The "common creator" myth

Mutations cover the spectrum - they can add information (e.g. insertions), delete information (deletions), or vary the information without changing the total amount of it (substitutions). Insertions and deletions (indels) can also result in frameshift mutations (if the resulting change isn't some multiple of 3 nucleotides).Here's a link to an article describing a 92-base-pair deletion mutation that occurred in the human lineage after it split from the chimp lineage (note that 92 isn't a multiple of 3, so this deletion resulted in a frameshift mutation): PNASDeletions can be anywhere on a spectrum of effects, from beneficial, to neutral, to harmful. Likewise for mutations that add information, or mutations which don't alter the amount of information.A given mutation can also be a mixed bag - it may make humans more susceptible to some diseases, but increase their intelligence compared to other primates. Another mutation may thwart malaria in mosquito-infested areas, but cause homozygous individuals to have sickle-cell anemia.Mutations also vary greatly in magnitude of the sequence affected ): from point mutations, to a gene (part or whole), to a group of genes, to a chromosome, to the whole genome. Note that the size of sequence change is not necessarily proportional to its effect on the organism. For example, a tiny point mutation may be lethal in some instances, while a wholesale duplication of the genome (polyploidy) may have little visible effect on the physical appearance of the organism (for example, the red viscach rat has nearly twice the number of chromosomes as its nearest relative, with the exception of the sex chromosomes - but you can't tell it's a tetraploid simply by outward appearance.)One of the common ways in which mutations cause increase in genetic information is the combination of gene duplication (caused by uneven crossover during replication) followed by point mutation. Many instances of such "gene families" are known. Compare the various hemoglobins for examples, or the bloodclotting proteins (and other serine proteases). You can peer even deeper into evolutionary time by comparing hemoglobins with myoglobin, and deeper still with a comparison to leghemoglobin from plants - but when you go back that far, simple sequence comparisons alone are inadequate, and the best method for comparing them is to perform a structural comparison using VAST - Vector Alignment Search Tool. I recently used VAST to compare horse myoglobin and yellow lupine leghemoglobin (using the Cn3D - "See in 3-D" - structure viewer, and was awed at how similar the structures are after all these eons of evolution). Which reminds me, I wanted to clarify something about evolutionary rates: particularly crucial proteins generally evolve quite slowly (such as histones, cytochromes, etc) while less crucial ones evolve more rapidly.Fortunately, wonderful comparison tools are all available online (BLAST = Basic Local Alignment Search Tool, VAST, etc.), so you can do all these data comparisons for yourself. The National Center for Biotechnology Information (NCBI) has great tutorials online.

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Mutations cover the spectrum - they can add information (e.g. insertions), delete information (deletions), or vary the information without changing the total amount of it (substitutions). Insertions and deletions (indels) can also result in frameshift mutations (if the resulting change isn't some multiple of 3 nucleotides).

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I was under the impression that the information contained in a gene depended on the activity of the protein it coded for. A stretch of 100 random amino acids that have no activity and bind to nothing has less informtaion than the 52 amino acid protein ferredoxin that is part of the metabolic pathway of anaerobic bacteria. A one base insertion can render the coded protein useless to the organism, or it can give the protein function as in the case of the nylon bug. Subtraction of code may cause a change in binding specificty, or an increase in enzyme activty. Or, a subtraction of bases may have the opposite effect. In one of the bacterial systems I work with, the subtraction of the first 15 or so amino acids would result in internalization instead of transport to the extracellular mileu. This is how I view information in the DNA sequence, by the functionality of the coded or mature protein.Added in Edit:

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Fortunately, wonderful comparison tools are all available online (BLAST = Basic Local Alignment Search Tool, VAST, etc.), so you can do all these data comparisons for yourself. The National Center for Biotechnology Information (NCBI) has great tutorials online.

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I think creationists call these the "tools of the devil". Only an evil tool would support the theory of evolution so completely.

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Which reminds me, I wanted to clarify something about evolutionary rates: particularly crucial proteins generally evolve quite slowly (such as histones, cytochromes, etc) while less crucial ones evolve more rapidly.

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This is why work with molecular clocks use mutations in neutral locations in the homologous genomes to measure mutation rates. This gives them an idea of the basal mutation rate, and has had limited success in matching rates with fossil species divergence times. This method has not been fully accepted within science (for very good reasons), but it does have some promise.This message has been edited by Loudmouth, 07-21-2004 12:18 AMThis message has been edited by Loudmouth, 07-21-2004 12:23 AM

Thank you all for the info.I'm still around. I just haven't been able to get back to reply. I'll do so as soon as I can.

Hey Dawg, will you be careful? If you keep asking good questions and thinking about the answer we might lose you as a YEC'er. We don't have enough that are coherant so we don't want you to go too far, ok?

Hangdawg13 responds to me:

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In order to eliminate something, there needs to be something pushing for elimination.

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You might say that a lack of vitiman C would cause the immune system to be so weakened as to weed out those individuals

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No, you might not. Despite what many people claim, vitamin C does not radically bolster the immune system. It does not prevent colds, it does not make them go away any faster.

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Humans and other primates get sufficient vitamin C from their diets, thus they do not need to synthesize it for themselves. So if they were to experience a mutation in their ascorbic acid synthesis genes (again, begging the question of why they would have such genes in the first place), they would never notice it.

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Where does the Vitiman C come from in our diet?

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(*blink!*)You did not just say that, did you?Are you seriously asking where vitamin C comes from in our diet? Well, for the average modern American diet, we get most of our vitamin C from potatoes. Fruits and vegetables are good sources of vitamin C.

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Now, answer the question: Why would a designer who has decided that the organism is going to acquire it's ascorbic acid via diet put in a BROKEN ascorbic acid synthesis gene?

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If you'll be patient, I'll get around to that

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No, I'm impatient for that is the crux of the matter: Why would a designer but in a broken system?

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Quite a fair way. It's because of these mutations that we are able to create genetic family trees showing the path of evolution.

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I need to know more specifically what our first ancestor was that did not have this mutation.

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No, you don't. Tell me what difference it would make to know if such-and-such species were the direct ancestor?

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what does the fossil evidence show of him?

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Fossils are very poor sources of DNA. We don't make the determination from fossil evidence. We make it from genetic evidence. As I said, there are molecular clocks from which we can determine when a certain mutation took place. That evidence does not tell us which specific species it took place in directly. Instead, it gives us a timeline of when it happened.You are asking the wrong question.

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I need to know the differencences that exist between us and him as in the mutations that have accrued.

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No, you don't. You're simply going down the road of claiming that because we don't know everything, that means we know nothing.

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We have genetic clocks that show us how quickly organisms mutate.

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So how fast do primates mutate? How many mutations per generation?

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Why don't you go look it up?The human mutation rate is approximately one per billion base pairs. This puts each human at having three to six mutations compared to his parents, on average.

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Only a few of the splinters of the mammalian ancestor acquired the broken GLO.

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What others besides humans and primates?

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Why don't you go look it up? Why do I have to do your homework for you? Especially since I already told you...weren't you paying attention?

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Rrhain
WWJD? JWRTFM!

Hangdawg13 responds to contracycle:

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What does the ascorbic acid gene do now that it is broken as you say?

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Nothing. That's why it's called "broken."The chemical process, as I already explained to you, involves a multi-step process converting glucose into ascorbic acid. If I recall the process correctly, it is in step four that the process breaks down. It goes something like this:The presence of glucose triggers a gene to produce an enzyme that converts the glucose into the next chemical product. The presence of that chemical product triggers a gene to produce an enzyme that converts it into the next chemical product. The presence of that chemical product triggers a gene to produce an enzyme that converts it into the next chemical product. Eventually, this results in a molecule of ascorbic acid.On the fourth step of this chain, the enzyme created does not convert the product. Thus, no ascorbic acid is produced.

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How many identical 'broken' genes like this one do we share with primates or other mammals?

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Quite a few. Why don't you do some research and get back to us? Why do we have to do your homework for you?

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and what do THESE broken genes do now that they are broken?

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Again, nothing. That's why they're broken.

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Rrhain
WWJD? JWRTFM!

Hangdawg13 writes:

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Adam and Eve's original diet was fruit.

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No, they ate meat. Abel was a shepherd, after all.

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Rrhain
WWJD? JWRTFM!

Thank you for your reply. That was my next question. Well, I'll put the common virus theory on the backburner unless other information arises. Whew... thats a lot of info... and much of it is over my head since I lack a background in genetics.
I attempted to understand as much as I could though.Something I would like to know that this page could not answer is how often do pseudogenes form today?

Thank you for your reply. Wow... Half is a lot. I realize genetic viruses work differently than computer viruses, but my computer had only ten viruses on it at one time and almost quit working. It had to have the hard drive totally reformatted. Nah.. its very interesting.

Well, I must point out that Bio dude also said that some viruses attack certain genes greatly improving the odds, but still not to an acceptable level. So I will set my common virus theory aside.I understand ERV's much better after reading that article from talkorigins as well. Thanks for the summary.

Thank you for your reply. As far as I know the latter. Yes. It makes me wonder, though, how an organism with all of the "broken" genes fixed would compare with the original.

Haha... Fortunately, I've "evolved" a thick skull, an open mind, and an intense desire for warfare, be it with guns or brains, so I wouldn't count on me becoming an ex-YEC'er any time soon.

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Well, I must point out that Bio dude also said that some viruses attack certain genes greatly improving the odds, but still not to an acceptable level. So I will set my common virus theory aside.

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I don't know about "greatly improving the odds" because each insertion has to spread through the entire population. On top of that, this ERV has to be in a germ line cell (sperm or egg). That egg or sperm has to grow to an adult. That adult has to have children, and his lineage must include every man woman and child alive today. And this has to happen for every species out there. On top of that, the mutations within the ERV have to match up with evolutionary predictions. The pattern of ERV insertion has to match up with the patterns found in supposedly "different kinds". The chances of two insertions being the same between two species is only the tip of the probability iceberg.What would be the testable creationist theory that explains these insertions? It would seem to me that evolutionary theories are able to predict the occurence of ERV insertions in homologous positions between different species quite well. The pattern of olfactory pseudogenes that someone else mentioned in another thread also is consistent with common descent and evolutionary predictions. Also, the mutations found within the ERV insertions also follow patterns of common descent and evolutionary pathways. That is, descendants inherit the mutations from the parent species and then add their own, which future descendents then pass on to subsequent generations and species.The problem I have is that creationists (not you in particular) ignore this type of evidence. They fail to understand the underlying mechansisms that create features in DNA, such as the random insertion of viral sequences and the disruption of functional genes. On top of that, they think that there are just a few isolated cases when in fact we share thousands of pseudogenes with other mammals, and numerous ERV insertions. If evolution and common descent were not true, then we would not expect such a high rate of correlation between the patterns we would expect and the patterns we observe. The theory of evolution, by this thread alone, is not just a cooked up fairy tale, but a theory that has very concrete, testable, and falsifiable evidence. The only way to avoid this evidence is to handwave it away by cooking up an ad hoc hypothesis that has no supporting evidence (eg, there was a virus in the past that always inserted in the same genomic position).

Alright, two more questions I have not found an answer to:At what rate are pseudogenes forming today? How often do new or varied forms of ERV's enter our genome? And what on average is the difference in number of mutations between 2 average people? What are the differences between a human and an ape?Edited to add: Oops, guess thats 4 questions.I found an article here: http://www.cs.unc.edu/~plaisted/ce/index.htmlThat discusses mitochondrial mutation rates and such which point to humanity being approx. 6000-10000 years old. (Avg of 18 differences in Mit DNA between two people; 33 generations per mutation; 20 year generations)I was wondering if there is a similar comparison with DNA in the nucleus between people and apes.This message has been edited by Hangdawg13, 07-23-2004 01:26 AM

They only worked the ground and ate meat after the fall.This really, hasn't much to do with the debate though.