The "common creator" myth

I thought that nickname came from their practice of eating limefruits (or similar citrus fruits) on their long boat journeys because the rest of their diet didn't contain enough fresh vegetables/fruits.This is the reason why dieticians (sp?) argue for a varied diet all the time. If you just eat meat, you're going to have a lot of trouble with lack of vitamins.This message has been edited by Melchior, 07-19-2004 11:18 AM

Exactly. It was finding a source of vitamin C to prevent scurvy.

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Aslan is not a Tame Lion

You've never heard of scurvy?

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The Laminator

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Wah? Of course I have. That's why I posted. But it was the statement "The vitamin C comes from all sorts of foods.. Capt Cook gave the British the nickname "limies" because of it." which confused me because it made it sound like limies was derived from something else than the citrus fruit.

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First of all, how do you know what is a mistake?

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vitC is not produced in the body. That is the first clue. The second clue is that there isn't any RNA product for that gene. That is, the gene isn't turned on. We then look at the gene in other organisms that controls vitC production and try and find a similar gene in humans/primates. We find the same gene in humans/apes, but the sequence is slightly different. It is called a pseudogene because it resembles other functional genes in other organisms, but does nothing in the organism under examination. It is like finding a chip in a computer that isn't hooked up to anything. It obviously had a function at one time but now it is just taking up space.We know which GLO's (gene responsible for the enzyme that makes vitC). In fact, a rat GLO gene was inserted into a monkey cell line and functinal GLO was measured.
1. Expression in monkey cells of the missing enzyme in L-ascorbic acid biosynthesis, L-gulono-gamma-lactone oxidase - PubMedThe pseudogene may have been partially created by a retroviral insertion. Also, the absence of vitC may have led to a higher free radical concentration in the blood and led to higher mutation rates. This may have helped speed up primate and human evolution:
1. Retroviruses, ascorbate, and mutations, in the evolution of Homo sapiens - PubMed
2. Did the loss of endogenous ascorbate propel the evolution of Anthropoidea and Homo sapiens? - PubMedSome in the health field are even talking about reinserting a new GLO gene into humans to correct for the pseudogene:
1. Homo sapiens ascorbicus, a biochemically corrected robust human mutant - PubMedIf we go by the "common creator, common creation" then why are there pseudogenes? Why are there stretches of DNA that are non-functional in humans/apes but almost the same exact sequence in other animals is functional? Human's don't do this when they design things, and therefore it can be argued that anything intelligent wouldn't design this way either. They don't include parts that don't work just because similar designs have the same, but functional parts. What does make sense is that the gene was knocked out, and the remanants remained in subsequent generations. The fact that we find the same knocked-out, ineffective gene in both apes and humans supports the theory that we had the same common ancestor, or the same "great great grandfather" if you will. It is amazing that once pseudogenes were found in other organisms such a relationship between apes and humans was PREDICTED by the theory of evolution. The first evidence for human/ape common ancestory was not pseudogenes, but the fossil record. The next question is why non-functional DNA should support what we find in the fossil record, and also why this non-functional DNA should support the theory of evolution so spectacularly.

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So you would have to have the DNA code of the parents AND kids to know if something is a mistake? If this is the case, I am confused as to how we know that we share the same "mistakes" as monkeys and not the same design patterns.

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You would find the mistake before knowing who the parents were. Take the kid mentioned in other threads that has a mutation in his myostatin gene, which has caused him to have large muscles. We would expect that his parents both have one copy of the mutated gene. Of course, it is possible that one of the child's genes spontaneously mutated. However, if every single one of his brothers and sisters had the same mutation, then we would expect the parents to be the source.As to design patterns, what does a broken gene do for "design patterns". It is like asking what kind of house a broken hammer can build. It CAN'T build a house, and in the same way a pseudogene does not add to the design pattern. There are examples of pseudogenes that are transcribed and do affect the cell, but then these are no longer pseudogenes but rather full fledged genes. Also, HERV's are viral insertions found in humans. Just like pseudogenes, they also support common ancestory between humans and apes. Go to http://www.pubmed.com and search for "ERV human evolution".

Thank you for your reply. So would this gene be classified "junk DNA"? I've heard that possibly 90% or more of our genome is junk DNA and is supposedly leftovers from billinea of evolution. But I've also heard that there have been recent discoveries that this junk DNA serves a purpose after all.Also, this WOULD be relevant to the info/complex debate. If these mutations are common, this would be a source of significant reduction in information. True.

This really has nothing to do with the pseudogenes mystery, but I just thought I'd point out that according to the Bible, Adam and Eve's original diet was fruit.

You don't get to say that until you define what you are talking about. What is "information" how do you calculate a reduction? A mutation that is "harmful" may be an increase in genetic information there is not connectionb between it's affect and the amount of information change it represents.

Thank you for your reply. Ok. Thanks for clarifying that for me. I was under the impression from the info/complex debate that mutations do not ever loose information, but only change it and add to it. Does this mean they are EXACTLY different as described in the OP? In other words both humans and apes have gcd 'A' dcg : same letter same place in the code that neutralizes it? This sounds very important. Does this mean a retrovirus can infect a person or ape and leave them with genetic mutations? Just makes me wonder if humans and monkeys could have been hit with the same virus that caused the same mutations in both. I thought free radicals were what caused cells to break down quicker leading to earlier death. Without free radicals wouldn't we live longer healthier lives? It seems like this affect would outshine the evolutionary benefits (which, after all our debating in the info/comp forum I'm still not sure actually exist), especially when most mutations are not beneficial. It seems to me that this would be about like giving everyone a piece of uranium to put in their pants so that humans will evolve quicker... But this is just my opinion. Merely speculation here, but as another thought, perhaps our creator created us with the functional gene which produced ascorbic acid which knocked out free radicles and was one of several causes for the long lifespans mentioned in the Bible (up to 800-900 years). Viruses are commonly spread from apes to men. Soon after the flood a virus hit the whole (small) population of both apes and men causing the mutation and the shorter lifespans as described after the flood.Could you please explain the meaning and significance of a retroelement? Also, this says that code is missing from the GLO gene. I was under the impression that an added letter made it non-functional. I assume the former is correct. Sounds like a good idea to me. I described a possible scenario above. Please tell me what you think about it. Could you please point me to this evidence? I was under the impression that no undisputed missing link had been found, partly because the slightest possibility of a "missing link" sends scientists into a joyful frenzy. Like I mentioned in another post, I was under the impression from our other debate that mutations never stopped the function, but only changed it. This makes me curious as to the stats of the percentages of mutations that cause pseudogenes. How many pseudogenes to we carry in our code? I mentioned junk DNA in my other post. Does this have anything to do with junk DNA? I read a few of the articles, but failed to see how this supports common ancestory. Let me make sure I'm understanding correctly. An endogenous retrovirus is a virus that proliferates in it's host over and over again by hijacking host cell's for RNA reproduction. An exogenous retrovirus goes from host to host doing this?Thank you again for all of this info. It's been very helpful.

Would you like to enlighten us on what purpose these pseudogenes serve?Reminds me of an outer limit episode I saw a while ago. This doctor discovered that the pseudogenes actually code for christmas future.

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The Laminator

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Yes. There are actually a number of different ways this can happen but the simplest is a virus inserting its DNA in the middle of a functioning gene. As you can imagine this messes up the gene’s sequence and is likely to leave a gene dysfunctional. Of course to be passed on to offspring (and therefore to be of much interest evolutionarily) the virus would have to insert its DNA in a sperm or egg cell. First off I (personally) don’t think it likely that a virus or other mobile element caused the mutation in the GLO gene, all the primates share a deletion that means that the rest of the gene is out of frame (because DNA is read in groups of three letters at a time deleting one letter ruins anything that comes after that letter.) Mobile elements are good and making lots of different genetic rearrangements, point deletions are not one of them.Still, even if the mutation is due to a virus it is incredibly unlikely that the exact same mutation occurred in apes and humans independently. We have 3 billion base pairs of DNA, do you think it is more likely that a retrovirus has inserted DNA copy into the exact same spot in monkeys and apes and humans or that an ancestor of all these 'groups' (I wouldn't actually call humans a group distinct form apes but that's besides the point) contained this insertion and passed it on to all its descendants.In the interest of full disclosure retroviruses and other mobile elements do actually "look" for certain target sites to insert their DNA. However these target sites are usually on a few DNA letters long meaning rather than having a few billion spots that they could insert in they probably have a few thousand — it’s still highly unlikely that two unrelated lineages would carry the same insertion in the same spot. It’s the same thing that I have tried to explain above, if an ERV is in the same spot in the genome of a monkey and a man but not a prosimian then we can say that the ERV inserted in that spot after a common ancestor between prosimians, monkeys and humans but before or in a common ancestor between humans and monkeys. By looking at lots and lots of such sequences in lots and lots of different organism you can draw cladograms (family trees if you like) detailing when different groups of animals branched off into different lineages.EDIT: You know, instead of writing that reply I could have linked to this exellent piece from talk.originsThis message has been edited by biochem_geek, 07-20-2004 12:01 AM

Yep. Junk DNA is actually a term that gets misinterpreted a little bit, if by junk you mean sequences of DNA that don’t ever get made into mRNA (or functional RNAs to be pedantic) then the human genome is about 98.5% junk. It is true that is becoming clear that pieces of junk DNA regulate the expression of the rest — but I think most people thought that would happen. It was just a matter of looking at the genes - a system we could understand — first.Also around half of the genome is from mobile elements, genetic parasites like the LINE-1 and Alu elements that copy themselves to different locations and doesn’t really much explanation beyond the parasites success and using us as a host. There is a school of thought that such elements might be favoured by natural selection because of benefits to the host genome. Although they certainly can provide some nifty things for a host (Drosophila telomeres and aspects of the vertebrate immune system are the result of domesticated mobile elements) I think overall that their presence is deleterious to the host and better described by them acting as parasites. It’s an interesting topic and I could talk about it for days but should probably stop now before I bore anyone still reading this to death Obviously stuff like pseudogenes really just are junk being carried along for the ride.This message has been edited by biochem_geek, 07-20-2004 12:02 AM

Thank YOU for your replies as well.

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Ok. Thanks for clarifying that for me. I was under the impression from the info/complex debate that mutations do not ever loose information, but only change it and add to it.

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Info/complexity can be gained, lost, or go unchanged because of mutations. Natural selection decides which is better within the given environment.

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Does this mean they are EXACTLY different as described in the OP? In other words both humans and apes have gcd 'A' dcg : same letter same place in the code that neutralizes it?

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As another poster above mentioned, there is also a point mutation that caused the gene to be out of frame. The best explanation for two species having the same exact insertion in the same exact spot is common ancestory since the probability of two species having the same mutation by chance is astronomical (1 in 3 billion).

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Merely speculation here, but as another thought, perhaps our creator created us with the functional gene which produced ascorbic acid which knocked out free radicles and was one of several causes for the long lifespans mentioned in the Bible (up to 800-900 years). Viruses are commonly spread from apes to men. Soon after the flood a virus hit the whole (small) population of both apes and men causing the mutation and the shorter lifespans as described after the flood.

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Retroviruses randomly insert into the genome. They have a preference for areas in the genome that are actively transcribed, but they are still random. Just like the mutation above, the chances of two species having the same insertion at the same spot in the genome is highly improbable (again, 1 in 3 billion). The fact that we find numerous such insertions that are the same in chimps and humans is VERY strong support for common ancestory, not common design. It would be like two people having the same fingerprints, retinal pattern, social security number, name, age, birthdate, and ice cream flavor preference.Viruses don't seek out one base in the genome, they RANDOMLY insert. Also, this insertion has to be a mistake on the part of the virus. That is, the insertion is a failed attempt at using that cell to create more viruses. Second, it has to have this error in a sperm or an egg. Third, this sperm or egg then has to grow up to be an adult. Fourth, this insertion then has to spread through the entire population through reproductive success. Even today there are human ERV (endogenous retroviral insertions) that not everybody has. That is, the ERV has not spread through the whole population. We have observed the insertion of retroviruses and we know that they are random. We have scanned the human genome for ERV's, and we know that they are spread randomly through the genome.For your scenario to work you would need two things to happen that have never been observed:1. Non-random, base specific insertion of a partial retroviral sequence.2. The same non-random, base specific insertion happening across several species, at the same time, population wide.

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I thought free radicals were what caused cells to break down quicker leading to earlier death.

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If concentration of free radicals is high enough, yes. Just as a little aside, neutrophils (a white blood cell) commits suicide by engulfing foreign material such as viruses or bacteria and releasing large amounts of oxygen free radicals. In the right conditions, free radicals are actually useful.In relation to mutation rates, a slightly higher concentration can elevate the mutation rate without significantly affecting lifespans. There are other molecules in the body that also bind free radicals, such as urea.

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Could you please point me to this evidence? I was under the impression that no undisputed missing link had been found, partly because the slightest possibility of a "missing link" sends scientists into a joyful frenzy.

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There are still some gaps that science would like to fill, but the fossils in hand already support common ancestory for new world apes and humans. We may not know the exact lineage, but the theory of common ancestory has been evidenced in the fossil record. Go here for a run down of the numerous species and the hundreds of fossils. These are undisputed links between man and ape. They are only disputed by creationists, and only then because of religious issues, not scientific ones.

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Like I mentioned in another post, I was under the impression from our other debate that mutations never stopped the function, but only changed it.

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Sorry if I caused any misunderstanding. Mutations can and do knockout gene function. Whether or not that mutation spreads through the population depends on it's benefice or detriment with regard to fitness.

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I read a few of the articles, but failed to see how this supports common ancestory. Let me make sure I'm understanding correctly. An endogenous retrovirus is a virus that proliferates in it's host over and over again by hijacking host cell's for RNA reproduction. An exogenous retrovirus goes from host to host doing this?

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Just in case my explanation above is hard to explain, I will try and give another description. ENDOGENOUS sequences are failed attempts at hijacking the cell. The full genome of the virus was not able to insert, and so the virus was unable to use the host cell to make more copies of itself. This insertion can either spread through the population or disappear after a few generations because a certain lineage dies out.Some viral insertions have been shown to be beneficial, such as one that is involved in placental development in mammals. In fact, it might have been an important step in going from marsupialism to placentalism. Other viral insertions do nothing, and still others cause cancer in somatic cells or other developmental problems. In other words, insertions are random with respect to reproductive fitness, just like random mutations are. In fact, insertions are treated AS mutations since their insertion is close to random and their effects are random.Just a quick summary. The important aspects of retroviral insertions are:1. Close to random insertion (slight preference to areas of the genome that are actively producing RNA).2. ERV's are broken viral sequences.3. The only mechanism for spreading an ERV to the rest of the population is through reproductive success.4. ERV's are random with respect to benefice, neutrality, or detriment.5. ERV "trees" (cladograms constructed through ERV comparisons between species) reflect what we see in the fossil record.

Just thought I would post some of the primary literature that relates to human pseudogenes. This article describes research that found 8,000 pseudogenes in the human genome. Being that there are approx 32,000 active genes in the human genome, it would be very surprising that humans could survive losing 20% of their genes during "The Fall" and survive. This article describes research that found 5,000 pseudogenes in mice. 40% of those pseudogenes are shared by humans, while 60% occured after the divergence of the mouse and human lineages.This message has been edited by Loudmouth, 07-20-2004 04:12 PM

Hi Hangdawg,Sorry about the lack of replies in the last couple of days - I've not had the time to really sit down and type (I only normally get the chance to get two decent sized posts a day anyway).I'd like to focus you on a couple of things related to the original post:As you can see its' not just by comparing pure sequence data like a showed with the smileys in my first post. Things like (dormant) retroviruses and pseudogenes point to common ancestors as well, but it works in the same way - by looking at shared genetic events. As someone (I think was Rrhain) pointed out earlier, its not a matter of needing the parents' (or in this case common ancestors') DNA, its' a case of comparing the existing descendents. Comparing the DNA from your generation of your family would be sufficient to show how you were all related (ie sister, cousin, second cousin) without the need for your great great grandmothers' DNA sequence The question to ask when thinking about the evidence for common ancestry on the species scale is this:Which is more likely, that a particular retrovirus independently inserted into a genome at exactly the same place in two separate species, or that they just inherited the same artifact from a common ancestor?The second thing is about the way that you look at the pure sequence data. Try not to think about the morphological differences between species, more about what the pure sequences (and the differences) tell you. There is something that keeps on getting said on these boards that I think is relevent here: most mutations are neutral! Most base changes don't have the slightest bit to do with whether a species walks on two legs or whether it has an opposable thumb, they just turn up from time to time and get passed from one generation to another. That's what you are effectively looking at when you compare sequences - the accumulation of neutral mutations overr time.This message has been edited by Ooook!, 07-20-2004 01:43 PM