Aaaah the "29 proofs of macro-evolution"! The 29 proofs which the evolutionists never post even after being asked to show just one through hundreds of posts! The 29 proofs which you have been bashing science for hundreds of posts in order not to give them! But wait, did you not say that there is no proof in science? Did you not say that dozens of times? Were you lying then or are you lying now? Or are you perhaps trying to tell me that evolution is not science by telling me that there is proof of evolution?
Those 29 proofs are no proof at all. I saw a lot of them when they were originally posted on FR over a year ago. Some are proofs of micro-evolution. Some are not proofs at all. All of them are so badly written that all they prove is the awful illiteracy of the author. However, since these seem to be the "Bible" of the evolutionists, I am sure you know it quite well. Pick the strongest of those proofs, post it here for all to see and we will discuss it. Hope I do not have to wait 150 years for the answer!
The title clearly says "29 Evidences." The Proof-Goof artlessly changes it to "29 Proofs."
Too many artless misunderstandings, forgettings, ill-reasonings. I pity the suckers who bite when you troll.
Those 29 proofs are no proof at all. I saw a lot of them when they were originally posted on FR over a year ago.
So which is it, al? Did we "never post" them, or did we post "a lot of them ... over a year ago"?
(Here we get a rare opportunity to see gore3000's mind at work, momentarily uncertain which form its envitable denial should take.)
Since gore3000 insists, here is one of the 29 points chosen at random. As you read this bear in mind gore3000's claim that "all of [these] are so badly written that all they prove is the awful illiteracy of the author." This should tell lurkers a great deal about gore3000's objectivity and crediblity. The fact that he has never bothered to repond to these with anything but ridicule, and has never specified any specific error of fact or of reasoning, should tell lurkers even more.
The support for common descent given by studies of molecular sequences can be phrased as a deductive argument. This argument is unique within this FAQ, as it is the only instance we can directly conclude that similarity implies relatedness. This conclusion depends upon the similarity of biological structures within a specific context: the similarity observed between ubiquitous genes from different species.
The following discussion is somewhat technical, so it is first presented in the outline of a deductive argument, which makes the logical thread easy to follow. Here are listed the premises of the argument followed by the conclusion and further discussion.
(P1) There are certain genes that all living organisms have because they perform very basic life functions; these genes are called ubiquitous genes.
(P2) Ubiquitous genes have no relationship with the specific functions of different species. For example, it doesn't matter whether you are a bacterium, a human, a frog, a whale, a hummingbird, a slug, a fungus, or a sea anemone - you have these ubiquitous genes, and they all perform the same basic biological function no matter what you are.
(P3) Any given ubiquitous protein has an extremely large number of different functionally equivalent forms (i.e. protein sequences).
(P4) Obviously, there is no a priori reason why every organism should have the same sequence or even similar sequences. No specific sequence is functionally necessary in any organism - all that is necessary is one of the large number of functionally equivalent forms of a given ubiquitous gene or protein.
(P5) There is one, and only one, observed mechanism which causes two different organisms to have ubiquitous proteins with similar sequences. That mechanism is heredity.
(C) It follows that organisms which have similar sequences for ubiquitous proteins are genealogically related, and the more similar the sequences, the closer the relationship.
Before the advent of DNA sequencing technology, the amino acid sequences of proteins were used to establish the phylogenetic relationships of species. Sequence studies with functional genes have centered on genes of proteins (or RNAs) that are ubiquitous (i.e. all organisms have them). This is done to insure that the comparisons are independent of the overall species phenotype.
For example, suppose we are comparing the protein sequence of a chimpanzee and that of a human. Both of these animals have many similar anatomical characters and functions, so we might expect their proteins to be similar too, regardless of whether they are genealogically related or not. However, we can compare the sequences of very basic genes that are used by all living organisms, such as the cytochrome c gene, which have no influence over specific chimpanzee or human characteristics.
Cytochrome c is an essential and ubiquitous protein found in all organisms, including eukaryotes and bacteria (Voet and Voet 1995, p. 24). The mitochondria of cells contain cytochrome c, where it transports electrons in the fundamental metabolic process of oxidative phosphorylation. The oxygen we breathe is used to generate energy in this process (Voet and Voet 1995, pp. 577-582).
Using a ubiquitous gene such as cytochrome c, there is no reason to assume that two different organisms should have the protein sequence, unless the two organisms are genealogically related. This is due in part to the functional redundancy of protein sequences and structures. Here, "functional redundancy" indicates that many different protein sequences form the same general structure and perform the same general biological role. Cytochrome c is an extremely functionally redundant protein, because many dissimilar sequences all form cytochrome c electron transport proteins. Functional redundancy need not be exact in terms of performance; some functional cytochrome c sequences may be slightly better at electron transport than others, but that is irrelevant for the purposes of this argument.
Decades of biochemical evidence have shown that most amino acid mutations, especially of surface residues, have no effect on protein function or on protein structure (Harris, Sanger et al. 1956; Li 1997, p. 2, Matthews 1996). A striking example is that of the c-type cytochromes from various bacteria, which have virtually no sequence similarity. Nevertheless, they all fold into the same three-dimensional structure, and they all perform the same biological role (Moore and Pettigrew 1990, pp. 161-223; Ptitsyn 1998).
Even within species, most amino acid mutations are functionally silent. For example, there are at least 250 different amino acid mutations known in human hemoglobin, carried by more than 3% of the world's population, that have no clinical manifestation in either heterozygotic or homozygotic individuals (Bunn and Forget 1986; Voet and Voet 1995, p. 235). The phenomenon of protein functional redundancy is very general, and is observed in all known proteins and genes, regardless of the species.
With this in mind, consider again the molecular sequences of cytochrome c. It has been shown that the human cytochrome c protein works just fine in yeast (a unicellular organism) that has had its own native cytochrome c gene deleted, even though yeast cytochrome c differs from human cytochrome c over 40% of the protein (Tanaka et. al 1988a; Tanaka et al. 1988b; Wallace and Tanaka 1994). In fact, the cytochrome c genes from tuna (fish), pigeon (bird), horse (mammal), Drosophila fly (insect), and rat (mammal) all function well in yeast that lack their own native yeast cytochrome c (Clements et al. 1989; Hickey et al. 1991; Koshy et al. 1992; Scarpulla and Nye 1986). Furthermore, extensive genetic analysis of cytochrome c has demonstrated that the majority of the protein sequence is unnecessary for its function in vivo (Hampsey 1986; Hampsey 1988). Only about a third of the 100 amino acids in cytochrome c are necessary to specify its function. Most of the amino acids in cytochrome c are hypervariable (i.e. they can be replaced by a large number of functionally equivalent amino acids) (Dickerson and Timkovich 1975). Importantly, Hubert Yockey has done a careful study in which he calculated that there are a minimum of 2.3 x 1093 possible functional cytochrome c protein sequences, based on these genetic mutational analyses (Hampsey 1986; Hampsey 1988; Yockey 1992, Ch. 6, p. 254). For perspective, the number 1093 is about one billion times larger than the number of atoms in the visible universe. Thus, functional cytochrome c sequences are virtually unlimited in number, and there is no a priori reason for two different species to have the same, or even mildly similar, cytochrome c protein sequences.
In terms of a scientific statistical analysis, the "null hypothesis" is that the identity of non-essential amino acids in the cytochrome c proteins from human and chimpanzee should be random with respect to one another. However, from the theory of common descent and our standard phylogenetic tree we know that humans and chimpanzees are quite closely related. We therefore predict, in spite of the odds, that human and chimpanzee cytochrome c sequences should be much more similar than, say, human and yeast cytochrome c - simply due to inheritance.
Humans and chimpanzees have the exact same cytochrome c protein sequence. The "null hypothesis" given above is false. In the absence of common descent, the chance of this occurrence is conservatively less than 10-93 (1 out of 1093). Thus, the high degree of similarity in these proteins is a spectacular corroboration of the theory of common descent. Furthermore, human and chimpanzee cytochrome c proteins differ by ~10 amino acids from all other mammals. The chance of this occurring in the absence of a hereditary mechanism is less than 10-29. The yeast Candida krusei is one of the most distantly related eukaryotic organisms from humans. Candida has 51 amino acid differences from the human sequence. A conservative estimate of this probability is less than 10-25.
One possible, yet unlikely, objection is that the slight differences in functional performance between the various cytochromes could be responsible for this sequence similarity. This objection is unlikely because of the incredibly high number of nearly equivalent sequences that would be phenotypically indistinguishable for any required level of performance. Additionally, nearly similar sequences do not necessarily give nearly similar levels of performance.
Nonetheless, for the sake of argument, let us assume that a cytochrome c that transports electrons faster is required in organisms with active metabolisms or with high rates of muscle contraction. If this were true, we might expect to observe a pattern of sequence similarity that correlates with similarity of environment or with physiological requirement. However, this is not observed. For example, bat cytochrome c is much more similar to human cytochrome c than to hummingbird cytochrome c; porpoise cytochrome c is much more similar to human cytochrome c than to shark cytochrome c. As stated earlier in prediction 3, the phylogenetic tree constructed from the cytochrome c data exactly recapitulates the relationships of major taxa as determined by the completely independent morphological data (McLaughlin and Dayhoff 1973). These facts only further support the idea that cytochrome c sequences are independent of phenotypic function (other than the obvious requirement for a functional cytochrome c that transports electrons).
The point of this prediction is subtly different from prediction 3, "Convergence of independent phylogenies." The evidence given above demonstrates that for many ubiquitous functional proteins (such as cytochrome c), there is an enormous number of equivalent sequences which could form that protein in any given organism. Whenever we find that two organisms have the same or very similar sequences for a ubiquitous protein, we know that something fishy is going on. Why would these two organisms have such similar ubiquitous proteins when the odds are astronomically against it? We know of only one reason for why two organisms would have two similar protein sequences in the absence of functional necessity: heredity. Thus, in such cases we can confidently deduce that the two organisms are genealogically related. In this sense, sequence similarity is not only a test of the theory of common descent; common descent is also a deduction from the principle of heredity and the observation of sequence similarity. Finally, the similarity observed for cytochrome c is not confined to this single ubiquitous protein; all ubiquitous proteins that have been compared between chimpanzees and humans are highly similar, and there have been many comparisons.
Without assuming the theory common descent, the most probable result is that the cytochrome c protein sequences in all these different organisms would be very different from each other. If this were the case, a phylogenetic analysis would be impossible, and this would provide very strong evidence for a genealogically unrelated, perhaps simultaneous, origin of species (Dickerson 1972; Yockey 1992; Li 1997).
Furthermore, the very basis of this argument could be undermined easily if it could be demonstrated (1) that species specific cytochrome c proteins were functional exclusively in their respective organisms, or (2) that no other cytochrome c sequence could function in an organism other than its own native cytochrome c, or (3) that a mechanism besides heredity can causally correlate the sequence of a ubiquitous protein with a specific organismic morphology.