I read it, and I'm having trouble finding an appropriate response to this:

"lol..yeah we share 80% of DNA with a worm...i sure dont think we look like Worms. 80% is a damn lot and we would definatly have some resemblence to a worm"

there are various other factors, you can check it out here as well, http://www.ornl.gov/sci/techresources/Human_Genome/project/info.shtml there is some stuff on the difference between humans and worms, plus flys etc.

http://www.slideshare.net/pubudu/genomics

Any idea what worm species he was referring to?  It must be one remarkable worm.  Of course it's interesting that this person brought that up as though it were a significant problem.  We share over 98% of our genome with chimps.  Of course it's also entirely possible that the person was misrepresenting reality.  To say we share 80% of our DNA with a worm would be different than saying a worm shares 80% of its DNA with us.  I imagina all animals have a lot of common genes.  But not every gene present in us will be present in a worm, maybe only 20% of the genes in the worm genome is not also shared by us but considerably less of our own genome is shared with the worm...if that didn't make sense let me know I'll try to clarify.

He then falls back on the classic complexity argument.  Darwin's contribution to evolution is actually anything but dead, genetics is doing nothing at all but confirming the common sense principle of natural selection.  Darwin attempted to show how accumulative mutations selected favoribly by the environment could lead over time to new species.  All evolution is microevolution.  In reality there is no such thing as macroevolution.  Macroevolution is just accumulated microevolution.  The fallacy being commited by creationists who assert that microevolution could never lead to "macroevolution" is the Continuum Fallacy, also known as the fallacy of the beard (http://en.wikipedia.org/wiki/Continuum_fallacy).  We know that microevolution happens.  That's all we need to know.  It helps that we know that all genomes are related, exactly what you would expect if all life evolved from a single common ancestor. 

The person is also cherry picking (http://en.wikipedia.org/wiki/Cherry_picking) his or her facts, always fun.  The reason why anthropologists and paleontologists classify bones the way they do is because bone and skeletal structures in certain differing species have distinct shapes and features.  The skull of a man is distinct from the skull of an ape in many ways that I won't get into, but can be read about by anyone interested in researching it seriously.  They can determine a transitional skull by how the skull shares features distinct to two different species.  Australopithecine skulls have features that are distinct to modern apes, and not all found in modern humans, but also features that are distinct to modern humans and not all found in modern apes.  That strongly suggests that australopithecines were more closely related to apes than we are.  They did not evolve from apes, but they were more closely related to the ancestor we share with modern apes.

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Firstly, there is an important matter to consider. The bulk of your post was rhetoric, your personal feelings, and emotions, mixed in with exclamations and confusing statements, your own opinions on ideas. You will note when you read my response that in my post I displayed no emotions whatsoever. Emotion is irrelevant to this debate. Your personal opinion is irrelevant. It does not matter whether you think evolution is "retarded" or not. It certainly does not matter whether you think it makes life meaningless, or what consequences result for society. These are consequential arguments, mixed with your personal opinion and should not form a part of your argument. Your feelings, emotions, and personal opinions do not have a place in any argument. They are worthless in these matters. Please check them out at the front door before engaging in this debate, and try to keep the rhetoric to a minimum please, because it too, is irrelevant. 

Now, to turn to your empirical propositions...

The argument being employed is incorrect. To understand the reasons for this it is necessary to understand certain background knowledge of concepts. This is puzzling since what is about to be mentioned is taught to every genetics student, which makes me suspect that your interlocutor is lying.

Firstly, especially in Eukaryota, there is no relationship between genome size, in nucleotide pairs, with morphology or phenotype. The human genome consists of 3.2 billion base pairs. The amoeba genome consists of 670 billion base pairs. The pufferfish has a genome of 4 billion base pairs. The virtually identical Fugu rubripes has 40 million. The relationship is more refined when discussing the number of genes or coding sequences, but nowhere near accurate. There is no direct relationship between morphology and gene sequences. Especially in higher Eukaryota, this depends mostly on Hox genes and morphenogenesis. For example, A particularly special method of control is available in Eukaryota. Eukaryotic pre-mRNA is spliced to make mature mRNA (as well as being capped and polyadenylated). The splicing is regulated by a series of splice sites or splice junctions that determine the cleaving of the pre-mRNA by the snRNP. The choice of splice sites can be regulated to form alternative splice sites to form alternatively spliced mRNA. This pathway is extremely important in many developmental pathways and other control mechanisms. In some cases, alternative splicing can produce a vast number of different proteins from the same gene. In the most extreme cases, more mRNA can be synthesized from a single gene than the number of genes in the entire organism. In Drosophila, a gene called DSCAM has four regions, each of which has a choice of exons and a choice of splice sites, with the necessity of there being an exon from each region to from the mature DSCAM. In theory, 38,016 different mRNA could be made from the single DSCAM gene, although only several of them are actually synthesized in Drosophila. Nonetheless, it demonstrates something important. To say, for example, that "Drosophila has 2-3 times the number of genes that the yeast does" is in no way a measure of complexity of Drosophila compared to yeast (Drosophila is orders of magnitude more complex than yeast is). This shows the perils of assigning the complexity of an organism based on its gene count.

 The genetic changes that are permanent are called mutations. Mutation rates in the somatic line need to be kept low to protect the individual organism. High mutation rates in the somatic line will cause cancers and the proliferation of unwanted rogue cells called tumors. At the same time, changes in the germ line that can be propagated along the germ line need to be able to passed on, but mutation rates in the germ line cannot be too high because the integrity of the genomes needs to be protected. Mutation rates are extremely low. Based on experiments with E Coli indicate that the accuracy of DNA replication is 1 in 10^9 errors. The mutation rate of sequences of genes can be estimated by comparing the genomes of organisms, which leads to the molecular clock hypothesis. The molecular clock will run fastest for non-conserved sequences like introns, and will run the slowest for the most conserved protein sequences. For example, by using the fossil record to note the amount of time between the divergence of two organisms, it is possible to note how fast different gene sequences mutate. This technique will always underestimate the rate of mutation, because most deleterious mutations for conserved sequences will be eliminated by natural selection. For this reason, it is useful to compare amino acid sequences of conserved proteins to those of a sequence of amino acids called fibrinopeptides. Fibrinopeptides are the discarded sequences from fibrinogen, which is a central protein in the coagulation pathway. The function of fibrinopeptides does not seem to depend on their sequence. In this way, fibrinopeptides act as a "master clock" of mutation rates, and the fibrinopeptides sequences between two diverged lines are compared, the results are in good agreement with those of conserved sequences. One more thing to note is that the size of the genome in terms of number of functional proteins seems to be limited by mutation rates. The balance between the need for preservation of genomic integrity and the necessity of genetic change for the adaption of organisms and continued phenotypic change is maintained by evolutionary processes. If the mutation rate was 10 times faster, then the genome would be limited to about 6,000 proteins, and evolution would have stopped at the complexity of a fruit fly. In general and overall, what this indicates is that for proteins, the molecular clock runs fastest for those that are the least conserved, but ultimately, the relationship between phenotype and genotype is so fluid that organisms which are multicellular Eukaryota will have extremely similar and conserved sequences where they share DNA. For example:

 Percentage divergence in amino acids between conserved domain of haemoglobin :

Human/Lamprey (divergence: 550 million years ago) 35%

Human /Shark (Divergence: 520 million years) 51%

Human/tuna fish (450 million years) 55%

Human/frog (350 million years) 56%

 Human/chicken (320 million years) 70%

Human/lizard (270 million years) 77%

Bird/Crocodile (220 million years) 76%

 Human/Kangaroo (170 million years) 81% Human/Sloth/Mouse/Elephant/Rabbit/Pig/Sheep/Whale/Cat/Dog/rat All between 150 and 50 million years, all 80-85% related in this domain

Human/orangutang (10 million years) 98%

Human/chimp (7 million years) 100%

There is an obvious reason for these observations. Multicellular Eukaryota, being much bigger and much more complex than Prokaryota, are actually much less diverse. There are vastly more fundamental constraints and requisites on physiology, cell dynamics and anatomy in a multicellular organism than in a single-celled one. As a result, Prokaryota are vastly more diverse than multicellular Eukaryota, and are also much more diverse than Single-celled eukaryote (since Eukaryota are much more complex than prokaryota, and single-celled Eukaryota, in turn, are much more diverse than multicellular Eukaryota). This is evident if we examine the base-pair span relationship in different domains of life:

The majority of changes between multicellular organisms are quantitative for this reason. Multicellular organisms are vastly more rigidly similar in biochemistry than are any prokaryota. I share a higher percentage of DNA with the potted plant on my desk than do two prokaryotic species picked at random. It is for this reason that bacteria account for 99% of all species on Earth, and will always be the dominant arm of the biosphere as long as sustainable life exists on the planet. This is also why for the bulk of geological time, our ancestry were single celled organisms. So, again, it is necessary iterate that in terms of the biochemical spectrum, all multicellular Eukaryota are extremely closely related and that the generation of new species is so incremental and in terms of time slower than bacterial change is merely because bacteria reproduce exponentially faster. This is one way we can use them to determine things like the molecular clock, the rate at which mutations occur and the rate at which certain critical proteins alter. In the germ cell line of the E coli stomach bacteria, after amplifying a colony to several billion specimens, we can perform an experiment where we breed the E Coli in a glucose agar and track the rate of deleterious mutations of the enzyme required to process lactose, by means of tagging the organisms in such a way that they become apparant when it mutates. In my essay on genomics, I can go through exact details through how evolution works despite the fact that the genome is ultra high-fidelity, and go through vastly better detail on how we track and establish the relationships of homologous sequencing. All that we need to understand now is that there is a directly proportional relationship found in the mutation changes in any orthologous gene in any two species and the time since those two diverged from a common ancestor.

For this reason, the utterly vast majority of mechanisms common to life were in place by the time the transition to multicellular Eukaryota was made after the rise of the Eukaryotes during the Oxygen Catastrophe. Granted, we can observe animal evolution very well, and our molecular techniques allow us to read it just as well as we would bacterial evolution, however, we must remember that we share far more in common with say, tucans, than the average soil bacteria shares with the average bog bacteria, and when examining the phenotype diversity of animals, we tend to forget this. Consider this: We use Drosophila as an invertebrae model where they take out or add individual genes to see what happens. So we end up with all sorts of odd mutants, like ones with three extra pairs of wings, or legs, or missing legs and wings, or a mismatched development plan. This is how we found all the Hox Genes associated with the three-part development plan. Actually, Drosophila is such a good model that we often use it as a model of vertebrae even though it is not a vertebrae itself, because it is genetically so similar to vertebrae, and because all vertebrae are, in many senses, basically the same. It was this very precise homology that led us to theorize that there may have been a massive divergence event several hundred million years ago, a whole-scale duplication, this being called an Ohnology. We tend to think that life on Earth is very diverse and different. But that’s not true, essentially, all life on Earth is the same, we all have the same and the similarity is directly proportional to physiological and anatomic complexity. Vertebrae are modular, they consist entirely of the same proteomic spectrum, the only originality coming from the reshuffling of modular domains. More and more, we are discovering that the only real differences between all the vertebrae are really quantitative, or modular. In this regard, it is necessary to examine the exact mechanisms of how Eukaryotic regulatory DNA creates complex biomolecular structures, they have to do with such concepts as Hox genes, heterochromatin, the position variegation effect, Helicase and nucleosome binding complexes etc. Hox genes explain why multicellular organisms arose so fast (The Cambrian explosion) and why animal evolution happens much faster than bacterial (in terms of generations, not years) and how phenotypic diversity and complex multicellular structures form and develop. This, in essence is evolutionary developmental biology, the synthesis of embryology with evolution. It is a radical new field which overturns old thinking. Namely, instead of a vast number of tiny incremental changes driving animal evolution, more significant changes in the genes controlling the in utero development of the organism allow for the development of new structures in utero.

So, in order to truly understand why multicellular organisms, which such similar genomes, look so phenotypically diverse, one must have at least a glimmer of basic understanding of devo genetics. To this end, I put together some notes that scratch the surface.

Cell differentiation

The key question in developmental biology is this: A multicellular organism has numerous different cell types, a body arranged of a precisely positioned array of such different cell types. Because the cell types are so phenotypically diverse, researchers originally suspected that they might undergo selective loss of genes during development. But this is not the case. Every cell in the body of an organism holds precisely the same genetic material. It is not deleted during development. Instead, different cells accumulate different proteins and RNA, which determines their phenotypes. When a cell has committed to a differential type, such changes are usually irreversible. And all descendants of differentiated cells retain the same phenotype and the same expression pattern.  This remarkable feat, called cell memory, underlies the existence of multicellular organisms.  The underlying initiators that develop this remarkable set of different cells expressing different genes, yet all with the same genome,  are gene regulatory proteins.

 The key question under discussion is thus. Multicellular organisms appear very different phenotypically, yet have highly conserved genomes compared to protozoa. The key function that ensures this phenotypic diversity comes from the decisions made during embryogenisis, and the evolutionary mechanisms that shape these. This is broadly referred to as evolutionary developmental biology. The first principle necessary to understand it even in the most basic fashion is gene control command.

A genome is much more than a protein code. Within the genome are sequences that dictate where, when and at what rate each gene is to be expressed. Immensely complex pathways of gene regulation are the principle methods by which cells adjust quickly to their external environs, and the method by which a multicellular organism is built from many different cell types with vastly diverse phenotypes, yet each of which hold exactly the same genome, through the process of cell differentiation. The gene expression pattern of a cell will determine what genes it expresses, and that will ultimately determine the cell itself. Regulation of genes occurs at many steps from the process from DNA to RNA to protein, and although in principle all of these steps can be regulated, for any one gene, only a few regulatory pathways are likely to be important. To truly understand the complex modular mechanisms that govern evolutioanry development, it is therefore necessary to have a complete understanding of all transcriptional and posttranscriptional command.So, the most important basic principles that I think you absolutely must know stripped to the bare essentials are as thus:

 Positive self-regulation

One of the simplest methods of ensuring that all descendant generations of a cell will express a protein which is expressed in the original cell is where the protein in question regulates its own synthesis, usually in combination with other proteins. We have already seen an example of this with the GR-Glucocorticoid complex. This simple mechanism, which is very widely used by many different cell types, ensures that all descendants will retain that protein and continue its synthesis.

Another mechanism that is similar in simplicity is a pair of genes that repress each other's synthesis. This allows the cell to quickly switch between two "types". This occurs most in viral genomes. Viruses exist in two pathways in cells, prophage and lytic. They can switch between the two very quickly. A pair of gene regulatory proteins command this. They repress each other's synthesis, and activate their own. Each activates and represses their own appropriate cascade of proteins for the initiation of either pathway. The switch mechanism that exists in viruses demonstrates something common in cell differentiation: By means of combinatorial control, a single gene regulatory protein can initiate differentiation by itself. 

-Gene regulatory stripes in the Drosophila embryo

As shall be discussed when delving into developmental biology, differentiated group of cells is often preceded by a common cytoplasm with multiple nuclei. This is called the syncytium. The syncytium is lined with nuclei and has a gradient of different gene regulatory proteins that extend down the anterior-posterior axis of the cell. As a result, different nuclei are exposed to different GRP. One well studied example of this occurs in Drosophila embryonic development. A gene called eve (even-skipped) is a critical gene in its regulation of embryonic development.  The eve gene is expressed in seven distinct "stripes" across the axis. This is an extremely impressive feat of positional information encoding. How is it accomplished? There are seven command regions upstream of the eve promoter. These seven modules have DNA-binding sequences that allow for combinatorial regulation. The modularity of the eve command regions, and their responses to the different concentrations of GRP along the AP axis, was demonstrated when module 2 was removed from the genome and inserted upstream of the promotor of the lacZ gene which encodes Beta-Galactosidase. When it was inserted back into the genome of Drosophila in embryonic development, a distinct stripe of B-Galactosidase was developed in precisely the same position as the second stripe of the even gene.

The module is regulated by four gene regulatory proteins, called Bicoid, Kruppel, Hunchback and Giant (the gene regulatory proteins are named for the phenotype that results from its deletion).  These four proteins are present on different gradients throughout the anterior-posterior axis. They determine the expression of module 2 of eve. The result of the exposure of the different gradients of the four GRP across the syncytium is that eve is epxressed in seven stripes. The second stripe is determined by these four proteins, and they need to be present in the correct combination for module 2 of eve to be expressed. Note that these proteins are ubiquitous in Drosophila development and via combinatorial control are responsible for the development of many processes in morphenogenesis.  Hunchback and Bicoid are repressors while Kruppel and Giant are activators. The two repressors need to be absent and the two activtators need to be present in high concentration, and this condition is only met across the AP gradient at the positional stripe that is commanded by the second module. The other modules work on similar principles.

-Combinatorial control in the initiation of a protein cascade

We have already seen how cell differentiation is generated by the response of cells to positional information and that this ensures they express different sets of RNA and Protein, since they are under the command of different GRP. We have already seen that a single GRP can be the key to the initiation of multiple proteins, and that single GRP can be part of a GRP complex that determines the transcription of multiple proteins. This is very important in cell differentiation, where different nuclei in a common cytoplasm are exposed to different GRP across the AP gradient. In myoblasts, which are a form of stem cells that can differentiate into the various forms of muscle cell, skeletal muscles are formed by the fusing of many thousands of myoblasts to form a syncytium. The initiator GRP that triggers the battery of genes downstream is called Mf2, and mf2 triggers the regulation of a cascade of proteins that differentiate myoblasts into mature myocytes, hence providing an impressive example of how a single GRP can initiate differentiation from stem cells.

-A single GRP as being responsible for a cascade

One striking result of combinatorial control and AP gradients is that a  single GRP can initiate the transcription of multiple proteins. Even more striking is the suggestion that it might be able to initiate the formation of an entire organ. One example of this is the protein called Ey, called eyeless, which triggers a battery of genes responsible for eye development. This was strikingly demonstrated when it was transiently activated in a cell line destined to form the leg of the Drosophila. The researchers found a perfectly formed Drosophila eye growing on the leg of the fly.

Another form of gene regulation that can be inherited is DNA methylation pattern. Methylation  of CG dinucleotides locks genes in transcriptionally silent states. In vertebrae DNA, the methylation of CG dinucleotides constitutes an alteration in gene expression controlled by direct modifiction of the chemical constituency of the DNA sequence. It has absolutely no effect on base pairing to methylate CG dinucleotides. More importantly, it binds a set of initiator proteins that recognize methylated DNA and serve to condense the chromatin into a silent formation. The methylation of CpG can be inherited. An enzyme called maintanence methyltranferase facilitates the inheritance. DNA is replicated semiconservitavely, so one strand is present in each copy from the parent cell. One strand will have a methylated CpG, which is recognized by MM which allows the methylation of the other side as well, which allows the methylation to propogate throughout the lineage of that cell. DNA methylation cannot initiate gene silencing. That much is clear since methylated genes in the presence of the GRP will continue transcribing. Rather, with the loss of the GRP, methylation locks genes as transcriptionally silent. Whenever enhancers are lost and the assembly of transcription factors at the promoter is not enhanced, the gene can still transcribe at very low levels. This phenomenon is called leaky transcription. DNA methylation prevents it. In mouse embryonic development, shortly after embryogeneisis formation, there is a wave of demethylation, methylation patterns are then reestablished by de novo methyltransferases, which do not need a CpG template. The deletion of any enzymes involved in demethylation is lethal, which suggests that the mice die because of the leaky transcription of genes that should be off. Methylation facilitates the binding of Atp-driven remodelling complexes and CRC and HDAT which condense the DNA and silence it.

 Imprinting

 A final mechanism to consider is imprinting. This is where the activation of a gene in diploid organisms depends on its parental derivation. The most well studied example is Igf2, Insulin-like growth factor in mice. Important in prenatal development, mice without it are half the normal size. Only the paternal copy is activated. When the maternal copy is mutated, the mouse is healthy, when the paternal one is inactivated, the mouse is stunted. This is due to imprinting. Methylation of the sequence allows the cell to distinguish between a(p) and a(m). This imprint is not lost during embryonic demethylation. Normally, methylation locks genes as silent. Here it does the opposite. The methylation targets the insulator region, and methylation of  the insulator allows the transcritpion of Igf2 in paternal cells. IN maternal cells, the methylation is blocked by the binding of a universal insulating regulator factor called CPFC, which binds to the insulator and blocks methylation, hence blocking transcription.

I am suspicious. If you were telling the truth, you would be able to refute your own arguments without problems.

Finally, it is time to consider your argumentative assertion pertaining to molecular biology. It is commonly asserted by those who wish to propogate these assertions that being the Charles Darwin did not understand molecular biology, evolution is invalidated since cellular systems cannot evolve. However, this is complete nonsense. The discoveries that we have made in genetics and molecular biology have only affirmed the principles of evolution. In fact, in reverse genetics, we do most of our work by virtue of employing homology. The modular nature of genetic systems in developmental and evolutionary biology, the employment of tracking by means of transposable elements and CSSR, duplication, divergence, recombination, have all painted a picture of life that points to common descent. Genetics and molecular biology have affirmed it (evolution) to high order. They are now an integral part of evolutionary biology. It is impossible to understand genetics without understanding evolution, or vice-versa. It is true that Darwin did not understand genetics. However, the modern picture of evolution, as we understand it today, was also not understood by Darwin. In the modern synthesis, no field of biology can possibly be understood without respect to evolutionary biology. It is the central unifying theorom of biology. It links developmental biology, molecular biology, structural biology, microbiology, anatomy, genetics, proteomics, transcriptomics, computational biology, biochemistry, histology, cytology, zoology, botany and mycology. Nothing in biology makes sense except in light of evolutionary biology.

 #1 tell em to back to studying cause there gonna fail unless they go to Liberty. Demand some references for this astounding discovery, cause he won't find any. There is no way worms like c. elegans or any other type of worm has 80% identical DNA that is just nonesense. They may share a large percentage of related proteins but this is an entirely different statement. And even in this case at the nt level for those conserved protein sequences the nt differences are not 80% identical between these species.

#2 if he doesn't get #1 then there is nothing else to respond to, so wait until he proves that worms have 80% identical DNA, then move to the next item in the list

Thank you peoples. I've given him the link to this page, And I hope he reads it. If he really is studying in this field.