shows a more complex and elaborate role for the body's hard-working G protein-coupled receptors (GPCRs) than previously thought, suggesting a conceptual advance in the fields of biochemistry and pharmacology. With more than 800 members in the human genome, GPCRs are the largest family of proteins involved in decoding signals as they come into the cell and then adapt the cell's function in response. NIDA is part of the National Institutes of Health.

Manipulating how cells respond to signals is key to developing new medications. Although pharmacologists have studied GPCRs for many years, there is still a debate on how they operate—are they isolated units that randomly collide with each other or are they deliberately coupled together to receive signals? The NIDA scientists conclude that GPCRs form part of very elaborate pre-coupled macromolecular complexes. Simply put, they act as little computing devices that optimally gather and process information coming into the cell, allowing the cells to adapt and change their function.

"These findings represent many years of complex and highly nuanced science, following the trail as chemical signals travel through the body at the cellular level," said NIDA Director Nora D. Volkow, M.D. "This remarkable discovery will open new avenues for medication development for addiction, pain and other conditions, offering more precise targets with fewer side effects."

"The specific macromolecular complex investigated in this study has therapeutic implications not only for addiction, but also for Parkinson's disease and schizophrenia," said Dr. Sergi Ferré, who led the team of scientists. "Discovering that these protein interact with other signals in preformed complexes gives us more precise targets for medication development."

To unravel the complex journey of the body's GPCRs, scientists used biophysical tools, including fluorescent biosensors; biochemical tools, such as cell signaling in neuronal cultures; as well as computational models."

My comment: Diet, climate, stress factors, social interactions, physical activity, toxicants and other inputs generate signals that travel from cell to cell throughout the body. Signals are typically transmitted by non coding RNA molecules, such as microRNAs. G protein-coupled receptors DECODE these important signals so that cellular mechanisms can alter the way DNA is read into transcription. This decoding contributes to histone markers, DNA methylation profiles and RNA epigenetics.

Changes in organisms are based on these Intelligent mechanisms, not random errors. There's no mechanism for evolution. Don't get lost.


DNA methylation plays key role in stem cell differentiation

DNA methylation plays key role in stem cell differentiation


Excerpt: "Northwestern Medicine scientists have discovered how the process of DNA methylation regulates the development of spinal cord motor neurons, according to a study published in the journal Cell Stem Cell.

DNA methylation, an epigenetic mechanism that determines whether or not a gene is expressed, guides stem cells as they transform from blank slates into specialized cells, according to Evangelos Kiskinis, Ph.D., assistant professor of Neurology in the Division of Neuromuscular Disease and senior author of the study.

Motor neurons are highly specialized neuronal cells that connect the central nervous system to muscle and degenerate in amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease.

"If you look at DNA methylation patterns in ALS patients, they are all over the place," said Kiskinis, who is also a professor of Physiology. "Is it a driver of disease, or is it just a byproduct? Our study provides us with a platform to address these intriguing questions."

The investigators used a variety of cutting-edge technologies—including single cell RNA-Sequencing and a methylation-focused adaption of CRISPR-Cas9 gene editing, known as epigenetic editing—to create a series of stem cells that each lacked different enzymes that trigger DNA methylation.

After analyzing the stem cells along with the differentiating neural progenitors and the motor neuron populations, Alberto Ortega, Ph.D., senior postdoctoral fellow in Kiskinis' laboratory and lead author on the study, concluded that the enzyme DNMT3A triggered DNA methylation, which in turn repressed or counterintuitively activated the key transcription factors that controlled differentiation of stem cells into spinal cord motor neurons.

"DNA methylation governs gene expression potential and hence cell identity," Kiskinis said. "As stem cells transition from early progenitors to committed progenitors to developed neurons, DNA methylation allows for the induction or suppression of key transcription factors. In turn, those transcription factors govern cell type function and specificity."
"Our study nicely shows the importance of epigenetics on controlling different steps of the development of the human central nervous system by tuning the expression levels of transcription factors," Ortega added.

In addition, the scientists found irregular DNA methylation patterns could have downstream consequences related to the function of these neurons, according to Kiskinis.

"It seems if you don't set your DNA methylation patterns correctly, there's a cascade of irregular gene expression that results in defective cells," Kiskinis said. "This is intriguing, because people usually think about methylation in the context of cell differentiation—the role in developed neurons is largely overlooked."
Further investigation could shed light on spinal cord diseases, as patients with ALS have irregular patterns of methylation, according to Kiskinis. In addition, patients with ALS exhibit a high rate of genetic variants associated with the DMNT3A enzyme—another puzzling link."

My comment: DNA methylation patterns that are necessary for cellular differentiation are regulated by non-coding RNA molecules, such as microRNAs, piRNAs, siRNAs and lncRNAs. The DNA has no control over cellular differentiation. Irregular patterns of methylation are linked to genetic variants i.e. genetic degradation. This is once again a clear evidence that aberrant methylation patterns result in genetic degradation. That's why there's no mechanism for evolution. Don't be deceived.


The obvious link between epigenetic factors and genetic mutations

Due to rapid genetic degradation scientists try to repair human DNA


Excerpt: "The new editors allow researchers to rewrite all four bases that store information in DNA and RNA. Those four bases are adenine (A) which pairs with thymine (T) (or uracil (U) in RNA), and guanine (G) pairs with cytosine (C). Mutations that change C-G base pairs to T-A pairs happen 100 to 500 times every day in human cells. Most of those mutations are probably benign, but some may alter a protein’s structure and function, or interfere with gene activity, leading to disease. About half of the 32,000 mutations associated with human genetic diseases are this type of C-G to T-A change, says Liu, a Howard Hughes Medical Institute investigator at Harvard University. Until now, there was little anyone could do about it, he says."


Excerpt: "Single‐gene and genome sequencing studies have identified base substitution mutations as a causative mechanism in human genetic diseases and cancer. These mutations do not occur randomly but are often enriched at specific DNA (deoxyribonucleic acid) sequences. The genome of most human cells contains about 50 million 5‐methylcytosine bases, the majority of them occurring at the CpG dinucleotide sequence. Methylated CpG dinucleotides are the targets of many of the mutations, mostly transition mutations (C→T or G→A), found in genetic disorders and in malignant tumours. The mechanisms that increase mutations at CpG sites include spontaneous deamination of 5‐methylcytosine and preferential interaction of such sequences with physical or chemical carcinogens. As a consequence of enhanced mutagenesis at methylated CpGs, the CpG frequency in mammalian genomes has been strongly depleted over evolutionary time."

Key Concepts

  • Methylated CpG sequences are preferentially mutated.
  • Deamination of 5‐methylcytosine leads to transition mutations at CpGs.
  • Exogenous carcinogens target methylated CpGs.
  • CpG mutations are frequent in genetic diseases and cancer.
  • DNA repair may be affected by methylation of CpG sequences.

My comment: Deamination of 5-methylcytosine is often caused by oxidative stress (keywords: deamination oxidative stress). Oxidative stress is typically result of weak nutrition (or overnutrition), lack of exercise, mental stress, bad life habits (alcohol consumption or smoking) etc.

This is why DNA sequences (also called genes) are driven by lifestyle. Any change in organisms is based on epigenetic regulation of existing biological information or gradual but inevitable corruption of information. That's why there's no mechanism for evolution. Don't get lost.


The DNA gene is dead

More reasons why DNA doesn't determine traits


  • Now it's clear that a single length of DNA can be transcribed in multiple ways to produce many different RNAs, some coding for proteins and others constituting regulatory RNAs.
  • By starting and stopping in different places, the transcription machinery can generate a regulatory RNA from a length of DNA that overlaps a protein-coding gene.
  • The same sequences are being used for multiple functions. That introduces complications into the evolution of the genome, which had until recently been assumed to act through single DNA mutations affecting single genes.
  • Moreover, the code for another regulatory RNA might run in the opposite direction on the facing strand of DNA.
  • More fundamentally, it muddies scientists' conception of just what constitutes a gene. In the established definition, a gene is a discrete region of DNA that produces a single, identifiable protein in a cell. But the functioning of a protein often depends on a host of RNAs that control its activity. If a stretch of DNA known to be a protein-coding gene also produces regulatory RNAs essential for several other genes, is it somehow a part of all those other genes as well?
  • Multiple and overlapping genes can occupy a single strip of DNA that also produces several functional RNAs that don't encode proteins.
  • To make things even messier, the genetic code for a protein can be scattered far and wide around the genome. The ENCODE project revealed that about 90 percent of protein-coding genes possessed previously unknown coding fragments that were located far from the main gene, sometimes on other chromosomes.
  • Offering a radical new conception of the genome, Gingeras proposes shifting the focus away from protein-coding genes. Instead, he suggests that the fundamental units of the genome could be defined as functional RNA transcripts.

My comment: The cell uses the DNA for building different RNA-products. It's likely that the cell is able to choose appropriate strands of the DNA and build essential RNA transcripts for different purposes. Overlapping, embedded  and opposite-directional DNA strands tell us about very complex, designed mechanisms the cell uses for building RNA-products. After realising this complexity and the way the DNA is used, we should also understand that

- The DNA is not your destiny
- Genetic determinism is a serious heresy
- The DNA doesn't dictate traits of organisms
- The DNA has no control over cellular processes
- Mutations never lead to evolution but gradual degradation of the genome
- It's a waste of money to buy a DNA test. Those tests tell you about genetic markers left by epigenetic mechanisms and genetic errors. (http://www.els.net/WileyCDA/ElsArticle/refId-a0006159.html)


The theory of evolution is full of chicken-egg dilemmas

The most inconvenient chicken-egg dilemmas of the theory of evolution

Evolutionists' belief in their theory is so strong that they are blind to see the impossibility of their theory. Here's the most serious chicken-egg dilemmas.

RNA Pol-ii
1. RNA polymerase is an enzyme that is a complex molecular machine and is intended to synthesize RNA from either DNA or RNA. The RNA polymerase is composed of a number of complex proteins. But proteins can't be produced without the RNA polymerase. Where did it come from?

2. DNA repair mechanisms need several complex enzymes. If life originated in the primordial soup, the sun's UV rays, background radiation, etc. would have destroyed the first assumed DNA molecules just in hours without a functioning repair mechanism. Just DNA is not enough to build proteins because the cell also needs epigenetic information structures for protein production and thousands of other fully functional mechanisms and machines. Where did the DNA repair mechanisms come from?

3. A unicellular organism can not evolve into multi-cellularity because the necessary information needed for cell differentiation is given from parents to offspring. For example, a growing flatworm C Elegans (1031 cells) needs accurate information for its cellular differentiation and specialization.  It gets that information only from its predecessor by using non coding RNA molecules (lncRNAs and miRNAs). Where did the predecessor come from?

4. Bacterial life span varies from a few minutes to a maximum of weeks (bacteria are able to stay in a dormancy even for years but then they have stopped all functionality). They have to be replicated so that the population survives and continues to exist. How did the first assumed bacterium develop a super complex replication machinery just in a few hours or weeks?

5. An RNA thermometer is a temperature-sensitive non-coding RNA molecule which transmits information from outside world for the cell and helps it regulate gene expression. RNA-thermometers are widely used by bacteria and plants. It is coded from DNA by RNA-polymerase and modified by several complex mechanisms. The RNA thermometer is read by cellular reading machineries. Which evolved first, the sensor, the signal routing mechanism or the reading mechanism? There are hundreds of different receptors in living organisms responding to nutrients, climate, stressors, light, chemicals etc.

There are no observed answers to these chicken-egg problems. But they are very important issues and people should demand evolutionary biologists to give relevant answers (based on scientific evidence) for these problems.


Astronaut experiences rapid genetic alterations after epigenetic adaptation - Genetic degradation

Astronaut experiences rapid genetic alterations after epigenetic adaptation - Genetic degradation


Excerpt: "Scott and Mark Kelly are identical twin brothers — at least, they were until Scott spent a year living in space.

When Scott Kelly returned to Earth after a 340-day voyage aboard the International Space Station (ISS) two years ago, he was 2 inches taller than he'd been when he left. His body mass had decreased, his gut bacteria were completely different, and — according to preliminary findings from NASA researchers — his genetic code had changed significantly. (Interestingly, Scott Kelly has since shrunk back down to his initial prespaceflight height.)

A new NASA statement suggests the physical and mental stresses of Scott Kelly's year in orbit may have activated hundreds of "space genes" that altered the astronaut's immune system, bone formation, eyesight and other bodily processes. While most of these genetic changes reverted to normal following Scott Kelly's return to Earth, about 7 percent of the astronaut's genetic code remained alteredand it may stay that way permanently.

The changes are "thought to be from the stresses of space travel, which can cause changes in a cell’s biological pathways," the NASA statement said. "Such actions can trigger the assembly of new molecules, like a fat or protein, cellular degradation, and can turn genes on and off, which change cellular function."

Two Brothers

Scott spent nearly a year aboard the ISS as part of a unique NASA project called the Twins Study, which aims to reveal the long-term effects of space travel on the human body and mind. In March 2015, he flew up to the ISS to begin what would become the single longest space mission any astronaut has ever accomplished. Most astronauts stay aboard the ISS for six months at a time. Scott Kelly stayed in orbit for 340 days.

Meanwhile, Scott Kelly's identical twin brother, Mark (a retired astronaut, himself), remained on Earth as a control subject. The Kelly brothers are the only twin astronauts in history, NASA said. Because identical twins are born with identical DNA — the genetic code that tells cells when and how to work — the Kellys made ideal subjects for before-and-after comparison.

Researchers tested both Kelly brothers before, during and after Scott's year in space to map specific changes in the astronauts' physical and mental health. Most of Scott's physical changes — including his 2-inch height gain — proved to be temporary responses to the low-gravity, low-oxygen environment of space, NASA said.

However, genes involved in bone formation, oxygen deprivation, immune system responses and DNA repair remained transformed after Scott Kelly's return to Earth, NASA reported. The reason behind this could involve a complicated reaction to an unusual type of stress: the stress of space.

"Oftentimes, when the body encounters something foreign, an immune response is activated," Christopher Mason, a Twins Study researcher and an associate professor at Weill Cornell Medical College, told Business Insider. "The body thinks there’s a reason to defend itself. We know there are aspects of being in space that are not a pleasant experience, and this is the molecular manifestation of the body responding to that stress."

Understanding why and how these "space genes" activate will be crucial to planning longer manned space missions. The way NASA sees it, Scott Kelly's year in space is a significant "stepping stone to a three-year mission to Mars."

More than 200 researchers in 30 states are helping to analyze the Kelly brothers' various test results, looking for space-induced changes in Scott Kelly's cognition, metabolism, microbiome and many other physiological processes. NASA will publish the comprehensive findings of these tests in a single study later this year."

My comment: Life is not driven by gene sequences. Genes are driven by lifestyle. Scott Kelly experienced epigenetic alterations due to loss of gravity, stress factors, low contribution to bacterial environment etc. Modification on his epigenome triggered genetic alterations. Not 7% but a few hundreds of SNP and CNV mutations. After he came back to the Earth, his epigenome recovered but genetic alterations didn't. This is how organisms experience changes in nature. Environmental factors, such as diet type, stressors, climate, sensory stimuli, toxicants etc. contribute to organisms' epigenome through several types of receptors and RNA-mediated signaling mechanisms.

About 7 % of Scott Kelly's DNA expression profiles remained altered. Seems that he didn't evolve. Seems that there were no stable phenotypic alterations.

Any change in organisms is based on epigenetic regulation of existing biological information OR gradual but inevitable disappearance of information. That's why there's no mechanism for evolution.


Reasons why DNA doesn't determine traits

Multiple different information layers in the cell respond to environmental signals

1.  DNA sections (sequences) are never used directly by cellular mechanisms. Parts of the DNA are always read into a template RNA strand (transcription) before further processing. The template RNA is then modified by several complex mechanisms, such as alternative splicing machinery. The mature RNA-product is regulated by several epigenetic factors and mechanisms before final protein production. 

2. DNA genes need to be told at what level they are activated or silenced. This is regulated by several mechanisms and factors, such as chromatin structure and folding (3D genome). Histone epigenetic markers affect strongly the folding and shape of chromatin. Chromatin structure is organized by complex motor protein called condensin. It is able to form loops so that certain parts of the DNA can be in flanking state regulating the activity of transcription

3. Histone code is a biological database. Histones are structural proteins of chromosomes. Histones pack and order DNA into structures known as nucleosomes so that it fits within a cell’s nucleus. Each nucleosome contains two subunits, both made of histones H2A, H2B, H3 and H4 – known as core histones – with the linker histone H1 acting as a stabilizer. Many chemical modifications can be found in the tails of the histones. These include, but are not limited to acetylation, mono-, di-, or tri-methylation and ubiquitination, and can occur in different amino acids in the tails of the different histones.  
Any real histone code has the potential to be massively complex; each of the four standard histones can be simultaneously modified at multiple different sites with multiple different modifications. To give an idea of this complexity, histone H3 contains nineteen lysines known to be methylated—each can be un-, mono-, di- or tri-methylated. If modifications are independent, this allows a potential 419 or 280 billion different lysine methylation patterns, far more than the maximum number of histones in a human genome (6.4 Gb / ~150 bp = ~44 million histones if they are very tightly packed). And this does not include lysine acetylation (known for H3 at nine residues), arginine methylation (known for H3 at three residues) or threonine/serine/tyrosine phosphorylation (known for H3 at eight residues), not to mention modifications of other histones. (https://en.wikipedia.org/wiki/Histone_code)

Histone markers are regulated and maintained by long non coding RNA-molecules that have a crucial role in development of embryonic cells. Histone markers affect strongly traits of organisms. For example skull morphogenesis is regulated by histone deacetylases. Fur, coat and pigment colors are also regulated by histone markers. And thousands of other traits...

4. DNA methylation is involved in the regulation of several cellular processes such as chromatin stability, imprinting, X chromosome inactivation and carcinogenesis. It strongly affects alternative splicing and RNA polymerases. Methylation stabilizes the genome and disrupted or aberrant methylation patterns are often the reason for genetic errors.

5. Non coding RNA molecules are transcribed from the DNA by very complex mechanisms called RNA polymerases I and II. They are not direct copies of the DNA because of complex modifications. Their job is to transmit epigenetic markers (over 140 different types) for the DNA, histones and other RNA:s. In this way cells are able to get information from surrounding environment. RNA-molecules are often packed into transporters called extracellular vesicles.

6. Transcription factors are proteins produced by previous mechanisms 1.-5.

The cellular information can be categorized as follows:

A. DNA - 
a passive digital information layer, a library for production of RNAs.
B. DNA methylation - analog information layer, meta-data
C. Chromatin structure and folding - analog information

D. Histone markers - a digital database  CONVERTED to chromatin folding (A/D converter)
E. Epigenetic markers of RNA - both digital, analog and meta-data
F. Transcription factors - meta-data

All living organisms receive signals from surrounding environment. This means diet types, climate, stress factors, sensory stimuli, toxicants etc. Any change in organisms is due to epigenetic regulation of existing biological information or gradual but inevitable disappearance of information. That's why there's no mechanism for evolution. Don't get lost.