Summations Only

Can you support any of these claims with any evidence? If what you claim is true then there shouldn't be disease or aging. There wouldn't be any birth defects. Also, if proteins are specified as you claim then you should really tell the people at the HapMap program (http://www.hapmap.org). They are mapping genetic variation in humans and guess what? A lot of that variation includes proteins that differ at the amino acid level. Evolution is not undirected. Evolution is directed by selection. If evolution were truly random then detrimental mutations would be passed on at the same rate as neutral or beneficial mutations. This is not what we see. The rate of mutation in the coelacanth lineage is roughly the same for all other lineages. The difference here is that mutations which didn't change morphology were selected for. How so? You are confusing phenotype plasticity with evolution. Gene regulation can not explain how a bacteria that lacks an enzyme for metabolizing a specific sugar can acquire this enzyme through changing it's DNA sequence. Gene regulation does not involve a change in DNA sequence. Because that is exactly what we observe. For example, the Lederbergs were able to show that the mutations which confer antibiotic resistance in bacteria occur in the absence of bacteria (source). Luria and Delbruck were able to demonstrate that mutations which confer phage resistance occurs in the absence of phage (source). Both of these experiments demonstrate that there is no link between the processes which produce mutations and the needs of the organism. IOW, these experiments demonstrate that mutations are random with respect to fitness.So why do biologists claim that mutations are random? Because that is what they observe. No, it is an argument from incredulity which is a logical fallacy. If it was about probability you would have done the math for us. You haven't. Instead, you express how you can't believe it. That is incredulity, not improbability.

Just a few more examples:

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Science. 2005 Sep 9;309(5741):1693.
A human-specific gene in microglia.
Hayakawa T, Angata T, Lewis AL, Mikkelsen TS, Varki NM, Varki A.
SourceGlycobiology Research and Training Center, University of California at San Diego, La Jolla, CA 92093, USA.

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Abstract
Recent studies have shown multiple differences between humans and apes in sialic acid (Sia) biology, including Siglecs (Sia-recognizing-Ig-superfamily lectins). Comparisons with the chimpanzee genome indicate that human SIGLEC11 emerged through human-specific gene conversion by an adjacent pseudogene. Conversion involved 5 cent untranslated sequences and the Sia-recognition domain. This human protein shows reduced binding relative to the ancestral form but recognizes oligosialic acids, which are enriched in the brain. SIGLEC11 is expressed in human but not in chimpanzee brain microglia. Further studies will determine if this event was related to the evolution of Homo.

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Identification of human specific gene duplications relative to other primates by array CGH and quantitative PCR.
Armengol G, Knuutila S, Lozano JJ, Madrigal I, Caballn MR.
SourceDepartment of Animal Biology, Plant Biology and Ecology, Faculty of Biosciences, Universitat Autnoma de Barcelona (UAB), Barcelona, Spain.
Abstract
In order to identify human lineage specific (HLS) copy number differences (CNDs) compared to other primates, we performed pair wise comparisons (human vs. chimpanzee, gorilla and orangutan) by using cDNA array comparative genomic hybridization (CGH). A set of 23 genes with HLS duplications were identified, as well as other lineage differences in gene copy number specific of chimpanzee, gorilla and orangutan. Each species has gained more copies of specific genes rather than losing gene copies. Eleven of the 23 genes have only been observed to have undergone HLS duplication in Fortna et al. (2004) and in the present study. Then, seven of these 11 genes were analyzed by quantitative PCR in chimpanzee, gorilla and orangutan, as well as in other six primate species (Hylobates lar, Cercopithecus aethiops, Papio hamadryas, Macaca mulatta, Lagothrix lagothricha, and Saimiri sciureus). Six genes confirmed array CGH data, and four of them appeared to have bona fide HLS duplications (ABCB10, E2F6, CDH12, and TDG genes). We propose that these gene duplications have a potential to contribute to specific human phenotypes.

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This is a very, very good point. It is entirely possible to have two separate species that share all of the same genes where the differences between the species are due to differential expression of genes. Also, morphological differences can arise due to the relative differences in mRNA levels for a given gene, and when those genes are turned on during embryonic development and maturation. This is why the cutting edge of evolutionary research (at least in metazoans) focuses so strongly on Evo-Devo.

WK did a wonderful job of describing what a frameshift mutation is. I will only add this illustration: The result of the frameshift mutation in the human myosin gene was a dysfunctional protein due to the massive difference in amino acid sequence caused by the addition (or deletion) of DNA. The result was a weaker jaw muscle. A weaker jaw muscle requires less bone as an anchor. Less bone needed to anchor the jaw muscle allows for a larger cranium, and hence a larger brain.As a counterexample, take a look at this gorilla skull. Notice the massive crests necessary for anchoring the large jaw muscles.

Except the one that allowed for one of the most important evolutionary changes in the hominid lineage, the MYH frameshift mutation that allowed for the expansion of the brain.

Darwin was fighting the idea that Genesis posited a fixation of species. Darwin was suggesting that species were mutable, and that all animals from different kinds shared a common ancestor contrary to what Genesis claims.Also, the definition of species has changed since Darwin's time. With the advent of the Modern Synthesis in the 1930's we now describe speciation with respect to genetic flow instead of Linnaean groupings.

They are still different species of finch, are they not? How do you get separate populations of finches with species specific features? How is Genesis useful for understanding genetic flow, lineage specific mutations, and natural selection? Where can I read peer reviewed papers on the mechanism of speciation that is based on Genesis? How does this help us define what a species is?If you want to discuss cladistics and how it is done I would be happy to discuss it in another thread.

We are more interested in what you can evidence, not what you can see.

What all of these definitions are trying to get at is the underlying genetic mechanisms, those of inheritance and divergence. Even for asexual species you are still talking about a population that is constantly competing leading to cycles of founders and flushes as rare beneficial mutations appear in the population. With sexual species we try to adjust our definitions to reflect gene flow.When we say that two living populations are separate species what we are trying to relate is the idea that both species were once one species. Through whatever means, that ancestral population split and the two halves began building up differences as mutations accumulated through time.For fossil species we have are looking at the process in action. We can not directly look at the genotype, but we can look downstream of the genotype which is the phenotype. We can see how each branch started accumulating different mutations (or different selective pressures) as evidenced by a difference in morphology.At the foundation of the species definition is inheritance, and the mechanisms of genetics. The results of these simple mechanisms can be quite complex which makes a one-size-fits-all definition of species nearly impossible.