For nearly six decades now biologists have been promoting the idea that a chemical molecule, DNA, encodes biological program. There is sufficient evidence to show this perception is wrong. Listed below are a few important questions on this issue. If anybody would like to answer the question(s), please give the response indicating the serial order of the question. Comments are subject to moderation, if necessary.
I particularly call upon Pharyngula blogger P.Z. Myers, Associate Professor, University of Minnesota Morrris, to respond to the challenge posted here. He countered in a derogatory manner my articles published elsewhere in his two posts at Pharyngula dated March 29, 2010 and December 13, 2010. Going by his posts against my articles, he appears to claim excellent knowledge of molecular gene – the only person in the world who can tell what it is! Could you please tell the world how you define molecular gene?
I also specially invite The Secular Outpost blogger Taner Edis (The Secular Outpost Dec. 11, 2010) and Improbable Research blogger Marc Abrahams (Improbable Research Dec. 14, 2010) to respond to the challenge. They are also very much annoyed by my questioning the concept of molecular gene in the light of Quranic revelations.
The world does not expect the scientific community and science media to go against belief systems without scientifically examining the veracity of Scriptural revelations. Taking recourse to such unscientific method will only help diminish the trust of the public in scientific community. The scientific community and science media are creating a furor against God and religion without any scientific basis. Now here is the golden opportunity for you to prove what you say is correct. If there is a grain of truth and honesty in what you say, take up this challenge. The challenge is as follows.
The Quranic revelations of nonmaterial basis of life challenge the molecular gene and genome (see post 4 at http://quranscienceblog.blogspot.com). These revelations are falsifiable and hence scientific community cannot mislead the world by saying these are unscientific assertions. These revelations imply that it is impossible to create life from non-life chemically without involving a living cell or organism at any stage of the experiment. The revelations also declare that it will not be possible to restore life to a dead cell (or organism) through pure chemical means. That is the challenge.
A lot of work is now going on in many universities and institutes to chemically synthesize life. All these attempts have so far failed; in future also the result will not be different. That is what the Scriptural revelations predict.
Secondly I have posed several questions against the molecular gene. If it is possible to provide satisfactory answers, please do that.
The Quranic challenge can provide answer to the biggest question ever – is there God or not? If scientists succeed in creating life by chemical synthesis without using a living cell during the experiment or in bringing a dead cell back to life by chemical means, that will be the end of God. Until then, God exists. Insofar as the Quranic challenge is falsifiable, the argument of no God has no meaning in the true scientific tradition until it is proved wrong. A falsifiable statement is a scientific theory. Unless and until scientists create life without the help of living cell, the molecular gene theory stands unproven. Most importantly it proves God exists. The existence of God can be questioned by scientists only if they succeed in creating life from non-life thereby falsifying the Quranic revelation. Until then, scientific community’s shout against God is meaningless and unfounded.
Questions against the molecular gene concept are givne below.
1. Molecular gene (genome) – violation of chemical fundamentals
DNA (genome) is a chemical molecule. Its structure encodes chemical information which is deciphered in terms of its physical and chemical properties. Biologists say in addition to that its structure also encodes genetic program (biological information). Thus the genome is treated as constituting the genetic program responsible for the heritable characteristics and biological functioning of organism. An organism is thus reduced to mere bundle of molecules like any other chemical substance.
Even if superimposition of biological information over chemical information (constituted by the chemical structure) is taken for granted, it should conform to the well-established chemical fundamentals. By this canon biological information encoded by the genome should be specific to the structure. But in reality, the genome defies this chemical principle in several ways.
a) Changes in the phenotype of an individual during ontogenetic development and post-developmental stage reflect change of biological information content of the genome (originally carried in the zygote) with time. A genome even creates two or more phenotypically different biosystems (e.g., larva and butterfly) in several species (Figure 1).
How can a chemical molecule (i.e., genome in the zygote) encode information that changes with time?
If DNA encodes biological program, its constituent elements C, H, N, O and P should also encode genetic information at some preliminary level. This means other compounds of these elements in some combination should also exhibit signs of life. But why does this not happen? Is it not strange that there is only one molecule (DNA) in the whole universe that can encode genetic information?
If C, H, N, O and P do not encode genetic information, how does their combination acquire that information and where does the information come from?
b) DNA is supposed to encode only information required for protein synthesis. Accordingly, protein-coding DNA is recognized as ‘the gene’. Protein synthesis is not the whole story of “life”. An organism requires information for the synthesis of numerous other substances during its life, development of body structures and their functions, behaviour, instincts, etc. The members of Homo sapiens also have intelligence, consciousness, feelings and freewill.
How can DNA encode genetic information required for instincts, feelings, consciousness, likes and dislikes, etc.? Do biologists think protein is the sole basis of life?
c) It has been observed that an overwhelming 95% of DNA consists of non-coding DNA in eukaryotes and about 5% is constituted by the coding-DNA (or the genes). The non-coding DNA (ncDNA) is referred to as “junk DNA”. Though structurally comparable to coding DNA, surprisingly, the so-called junk DNA does not encode identical biological information (or vice versa).
How can this be explained based on chemistry?
d) It is believed that mitosis produces daughter cells with identical genome.
If the genomes of the cells in a body are identical, all the cells should carry identical information. But we find the tissues are structurally and functionally different. How can the tissues with identical genome (biological information) exhibit variable anatomy and function?
e) Recently, it has been shown that the genomes of different tissues are not identical [1]. This discovery sprang from an investigation into the underlying genetic causes of abdominal aortic aneurysms (AAA). The researchers found major genetic differences between blood cells and tissue cells of the same individuals. The finding calls into question one of the most basic assumptions of human genetics that DNA in every cell in the body is identical to every other cell. Apart from that, “This discovery may undercut the rationale behind numerous large-scale genetic studies conducted over the last 15 years, studies which were supposed to isolate the causes of scores of human diseases. Except for cancer, samples of diseased tissue are difficult or even impossible to take from living patients. Thus, the vast majority of genetic samples used in large-scale studies come in the form of blood. However, if it turns out that blood and tissue cells do not match genetically, these ambitious and expensive genome-wide association studies may prove to have been essentially flawed from the outset.” [2].
How is it possible for the genome of a parent cell (e.g., zygote) to create different genomes in the daughter cells? Is it not a clear proof that the genome does not constitute the biological program? Is this not enough to prove genetic information of the organism exists independently of the genome structure and it is according to that, cell structures including genome are produced? If genome is not identical in different tissues, how is it possible to determine the genome of the individual? Similarly when the genomes of male and female or different castes (polymorphs) are different, how is it possible to determine the genome of the species?
f) Studies at the molecular level fail to demonstrate the expected correspondence between genome and phenotype. The most spectacular example of this is the morphological dissimilarity between human being and chimpanzee despite a 98.7% similarity in their DNA [3]. Although evolutionary biologists speak of genomes of chimp and man as being almost identical to support of their argument of human evolution from an animal, and for establishing chimpanzee as the closest animal ancestor of human being, they have not enumerated so far the identical phenotypic characters in human and chimp in terms of anatomy, physiology, development and other biological features. In fact there is none! A chimp is not even 0.1% human being or a human being 0.1% chimp. A human being differs from chimp in every aspect and at every point of the body. The only similarity between chimp and man is in the DNA! The differences in traits, characteristic behaviour, instincts and capabilities between human (Homo sapiens) and chimpanzee (Pan sp.) are far greater than the small degree of sequence divergence (1.3%) could account for (Figure 2).
The chimp-human comparison is a case of similar genomes but dissimilar phenotypes. The reverse case is also known. Caenorhabditis elegans and C. briggsae are physically very similar organisms. It takes an expert to distinguish them. The two have near-identical biology, even down to the minutiae of developmental processes. Surprisingly, however, their genomes are not so similar. C. elegans has more than 700 chemoreceptor genes when C. briggsae gets on by just 430. There are also many genes unique to each of them [4]. Another anomaly is the lack of correspondence in the number of genes (taking for granted the meaninglessness of gene identification) with complexity of the organism. For example, fruit flies have fewer coding genes than roundworms, and rice plants have more than humans [5].
Are these not departures from the expected genome configuration (i.e., genetic information)-phenotype relationship? Secondly gene counts are also widely published in the journals. If the gene is not definable, how can it be counted? If single genes do not determine the phenotypic characters, what meaning is there in gene counts?
g) Many insects exhibit alternative morphologies (polyphenisms) based on differential gene expression rather than genetic polymorphism (differences in genes themselves). One of the best understood insect polyphenisms is the queen-worker dimorphism in honey bees. Both the queens and the workers are females but morphologically distinct forms. Besides, the queen is fertile whereas the worker is sterile. Studies conducted with the bee species Apis mellifera revealed that numerous genes appeared to be differentially expressed between the two castes [6]. The seven differentially expressed loci observed in the study belonged to at least five distinctly different functional groups. The queen and the worker castes in honey bee provide an unfailing proof of natural existence of similar genomes exhibiting dissimilar phenotypes.
How is it possible for similar genes (chemical structures supposed to be encoding similar information) to express differently?
h) “Pseudogenes are similar in sequence to normal genes, but they usually contain obvious disablements such as frameshifts or stop codons in the middle of coding domains. This prevents them from producing a functional product or having a detectable effect on the organism’s phenotype…. The boundary between living and dead genes is often not sharp. A pseudogene in one individual can be functional in a different isolate of the same species… and so technically is a gene only in one strain…. there are other pseudogenes that have entire coding regions without obvious disablements but do not appear to be expressed.” [7].
How can a chemical structure function as gene in one strain and fail to function similarly in another strain? Can it be explained chemically?
i) The variation observed in the use of triplet codes among organisms is another issue. Like the pseudogene this aspect is against chemical fundamentals and remains unexplained. The degenerate nature of the biological code implies several triplets coding per amino acid. Further, two amino acids have only one mRNA codon each; AUG for methionine and UGG for tryptophan. Hence 59 degenerate triplets code 18 amino acids; these 18 have two to six synonymous codons each. Choices between synonymous codons are not random; some codons in the set specific to an amino acid are used more than the others [8]. The ‘genome hypothesis’ which tries to explain the variation in codon use states that codon use is species-specific, i.e., each genome or type of genome shows a particular pattern of choices between synonymous codons. Thus overall codon usage differs between taxa; but codon bias is also influenced by other factors like gene length, gene expressivity (the amount of protein made per gene), environment and lifestyle of the organism [9]. The codon bias gives rise to the paradox whether protein evolution determined DNA sequence or DNA commanded protein evolution. Many such dilemmas remain in molecular evolution. The origin of bias in codon and anticodon frequencies continues to elude researchers [8].
Are these not departures from chemical principles? How can these be explained?
j) There are many kinds of DNA repairs. Rosenfeld gives a detailed account of the self-healing strategies of the ‘master molecule’. If a base is put in wrong place during replication, there are enzymes to correct the mistake. Purines, without any errors and without any damages drop out by the thousands every day presumably due to wear and tear of existence in the chromosomes only to be promptly replaced by insertases. A base can spontaneously undergo change. A cytosine, for example, will lose an amino group and become uracil. Uracil is perfectly at home in RNA but not in DNA. The enzymes called uracil glycosylases recognize the uracil, remove it and replace it with a new cytosine. Suppose that an error has occurred in one of the DNA strands say, a T has been put across from a G, where a C really belongs. This would give rise to two strands one with a G and the other with a T. The enzymatic apparatus ‘knows’ that cannot be correct, but how does it know whether to replace the C with a T on one strand, or the C with an A on the other? If the replacement takes place not on the right strand, the result would be either death of the cell or a mutation. How does it know which is the authentic original? [10].
How can a chemical structure (DNA) be aware of the change in its elemental composition and arrangement? How can it detect the ‘wrong’ one and ‘correct’ it with the genetic information encoded by it?
2. Phenomena of life and death remain unexplained in biology
a) Although biology is science of life and DNA is hailed as the blue print of life, biologists have not yet been able to define either the gene or “life”! The reason is very clear – DNA does not encode biological program.
If biologists cannot define molecular gene or “life”, what justification is there to still think that material gene is the driving force of life?
b) Another important fact that goes against the material gene is both dead body and its living counterpart are materially identical (including genome) but yet the dead body does not show any sign of life. Even if the genome undergoes certain changes at death, repair of those mutations should bring the dead cell or dead body back to life. A fundamental feature of chemical molecule is that it cannot lose its properties assigned by its structure. The genome appears to be an exception to this rule also. Going by the present concept of particulate genetic program, a cell carrying the genome should invariably show life properties. However a dead cell with its genome remaining intact fails to exhibit “life” clearly indicating the genome does not encode the biological program. When I put this question to Nature (Scitable), I received the least expected silly answer from its expert, which is no answer to my question at all. The Scitable answer [11] is reproduced below:
“Questions like yours about life and death spurred the earliest scientific inquiry and keep the field moving forward. It is possible for the genome to be intact in dead cells. For example, think about your local library: at night, nothing is going on and none of the books can be checked out, but all the books would still be there. Similarly, the genetic code is still present in dead cells; however, the absence of certain key biochemical processes, such as transcription and translation, makes reading the code (like checking books out from a library) impossible. Death can be understood at two levels: at the level of the organism and at the level of the cell. In the first case, death arrests all key biochemical processes. No key enzymes are available to translate mRNA and no amino acids are linked to create polypeptide chains. But in the second case death can also help other cells in the same body. This process is called programmed cell death (or apoptosis) and involves a series of biochemical events leading to changes in cell shape followed by cell death. These changes in cell shape include blebbing, which occurs when a portion of the cytoskeleton separates from the plasma membrane and creates an irregular bulge called a bleb. This is like the locking of a door — a change in cell structure arresting cell activity. The cell membrane also loses symmetry and detaches from the cytoskeleton, which leads to cell shrinkage, nuclear fragmentation, chromatin condensation, chromosomal DNA fragmentation, and the eventual damaging of the cell’s genome. All these processes make it harder for the cell’s transcription machinery to read the genetic code, just as locked doors make it difficult for us to check out books from the library at night. A second type of cell death can actually damage neighboring cells, like a fire in the library that spreads to the bookstore across the street. This type of cell death is called necrosis and results from acute cellular injury or infection. Cells undergoing necrosis eventually burst and release their cellular contents, which can damage neighboring cells and induce inflammation. You’re right: the genetic code is essential for all life. But key proteins required to read the genetic code stop working in dead cells. Despite the great wealth of information contained within the genetic code, a genome alone doesn’t lead to the creation of proteins that serve as the basis of life.”
Clearly there is no answer to the natural irreversible cessation of all biological activity (death) at some point of time during the life of an organism with all its material contents including genome intact. Since biologists believe an organism is nothing more than a chemical substance and every atom of the material is present in the dead body as it were before death, how is it possible to explain the cessation of biological activity of the organism (i.e., death) based on molecular gene concept. The phenomenon of death remains unexplained in biology even today. Further, the body starts decaying immediately after death. What makes the body resistant to microbial decomposition prior to death or susceptible to decay after death when the body has not undergone any change in its material constituents is also equally unexplainable. Clearly no chemical structure(s) in the cell encodes or constitutes the genetic program but the program exists independently of any chemical structure as stored information as in computer.
Can biologists offer valid scientific explanation for this anomaly to defend their assumption that DNA encodes biological program? To put it differently, how can a cell or body exist in two mutually exclusive (live and dead) states with no change in their material constituents?
3. The molecular gene remains undefinable
a) Although molecular biologists freely use the term “gene” and claim identification of genes for various characters and diseases, the “gene” remains unknown to them even today. According to geneticist Peter Portin, “The gene is no longer a fixed point on the chromosome, producing a single messenger RNA. Rather, most eukaryotic genes consist of split DNA sequences, often producing more than one mRNA by means of complex promoters and/or alternative splicing. Furthermore, DNA sequences are movable in certain respects, and proteins produced by a single gene are processed into their constituent parts. Moreover, in certain cases the primary transcript is edited before translation, using information from different genetic units and thereby demolishing the one-to-one correspondence between gene and messenger RNA. Finally, the occurrence of nested genes invalidates the simpler and earlier idea of the linear arrangement of genes in the linkage group, and gene assembly similarly confutes the idea of a simple one-to-one correspondence between the gene as the unit of transmission and of genetic function....” [12]. Other leading scientists like Thomas Fogle and Michel Morange also concede that there is no longer a precise definition of what could count as a gene [13, 14]. The objective of genomic research is to ultimately understand the relationships between heritable units and their phenotypes. But it appears that genome concept would not deliver that information. The genome organization is extremely complex. Genes reside within one another, share some of their DNA sequences, are transcribed and spliced in complex patterns, and can overlap in function with other genes of the same sequence families. “Today, in the era of genomic sequencing and intense effort to identify sites of expression, the declared goal is to search for genes, entities assumed to have physical integrity. Ironically, the sharper resolving power of modern investigative tools make less clear what, exactly, is meant by a molecular gene, and therefore, how this goal will be realized and what it will mean”, observes Fogle [13]. These findings clearly expose the meaninglessness of the concept of molecular gene (genome).
When the “gene” remains unknown to biologists, what justification is there in using the molecular gene concept to explain biological attributes and functions?
b) Horace Freeland Judson writing in Nature notes: “The phrases current in genetics that most plainly do violence to understanding begin “the gene for”: the gene for breast cancer, the gene for hypercholesterolaemia, the gene for schizophrenia, the gene for homosexuality, and so on. We know of course that there are no single genes for such things.” [15]. Yet we find even now in every biology journal the term “gene” is used in general sense as well as to indicate specific characters.
Although biologists find there is no single gene responsible for an attribute or disease and the journal editors accept it, the same people continue to publish the term “the gene for” even now. If there is no single gene for a character, why papers suggesting “the gene for” continue to be accepted for publication? Will the use of the term “the gene for” not corrupt science and mislead the people?
The findings in molecular biology given above not only invalidate the molecular gene (genome) but also prove Wilhelm Johannsen’s warnings against material gene (i.e., the gene should not be treated as material, and there is no single gene for each character) correct. Despite this, biologists ignore Johannsen’s non-physical gene and continue to stick to the molecular gene concept. Even after sixty years of worldwide research in molecular gene and genomics, the field of genetics remains as it was fifty years ago. What we have today in the name of molecular biology et al. is unscientific least worthwhile biological information. What justification is there in not rejecting the physical gene?
References
1. Gottlieb et al., “BAK1 gene variation and abdominal aortic aneurysms”, Human Mutation Vol. 30, 2009, pp. 1043. DOI: 10.1002/humu.21046.
2. DNA not the same in every cell of body: Major genetic differences between blood and tissue cells revealed,” ScienceDaily (July 16, 2009).
3. Wells, J. Homology in Biology: A Problem for Naturalistic Science. By Jonathan http://www.trueorigin.org/homology.asp Retrieved 24 November 2001.
4. M. Blaxter, M. 2003. Two worms are better than one. Nature 426:395-396.
5. W.W. Gibbs, W.W. 2003. The unseen genome: Gems among the junk. Scientific American 289, November 2003, pp. 46-53.
6. Evans, J.D. and Wheeler, D.E. 1999. Differential gene expression between developing queens and workers in the honeybee, Apis mellifera. Proc. Natl. Acad. Sci. USA. 96:5575-5580.
7. Snyder, M. and Gerstein, M. 2003. Genomics: Defining genes in the genomics era. Science 300:258- 260.
8. Grantham, R.L. Codon usage in molecular evolution. doi: 10.1038/npg.els.0001806.
9. Grantham, R. et al., 1981. Codon catalog usage is a genome strategy modulated for gene expressivity. Nucleic Acids Res. 9:43-47.
10. Rosenfeld, A. 1981. Master molecule heal thyself. Mosaic 12(1).
12. Portin, P. 1993. The concept of the gene: Short history and present status. The Quarterly Review of Biology 68:173-223.
13. Fogle, T. 2000. The dissolution of protein coding genes in molecular biology. In Peter Beurton, Raphael Falk, and Hans-Jörg Rheinberger, The Concept of the Gene in Development and Evolution. Historical and Epistemological Perspectives, Cambridge University Press, Cambridge, pp. 3-25.
14. Morange, M. 2000. The developmental gene concept: History and limits. In Peter Beurton, Raphael Falk, and Hans-Jörg Rheinberger (eds.), The Concept of the Gene in Development and Evolution. Historical and Epistemological Perspectives, Cambridge University Press, Cambridge, pp.193-215.
15. H. F. Judson, H.F. 2001. Talking about the genome. Nature 409:769.
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