The DNA code itself is universal and was a prediction.
A universal code was never a prediction of evolution. IÃ¢â‚¬â„¢ve noticed youÃ¢â‚¬â„¢ve made a lot of claims yet you seldom provide actual substance to back them. The fact we found a Ã¢â‚¬ËœcodeÃ¢â‚¬â„¢ in the DNA was overwhelming evidence against a naturalistic origin. It was so overwhelming that the co-discoverer (Francis Crick) dropped his belief in neo-Darwinism in favor of the silly panspermia theory (aliens seeded the planet with the information). We know from information science that is impossible for a code to arise naturalistically, it MUST have an intelligent source. Even in the book and subsequent movie Contact, Carl Sagan had enough sense to realize this truth (the movie makes this very claim), but Sagan didnÃ¢â‚¬â„¢t apply this truth to origins because his religious atheism got in the way.
Since the existence of a code itself refutes evolution, its universal nature can instead be viewed as solid evidence that there is ONE designer, not multiple designers.
Regarding Cytochrome-C, Deadlock already pointed out the illusion behind it, that you can make all kinds of relationships that evolutionists do not claim are due to recent common decent. I have a much wider chart on Cyto-C that includes more animals, and I would be willing to bet you that if I gave the labels of each animal a code you would not be able to make a coherent sequence of evolution that even remotely matches what evolutionists believe. There are also mosaics in the Cyto C sequence, such as the snake. It would be fun to see where you put the snake in the grand scheme of things.
He uses these bad numbers to say 120 point mutations would require 2,700,000 generations to propagate through the population. Yet this carried even more bad assumptions. He assumed mathematically that each point mutation must first propagate through the population before starting the next mutation. In reality mutations can occur simultaneously throughout the population. When these bad assumptions are removed then even with ridiculously low rate of only 1 mutation every 20 generations you get that 120 point mutations in only 2400 generations. That's barely a month for some microbes and well less than 50,000 years for humans.
Sorry to be so blunt, but this shows remarkable ignorance of genetics. To claim that a mutation can become fixed in a mere 20 generations (and claim this is a Ã¢â‚¬Å“ridiculously lowÃ¢â‚¬Â estimate) is a pipe dream. For one you forgot that microbes are asexual and humans are not (S@xual organisms add an additional 50% hurdle per generation when moving a mutation through a population). You are making your own bad assumptions, and most importantly you are completely ignoring an important mechanism, the cost of substitution. Each mutation must incur its own cost to reach fixation. Haldane believed this, and Kimura believed this (in fact the problem with the cost of substitution was a driving force behind why Kimura proposed the neutral theory in the first place). So it turns out that EdenÃ¢â‚¬â„¢s assumption that each mutation should be considered serially was actually not a bad assumption at all, and why I suspect he was keenly aware of the substitution problem. One particular cost of substitution (among others) is the cost of harmful mutations, a damning cost indeed that punches a big hole in common decent with a monkey-esque grandaddy. See my article on this:
A related debate I had with a biologist:
What they did do [computer simulations] was demonstrate that the argument that evolution couldn't happen with random mutations doesn't work.
Such programs proved no such thing. Random mutations cannot produce information without an intelligent source present to harness the data. See this pinned thread:
The DNA fingerprint of these ERVs are identical. It's like taking a picture on the Bangkok and in Dallas and both pictures being identical. The DNA of these ERVs can also be identified as an individual virus the same way you can be identified from all other people on Earth by your DNA. The damage done to the cell itself was even identical, like two sticks of dynamite creating identical pictures in two parts of a jungle. So we have an individual virus that invaded the exact same cell type in multiple species leaving the exact same damage to the cell and all these cells managed to survive the infection to continue reproducing. Then somehow after all this it follows the same species lineage that we infer from the fossil record. If that's not enough it also agrees with the fossil records timing of when the species split in the past. There is also a lot of other ERVs that did all these same things. So you can say it was put there for an unknown purpose but needing these things does not explain why all these things had to be exactly the same or why it had to match the sequence and timing already inferred from the fossil record.
This is mostly ad hoc story-telling. Evolutionists assume: 1) ancient infection in 2) our alleged simian ancestor, 3) the vast majority of ERVs have no function, 4) the events are random. Since we have already identified some ERVs that are highly conserved and clearly have function, this alone casts doubt on their argument. Another ugly problem for evolution again rears its head, namely convergent evolution. By itÃ¢â‚¬â„¢s very definition it is anti-evolutionary, since it describes similar traits in two organisms that cannot be attributed to common ancestry! So the problem is this - we find similar ERVs in organisms no evolutionist would dare claim is a recent common ancestor to humans .
[regarding nylon-eating bacteria] You say adaptation not random mutation and/or selection? Why does 9 days speak to anything? Of course it was an adaptation that required a random mutation to produce.
You apparently are missing rbarclayÃ¢â‚¬â„¢s point. The mutation happened too quickly and conveniently to be attributed to a random copying error in the DNA. Evolution theory doesnÃ¢â‚¬â„¢t accommodate non-random mutations because they clearly imply design.
1 - JBS Haldane, The Cost of Natural Selection, Journal of Genetics 55, pp 522 (1957)
2- Dupressoir A, Marceau G, Vernochet C, BÃƒÂ©nit L, Kanellopoulos C, Sapin V, Heidmann T (2005) Syncytin-A and syncytin-B, two fusogenic placenta-specific murine envelope genes of retroviral origin conserved in Muridae Proc Natl Acad Sci U S A. 102(3):725-730