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

https://www.algemeiner.com/2016/08/10/its-easy-to-be-an-atheist-if-you-ignore-science/

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

https://phys.org/news/2018-03-genes-dont-biologists.html

Summary:

- 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

http://epigenie.com/long-non-coding-rna-superhero-guardin-genome-dna-damage/

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.

https://www.ncbi.nlm.nih.gov/pubmed/29593331

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

http://www.biology-pages.info/R/RNA_Editing.html

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).

https://www.genome.gov/19016904/faq-about-genetic-and-genomic-science/

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.

https://www.nature.com/news/2009/090827/full/news.2009.864.html

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:

https://www.nature.com/news/past-5-000-years-prolific-for-changes-to-human-genome-1.11912#/b3

"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.

http://www.hgmd.cf.ac.uk/ac/index.php

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

http://news.mit.edu/2016/linking-rna-structure-and-function-cell-fate-0908

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.