Genetic Boundaries (Research Article)

This article will be a bit of a change of pace from what has been previously covered.  Up to now, the focus has been entirely on the created kind and the Linnaean species. However, in order to understand the deeper difference between a kind and a species, a surface knowledge of genetics and inheritance is required.   This article will introduce the concepts of DNA, RNA, and the genetics of inheritance. Because much of this article is fairly well-established science, there will likely be fewer citations in this articles than in previous articles.  However, this article is very important because it will be foundational to understanding much of the rest of the series.

Discovering DNA Structure

The story of the DNA molecule is one of the most well known in the scientific community. Most high school science students can tell you that James Watson and Francis Crick are the men responsible for discovering the structure of DNA. Contrary to popular understanding, however, Watson and Crick did not discover DNA.  That honor goes to the Swiss chemist Johann Miescher.  Miescher recognized the significance of what he discovered but did not pursue the discovery very far. It was the only 1869 and the technology simply did not exist to pursue what Miescher called “nuclein”[1]. In fact, the name “DNA” (deoxyribonucleic acid) was not coined until the 1880s when the five key nucleotides of DNA and RNA were isolated by Albrecht Kossel, who won a Nobel Prize for his work[2].  Kossel has been largely overlooked in the outpouring of accolades for Watson and Crick.  However, without his work, the DNA structure could never have been discovered.

It took science some time to recognize the significance of Kossel’s discovery. Most scientists were convinced that proteins were the molecule of heredity. However, some scientists were still interested in the structure of DNA. This problem began to receive more attention after the end of WWII which is when James Watson and Francis Crick became involved in the work. Watson and Crick were something of an odd pair. Neither was well regarded in the scientific community, and Crick was a physicist rather than a biologist who did not have his doctorate yet when he started working on DNA. Other, much more prestigious scientists were working on the DNA problem as well, including luminaries such as Erwin Chargaff, Linus Pauling, and Rosalind Franklin.  It was Chargaff, for example, who discovered that equal numbers of the bonding nucleotides were present in each DNA strand, though he did not grasp the bonding pattern that exists in the strand[3]. Yet it was the two misfits, who were something of a laughingstock in their field, who would discover the structure of DNA.

In April 1953, Watson and Crick published a single page paper in Nature outlining the DNA double helix structure they had discovered.  They proposed that the four nucleotides in DNA bonded in a certain pattern (discussed below) which explained the one to one correlation discovered by Chargaff[4].  Watson and Crick also recognized that the DNA double helix they described lent itself well to a copying mechanism and said so in their paper.  While their model was published nearly seventy years ago, and science has progressed massively since then, the model has held up with very minor tweaks and expansions. Watson, Crick, and Maurice Wilkins were awarded a Nobel Prize for their work on DNA. Despite her significant contributions, for which Watson and Crick acknowledged her in their paper, Rosalind Franklin was snubbed for a Nobel Prize, perhaps because she has passed away by the time it was awarded.


The DNA double helix structure is perhaps one of the most iconic images in science. With computer-generated imagery, it has become easy to demonstrate this structure to the scientific layman. However, DNA is an incredibly complex molecule that contains the information necessary for life.

In an ultimate sense, DNA is a code containing information.  This information must be extracted from the code in order to be used. However, before getting into that process, we need to examine what DNA actually is.

Deoxyribonucleic acid is a molecule made of three parts. The first part is the deoxyribose sugar molecule. Deoxyribose is a part of the backbone of the double helix. Deoxyribose is made by removing a single oxygen atom from a D-ribose[5] sugar molecule, producing a molecule with the molecular formula C5H10O4.  The ribose sugar loses one of its oxygen molecules by reacting with an enzyme called ribonucleotide reductase to create the deoxyribose sugar[6].  The deoxyribose sugar is incredibly important because it is the support for the nucleotides, that provide the scaffolding of the DNA strand and codes for the information in DNA.

However, the deoxyribose sugar is only half of the backbone required to build a strand of DNA. A second required piece is a phosphate group. The phosphate group consists of a phosphate molecule, and four oxygens, two of which bond to deoxyribose sugars, effectively replacing the oxygen in those sugars.  The phosphate group functions as a link between the deoxyribose sugars. In essence, it is the joiner molecule, that holds the DNA strand together.

The final piece of the DNA scaffold, the internal connecting links consists of nitrogenous bases. Nitrogenous bases come in two forms: pyrimidines and purines. There are three pyrimidines and two purines. Two of each are found in DNA and the third pyrimidine is a replacement for another pyrimidine in RNA. Purines will only bond with pyrimidines and vice versa. However, it gets more specific than that. Guanine, one of the purines, will only bond to the pyrimidine Cytosine and vice versa.  Thymine, a pyrimidine, will only bond to purine Adenine. Adenine is the one nitrogenous base that can bond to more than one partner, though not simultaneously. Besides thymine, it will also bond to Uracil, which is the pyrimidine found in RNA.  The assemblage of bonded nitrogenous bases founded on deoxyribose sugars and linked by phosphate groups provides the structure of the DNA double helix[7].

However, having a DNA strand is not nearly enough for heredity.  The strand must carry information on it. It does this using a remarkable three letter code sequence called codons, also discovered by Watson and Crick[8]. The human body requires twenty amino acids, the basic building blocks of proteins, to survive.  Conveniently, the code in DNA can provide the information for all of them. By combining the nitrogenous bases in particular arrangements, DNA enables the body to create long chains of amino acids that can be molded into proteins. The table below shows the available codons and what amino acids each code for.



































































The above chart illustrates the codons that code for a given amino acid. Note that some of them, such as Glycine (gly) have more than one codon(GGU, GGC, GGA, GGG) that carries the information to make it.  Others, such as Methionine,(met) have just one (AUG). Note also that the pyrimidine Thymine does not appear in the codon dictionary. In its place is the pyrimidine Uracil. This is because I have chosen to translate the codons that directly code for amino acids, which are found on RNA. RNA uses Uracil in place of thymine.  Notice also that three codons are labeled “STOP”.  These codons function as roadblocks in the code, indicating the end of a particular amino acid chain.  Interestingly, the Methionine codon (AUG) also serves as the “START” codon[9] [10]for eukaryotes[11].

The interesting thing about the DNA code is that the codons on DNA that are transcribed are actually not what codes for the amino acid chain.  They simply code for what is called RNA. RNA (ribonucleic acid) is a mirror image of the DNA strand that produced it, with Uracil substituted for Thymine. There are several types of RNA which we will get into shortly.  RNA is produced by a process called transcription.

In order to start the transcription process, the DNA strand must be unzipped. It must be unzipped in exactly the right place to ensure the correct RNA is created. However, the whole strand is not copied. Only one of the two sets of nucleotides are copied. The copied strand is called the template. This is referred to as asymmetric transcription.  This transcription is catalyzed by a special group of enzymes called RNA polymerases[12]. RNA polymerases unzip the DNA strand by breaking the hydrogen bonds that hold the purines and pyrimidines together. Having broken these bonds, the polymerase causes the DNA strand to unfold by pulling the strand through itself[13]. It then begins to pair RNA nucleotides to the portion of the DNA strand that it needs to copy. During the transcription process, a special type of RNA polymerase runs along the forming RNA strand and proofreads it, correcting mistakes as it finds them[14]. This ensures that the RNA strand produced is accurate to the DNA strand, but the exact mechanism is not understood[15].    These nucleotides bind together and form the RNA strand.


Once the RNA strand forms, it needs to be split from the DNA strand because, in order to create the strand, the RNA nucleotides hydrogen bonded to the DNA nucleotides. It also needs to rezip the DNA strand.  As the RNA polymerase pulls the DNA strand through it, a special enzyme comes behind and rezips the DNA strand shut. As the RNA strand completes, a special sequence is added to the end of the RNA consisting solely of adenine nucleotides.  This process is called polyadenylation[16].

A formed RNA strand can come in many forms, each of which has different functions. The primary type that we think of is messenger RNA (mRNA). Messenger RNA is the type of RNA that will be translated into proteins. Transfer RNA (tRNA) is involved in the translation process as is Ribosomal RNA (rRNA). Other types of RNA include micro RNA (miRNA) long non-coding RNA (lncRNA) and small nucleolar RNA (snoRNA) among others. All of these are created as part of the transcription process.

Once the mRNA strand has formed, it has to leave the nucleus, where the DNA is stored, and go out into the cytoplasm where specialized structures called ribosomes will translate it[17]. The mRNA is directed into the ribosome. As it is pulled through the ribosome, tRNA brings amino acids to the ribosome and matches them with the correct mRNA codon[18].  As they match up, a chain of amino acids begins to form, while the tRNA’s that brought them to the ribosome depart.  When the ribosome reaches one of the STOP codons, it ejects the mRNA strand and the amino acid chain is formed. This chain will be folded into a protein.



Making proteins is an important function of DNA and RNA, but DNA serves another critical function. It carries the information from one generation to the next. DNA is the molecule of heredity.  Because it codes for proteins, which are the building blocks of life, DNA in the gametes passes on the information in the parent to the offspring.  This is the process known as heredity.

Heredity is a complicated process that requires us to understand how DNA is stored. In eukaryotes, DNA is stored coiled in chromosomes. Chromosomes are packages containing at least part of the DNA of an organism. In most eukaryotes, chromosomes come paired, with genes coding for similar information on each of the pairs.  Each discrete, information containing sequences is called a gene for simplicity.  Organisms with two copies of all their genes are referred to as diploid, while those with only a single copy are called haploid. Diploid creatures inherit one set of their chromosomes from each parent. This leads to incredible uniqueness among individuals[19].

For most diploid organisms, the gametes they produce are haploid. This allows the male and female gametes to fuse and combine genetic information in the offspring. However, what information is passed from each parent is completely random. When a parent has two copies of a given gene, there is a fifty-fifty chance that a given one of those genes will be passed on to the offspring.  This is the genesis of heredity, and it was available to Darwin.

Heredity had been a puzzling problem for centuries when a monk named Gregor Mendel began his work on the topic. Mendel was an incredibly well-educated man and an excellent naturalist. He performed his classic work on the common pea plant. It took eight years of breeding, backcrossing, and outbreeding to complete his work, but in 1865 Mendel read his completed paper to the Brunn Natural History Society. The paper was incredibly detailed and groundbreaking. No one had ever attempted to perform a quantitative analysis of heredity before.  Mendel’s results were largely overlooked in his time, not even appearing publicly in English until the 1900s. However, since then, the results of his work have formed the backbone of modern genetics.

Mendelian Genetics

In order to perform his experiment, Mendel spent two whole years breeding thirty-four distinct varieties of peas in order to ensure they bred true[20]. Mendel then selected twenty-two and used them for his experiment. He crossed these true breeding strains to one another then bred the offspring to one another and looked at the resulting plants.

Mendel’s results were astounding. When he crossed plants that bred true for a single trait, such as flower color, he was able to predict the exact ratio of the resulting plants. Three-fourths of the offspring would have one color, while one fourth was another color. The most exciting part was it was predictable which color would be which.  This meant that one of the colors was consistently dominant over the other. Mendel gave us the modern genetic terms “dominant” and “recessive” to describe these traits. “Henceforth in this paper those characters which are transmitted entire, or almost unchanged in the hybridization, and therefore in themselves constitute the characters of the hybrid, are termed the dominant, and those which become latent in the process recessive. (emphasis his)[21]” What Mendel is saying is that a dominant trait will always appear when it is present, while a recessive trait will only appear in absence of a dominant trait.

Mendel did not stop there. He then bred two plants that bred true for multiple traits. One parent plant was true breeding dominant and the other was true breeding recessive. The first generation of offspring imitated the dominant parent completely. Both traits were identical to the dominant phenotype[22]. However, when the second-generation offspring were bred together, a 9:3:3:1 ratio resulted where nine of sixteen offspring were completely dominant, three of sixteen had dominant trait one and recessive trait two, three of sixteen had dominant trait two and recessive trait one, and just one of sixteen had both recessive traits.  This is exactly the expected outcome of two 3:1 ratios multiplied together.

Mendel did not know anything about DNA or the cell, but he did not need to.  He was able to deduce how heredity worked simply by observation of the phenotypes. Out of Mendel’s work grew the Law of Independent Assortment, which states that every trait sorts into each gamete independently of every other trait.  Essentially this means that each trait that a parent has an equal, independent chance of being passed to the offspring. Mendel’s work was also the genesis for the Law of Segregation, which states that each gamete will only receive one copy of the information for a given trait, meaning that offspring get half their information for each trait from each parent.  These laws allow us to use what is called a Punnett Square to determine the likelihood that an offspring will exhibit a given trait.

In the below Punnett Square, we are using the example of pea plants derived from Mendel, using a trihybrid cross[23]. The traits are represented by large and small letters.  The capital letters represent a dominant allele[24], while the small letters represent the recessive allele.  The three traits we are using in this Punnett Square are plant height, represented by Ts where tall is dominant and short is recessive, pea shape represented by Ws where wrinkled is dominant and smooth is recessive,  and pea color, represented by Ys where yellow is dominant, and green is recessive.  You will notice that one parent is completely heterozygous[25] while the other parent is homozygous[26] dominant for wrinkled peas, but homozygous recessive for yellow peas, meaning it will produce green peas.  This also means it can only give its offspring the information for wrinkled peas, and green peas.  The cross is represented as follows:

TtWwYy × TtWWyy

Book Punnett Square[27]

Before you get blown away by all the resulting genotypes[28], the image is actually color-coded to represent the resulting phenotypes. One resulting phenotype is a tall, wrinkled, yellow pea.  This accounts for 24 of the results.  A second phenotype is a tall, wrinkled, green pea, also accounting for 24 of the results.  The third possible phenotype is a short, wrinkled, yellow pea, accounting for eight of the results.  The final phenotype possible is short, wrinkled, green peas also accounting for eight results. Note that none of the phenotypes produced was smooth seeded. Because smooth seeds are recessive and only one parent had an allele with the information for them, this particular cross cannot produce a smooth pea in the first generation.

Some alleles exhibit a property known as codominance as well. This is the case in blood types for example. Type A and Type B blood are equally dominant, so when a person has both, they have type AB blood.  Type O is recessive to both, meaning even if someone has the genotype AO, they will exhibit the type A blood phenotype.  Other alleles exhibit incomplete dominance. This is the case in many flowers. When parents of two different colored true breeding strains are bred together, the flowers produced by the offspring are often a blend of the colors of the parents.


There is much more that could be discussed about Mendelian and non-Mendelian genetics and how it applies to heredity but that is beyond the scope of this series.  Before wrapping up this article with a discussion of how it all applies, there is one more topic which must be addressed, that of epigenetics. Epigenetics literally means “in addition to changes in genetic sequence[29]” but in practice it usually means regulation of alleles without any actual change in information.

The most well-known mechanism of epigenetic regulation is something known as DNA methylation. The term refers to the addition of a methyl group (CH3) to a section of the DNA strand. DNA methylation is postulated to serve as a sort of cellular memory in development[30]. Thus environmental influences can be carried over by the developing young and then passed on to their offspring.  This is typical of how epigenetics works.

While it is beyond the purposes of this series to go through all the aspects of epigenetics, it is important to understand that epigenetics does affect the phenotype of an organism. However, most epigenetic changes are established in the womb[31]. By the time a child is born, it appears that at least a sizeable part of their epigenome has already been established.  Epigenetics is also critical to regulating cells during development. If portions of the epigenome are disrupted during development, cells begin to explode automatically[32]. This underscores just how important the epigenome is to development and regulation of the genome.


This article has just barely scratched the surface of the DNA, how it works, the genome, and heredity. There is so much more depth we could delve into, and hundreds of papers are written about these topics every year.  However, hopefully, the basic background provided will help you understand the remainder of the article.

As referenced earlier in the chapter, DNA is the information for life.  The DNA strand contains all the information an organism needs to reproduce itself. This is, of course, presuming an organism exists, to begin with, but that’s an argument for a different time.  Presuming that organisms exist, and they have DNA, how does that DNA change? How is the massive variety in the world produced?

The answer evolutionists give is a mutation.  Mutations to the neo-Darwinists are the source of all new variation.  This requires that we examine what this powerful mechanism is that can create new variation. Does it work the way evolutionary dogma demands it does?

A mutation is any change in the nucleotide sequence of the DNA strand.  They represent a loss of genetic information and are almost always entirely deleterious. The few examples where organisms gained a benefit because of a mutation are, to my knowledge, exclusively a result of a lost function conferring a situational advantage. The most common example cited is antibiotic-resistant bacteria. However, the bacteria with the mutation providing antibiotic resistance are less able to survive in absence of the antibiotic. “In the absence of the selecting drugs, chromosomal mutations for resistance to antibiotics and other chemotherapeutic agents commonly engender a cost in the fitness of microorganisms.[33]” The fact that these beneficial mutations are, at best rare, is even acknowledged by evolutionists. “The punctuation is caused by natural selection as rare, beneficial mutations sweep successively through the population.[34]”  This is known as Haldane’s dilemma, named for the evolutionary geneticist who proposed it.  If a beneficial mutation occurs, it has to increase in a population, but it does so at an incredibly slow rate and can easily be selected out and eliminated.  This dilemma has still not been solved[35].

Even assuming beneficial mutations exist, which is by no means demonstrably certain, they are rare. However, mutations themselves are quite common and affect every part of the genome. For example, significant percentages of the genome are non-coding. In other words, it does not directly contain the information for a protein.  Thus, mutations in these sections of the DNA strand are called silent mutations. However, silent mutations are far from inert. In research on Escherichia coli, a typical laboratory organism, researchers revealed that silent mutations had massive deleterious effects. “These results demonstrate that silent mutations can severely inhibit several steps of gene expression in E. coli…[36]” In other words, silent mutations are not silent.  They are detrimental, which is exactly what creationists would expect[37]. The same could be said for the vast majority of other mutations as well.

This deleteriousness of mutations is incredibly destructive to typical Darwinian mechanisms.  Yet mutations are what evolutionists rely on to advance their dogma. “Phenotypic evolution occurs primarily by mutation of genes that interact with one another in the developmental process. The enormous amount of phenotypic diversity among different phyla or classes of organisms is a product of [the] accumulation of novel mutations and their conservation that have facilitated adaptation to different environments.[38]” This evolutionist is arguing that phenotypic changes, ie changes we can observe on the outside, are created due to mutations. Another author, in discussing a proposed evolutionary synthesis involving protein evolution said “…such changes largely occur through mutations in the cis-regulatory sequences of pleiotropic developmental regulatory loci and of the target genes within the vast networks they control.[39]” Obviously, mutations are key to the postulated evolutionary process. Ironically, forty years earlier, Mayr had tried to argue that evolution was not guided by mutation at all[40].

Barriers to Change

 Hopefully, the above information has given the reader some insight into how the genome works. However, there is more to explore. Just knowing how the genome and heredity works do not answer the fundamental question of origins: is there a limit to the possibility of change over periods of time? The answer to this question determines whether molecules to man evolution is a possibility, or if it can be eliminated out of hand.

The question being asked requires going back and examining what we demonstrated with heredity.  DNA is a code containing information.  This information is passed to the offspring. There is no debate over this point.  That being the case the offspring will get a copy of the same information as the parent.  There is no way to emphasize enough that the information an offspring gets is directly derived from the parents.  This means the offspring does not generate new information. The information is preexisting. The offspring gets a copy of a preexisting set of information.

Combining the two copies of DNA, one from each parent, does create a unique phenotype. The phenotypic expression could be significantly different than the parents, depending on what alleles the offspring inherits from each parent, but that actually does the opposite of what evolution requires. Instead of demonstrating limitless change, phenotypic variation demonstrates that there are limits to change.  Because phenotypic variation is entirely based on information derived from the parents and the epigenome, also inherited from the parents, it is based entirely on new combinations of existing information for the same traits.  There is no new information.

However, new information is a must for evolution.  To make a dog fly, new information would have to be placed in the dog genome to give it wings. The information currently in the dog genome does not contain the blueprint for a wing.  Countless other such examples could be cited. Without this new information, no matter how high you throw the dog, it will not fly.  Thus, the genome itself serves as an independent barrier to change.  New information must be introduced, yet there is no mechanism to introduce this information.

If no information is introduced, then where does variation come from?  As we have seen from Mendelian genetics, variation is built into the genome, but there are limits. Consider Mendel’s pea plant experiment. When he bred yellow and green peas, he never produced purple peas. His offspring could be green or yellow, depending on parent genotype, but never purple because the information for purple peas is not in the pea genome[41]. Even if every individual is heterozygous for every trait, there is still a hard limit already coded into the genome. While creationists accept heterozygosity and even believe that the kinds were created heterozygous, this still does not involve the creation of any new information[42].  The information was already there, it was simply passed on from parent to offspring. There are options, but the options are not limitless. Without this limitless information increase, evolution fails.

This article has been a very shallow overview of the field of genetics but to cover it in any great depth would require much more space than is available for this work. The key takeaways are that heredity is based on information that is found in the DNA.  The information in each creature creates its phenotype.  There is no mechanism to introduce new information into a lineage. Mutations are a failed explanation for this problem. Even if beneficial ones exist, they are incredibly infrequent, represent a loss of information, and generally represent a loss of function as well. No new information is added Without this new information, no new phenotypes will arise.  With no new phenotypes, there is no evolution.  No evolutionist will acknowledge this, but an objective view of observable science as presented in this article leads unavoidably to this conclusion.



[1] Robert Matthews “Who really discovered DNA?” Science Focus Accessed November 14, 2018.

[2] “Albrecht Kossel Facts” Accessed November 14, 2018

[3] Leslie A. Pray “Discovery of DNA Structure and Function: Watson and Crick.” Nature Education Volume 1 No. 1 (2008)

[4] James Watson and Francis Crick. “Molecular Structure of Nucleic Acids.” Nature Volume 171, No. 4356 (1953) Page 737.

[5] D-ribose is the naturally occurring form of ribose. L-ribose, it’s mirror image, is only produced in laboratory conditions so I will just use ribose for D-ribose in this book for simplicity.

[6] Pete Reichard and Anders Ehrenberg. “Ribonucleotide Reductase­–A Radical Enzyme.” Science Volume 221, No.4 (1983) Pages 514-519.

[7] Kevin Beck “What Are the Four Nitrogenous Bases of DNA?” Sciencing August 14,2018 Accessed November 14, 2018.

[8] James D. Watson and Andrew Berry. DNA New York: Alfred A. Knopf, 2003.

[9] H.A. Lutcke, K.C. Chow, F.S. Mickel, K.A. Moss, H.F. Kern, and G.A. Scheele. “Selection of AUG initiation codons differs in plants and animals.” The EMBO Journal Volume 6, No. 1 (1987) Pages 43-48.

[10] Marilyn Kozak. “Downstream secondary structure facilitates recognition of initiator codons by eukaryotic ribosomes.” Proceedings of the National Academy of Sciences Volume 8. (1990) Pages 83801-8305.

[11] Eukaryotes are living creatures with nuclei in their cells.

[12] Richard R. Burgess, Andrew A. Travers, John J. Dunn, and Ekkehard K.F. Bautz. “Factor Stimulating Transcription of RNA Polymerase.” Nature Volume 221 (1969) Pages 43-46.

[13] Andrey Revyakin, Chenyu Liu, Richard H. Ebright, and Terence R. Strick. “Abortive Initiation and Productive Initiations by RNA Polymerase Involve DNA Scrunching.” Science Volume 314 No. 5802 (2006) Pages 1139-1143.

[14] Margaritis Voliotis, Netta Cohen, Carmen Molina-Paris, and Tanniemola B. Liverpool. “Backtracking and Proofreading in DNA Transcription.” Physical Review Letters Volume 102, No. 258101 (2009) Pages 1-4.  

[15] Nikolay Zenkin, Yulia Yuzenkova and Konstantin Severinov. “Transcript-Assisted Transcriptional Proofreading.” Science Volume 313 No. 5786 (2006) Pages 518-520.

[16] Diana F. Colgan and James L. Manley. “Mechanism and regulation of mRNA polyadenylation.” Genes and Development Volume 11(1997) Pages 2755-2766.

[17] S. Brenner, F. Jacob, and M. Meselson. “An Unstable Intermediate Carrying Information From Genes to Ribosomes for Protein Synthesis.” Nature Volume 190 (1960). Pages 576-581.

[18] Michael Ibba and Dieter Soll. “Aminoacyl-tRNA Synthesis.” Annual Review of Biochemistry Volume 69 (2000) Pages 617-650.

[19] Samuel Levy, Granger Sutton, Pauline C. Ng, Lars Feuk, Aaron L. Halpern, Brian P. Walenz, Nelson Axelrod, Jiaqi Huang, Ewen F. Kirkness, Gennady Denisov, Yuan Lin, Jeffrey R. MacDonald, Andy Wing Chun Pang, Mary Shago, Timothy B. Stockwell, Alexia Tsiamouri, Veneet Bafna, Vikas Bansal, Saul A. Kravitz, Dana A. Busam, Karen Y. Beeson, Tina C. McIntosh, Karin A. Remington, Josep F. Abril, John Gill, Jon Borman, Yu-Hui Rogers, Marvin E. Frazier, Stephen W. Scherer, Robert L. Strausberg, and J. Craig Venter. “The Diplod Genome Sequence of an Individual Human.” PLOS B (2007)

[20] Gregor Mendel (translated William Bateson)“Experiments in Plant Hybridization” Verhandlungen des naturforschenden Vereines in Brunn Bulletin 4 (1865) Pages 3-47.

[21] Ibid

[22] Phenotype is the physical manifestation of the traits inherited from the parents.

[23] A Trihybrid cross involves three traits.

[24] An allele is one of the two sets of information for a given trait.

[25] Heterozygous means having both a dominant and a recessive allele for a given trait

[26] Homozygous means two of the same allele for a given trait.

[27] Created using the fantastic Punnett Square calculator at

[28] A genotype is the combination of alleles that produce the phenotype.

[29] Bob Weinhold “Epigenetics: The Science of Change.” Environmental Health Perspectives Volume 114, No. 3 (2006) Pages 160-167.

[30] Adrian Bird “DNA methylation patterns and epigenetic memory.” Genes & Development Volume 16 (2002) Pages 6-21.

[31] Craig A Cooney, Apurva A. Dave, and George L. Wolff. “Maternal Methyl Supplements in Mice Affect Epigenetic Variation and DNA Methylation of Offspring.” The Journal of Nutrition Volume 132 No. 8 (2002) Pages 2392S-2400S

[32] Laurie Jackson-Grusby, Caroline Beard, Richard Possemato, Matthew Tudor, Douglas Fambrough, Gyorgyi Csankovszki, Jessica Dausman, Peggy Lee, Christopher Wilson, Eric Lander, and Rudolf Jaenisch. “Loss of genomic methylation causes p53-dependent apoptosis and epigenetic deregulation.” Nature Genetics Volume 27 (2001) Pages 31-39.

[33] Bruce R. Levin, Veronique Perrot, and Nina Walker. “Compensatory Mutations, Antibiotic Resistance and the Population Genetics of Adaptive Evolution in Bacteria.” Genetics Volume 154 (2000) pages 985-997.

[34] Santiago F. Elena, Vaughn S. Cooper, and Richard Lenski. “Punctuated Evolution Caused by Selection of Rare Beneficial Mutations.” Science Volume 272 (1996) Pages 1802-1804.

[35] Don Batten. “Haldane’s dilemma has not been solved.” Journal of Creation Volume 19, No.1 (2005) Pages 20-21.

[36] Atilio Deana, Ricardo Ehrlich, and Claude Reiss. “Silent mutations in Escherichia coli ompA leader peptide region strongly affect transcription and translation in vivo.” Nucleic Acid Research Volume 26, No. 20 (1998) Pages 4778-4782.

[37] Alex Williams “Astonishing DNA complexity demolishes neo-Darwinism.” Journal of Creation Volume 21 No. 3 (2007) Pages 111-117.

[38] Masatoshi Nei “The new mutation theory of phenotypic evolution.” Proceedings of the National Academy of Sciences Volume 104, No. 30 (2007) Pages 12235-12242.

[39] Sean B. Carroll “Evo-Devo and an Expanding Evolutionary Synthesis: A Genetic Theory of Morphological Evolution.” Cell Volume 134, No. 1 (2008) Pages 25-36.

[40] Mayr, 1965.

[41] Mendel, 1865.

[42] Nathaniel Jeanson and Jason Lisle. “On the Origin of Eukaryotic Species Genotypic and Phenotypic Diversity.” Answers Research Journal Volume 9 (2016) Pages 81-122.

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