incorygible
Posts: 374
Joined: Feb. 2006
|
| Quote (afdave @ May 16 2006,10:58) | Shared ancestry predicts shared errors ... no problem. I agree. But Creationism predicts the same thing, namely, the Creator made apes and humans as separate kinds with functional GULO, then both might lose function through mutational degeneration. Big deal. This is what creationists expect. I would expect other species to lose the function in years to come also. What do we find in apes and humans? Voila! 95% similar broken GULO! No surprise there. Even if it is the same substitution (or deletion or whatever) in apes and humans, so what? Humans and Guinea Pigs have 36% (High percentage to use Inai's words) identical substitutions. Why shouldn't apes and humans also have an even higher % of identical substitutions?
Dr. Max does not even say the error itself is identical. He just says both apes and humans have broken GLO. But even if there were some "identicalness" this proves nothing for evolutionists. |
Dave, ONCE AGAIN: 'shared errors' is not the same as 'also contains errors'.
So I tell you what:
You stipulate that humans, apes and monkeys have the exact same 'shared error' that broke GULO. (You've already done as much with, "Big deal.")
In return, I'll hold my nose (something sure smells fishy) to go a huge step further in stipulating that guinea pigs have a very similar error. In other words, we'll accept, for the sake of argument, AiG's little song-and-dance contention that 36% shared 'lesions' indicates such a similarity. (Nevermind for the moment that others have pointed out that they conveniently ignored deletions, etc. to arrive at this figure, or the fact that 36% similarity is hardly a high index -- I'll stop calling them liars for a bit.)
So riddle me this...
We have about a thousand original kinds. (Again, others have contested this estimate as too few to have seeded the earth without some SERIOUS evolution going on, but I'll go with it.) Guinea pigs are part of one original kind (rodent-kind, rat-like-kind, small-furry-child-pet-kind, whatever). Humans are most definitely their own kind. Apes are a third. Monkeys may be a fourth (I'll include the monkey-kind you mention, but you can omit it when you tap-dance, if you wish). These kinds were created independently, but after the fall, random mutations resulted in broken genes like GULO.
Can you please tell me, why (oh why?! , when we look at broken GULO, 3 of the 4 kinds that share the break (out of a thousand or more) are exactly what common descent would predict? Furthermore, whenever we look at a broken gene like GULO, if it's broken in our kind, it's very likely to be broken in the ape kind, a little less likely (but still quite likely) to be broken in the monkey kind, not nearly as likely to be broken in the cat kind or the dog kind (but sometimes), and either not broken, or completely different, or not there at all in amphibian kinds and insect kinds and... Why do we see this, Dave? Even if we spot you the guinea pig GULO, and similar exceptions, we still see this pattern emerge so obviously you'd have to be blind not to see it, and you really need a predictive theory to explain it (i.e., something far better than "shit happened after the Fall", Dave). Common design might predict the working genes being similar in similar appearing species, but by your own admission, it has nothing to do with the broken ones -- creationists don't believe they were designed that way, right?
Do you really fall for "arguments" like the following from the AiG GULO screed:
| Quote | | "If a strong pattern of pseudogenic ‘shared mistakes’ can happen even once in an evolutionarily impossible manner, it can also happen again and again in an evolutionarily consistent manner. Now, more than ever, Occam’s razor dictates that ‘shared mistakes’ be approached in terms of parallel mutations rather than common evolutionary ancestry." |
Do you not see that first sentence as a huge non sequitur? Could we not just as well say, since we know of many exceptions where people have fallen from great heights unharmed, that we may as well start walking out of windows because all bets are off? Or would you rather apply a little probabilistic reasoning in that case? At this point, suit yourself.
Furthermore, speaking of probability, if you accept the AIG argument, you must agree with this:
| Quote | Of course, it is virtually inconceivable that these many identical nucleotide substitutions have arisen solely by chance:
‘Assuming an equal chance of substitution throughout the sequences, the probability of the same substitutions in both humans and guinea pigs occurring at the observed number of positions and more was calculated to be 1.84 X 10-12. This extremely small probability indicates the presence of many mutational hot spots in the sequences.’35
It has long been known that mutations are quite non-random in occurrence, but the variety and complexity of mutational hotspots has seldom been appreciated. Rogozin et al.36 have recently summarized our current knowledge of experimentally induced mutations. Many nucleotide motifs other than the earlier-discussed CG doublet can serve as mutational hotspots. It is now known that the sequence content tens of bases away from a given motif can influence the degree of its hotspot behaviour. Moreover, the propensity of nucleotide motifs to be mutational hotspots varies from gene to gene and from one region of the genome to another. Moreover, the foregoing considerations do not even touch the higher-level features of gene or chromatin structure as causes of mutational hotspot behaviour.37 The large relative number of parallel mutations in the guinea pig and primate GULO pseudogenes cannot be said to be unprecedented. Experimental evidence has already demonstrated that nucleotide substitutions (as well as indels, for that matter) can, unexpectedly, occur in a very strongly concerted manner.38 |
So, given these non-random 'hot spots' and other biochemical phenomena that we are just beginning to understand, I'm sure you would never say anything about mutation being entirely random when it came to the evolution of life, right? And you'd certainly never accept an argument against the probability of a genetic sequence that assumed such simplistic, purely random mutation, right?
Like this one:
http://www.answersingenesis.org/creation/v1/i1/figures.asp
or this one:
http://www.answersingenesis.org/creation/v17/i2/chance.asp
or this one:
http://www.answersingenesis.org/home/area/re2/chapter9.asp
or all the similar ones listed here:
http://www.answersingenesis.org/home/area/faq/probabilities.asp
You and your sources would remain consistent, right?
|
