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To: RightWingNilla
Nice summary of how trangenics are made, but I dont see how this supports your notion that the genome can't handle change which what I was arguing with you about in the first place. I have read hundreds of papers on "knockout" and "knock-in" mice and the results vary tremednously. Sometimes if the gene disrupts a critical developmental program, they die in the embryoinc stage. Sometimes the mice live longer. Clearly the genome can handle change.

Well, I tried to do make it as short as possible, perhaps it was too short. The purpose of the first quote was to show that if you wish to insert a new gene and have it work, you need to also insert other DNA that helps control the use of that gene. The one that expresses the gene for one thing. The purpose of the second was to show what would happen if a gene were duplicated. First of all, if it ends up in a vital part of the genome, the individual would die, this however is a small (but if it happens to you a very significant problem). If it does not however, some things can happen - it may dissappear - even in populations which have been 'seeded' with the extra gene. Chances are even more abominable in real life since no one else would have that gene (mendellian genetics again). However, the real big problem after all the above is that even though the test is being conducted with a new gene which should produce some phenotype changes in the individual - they cannot distinguish the individuals who have the new gene and those who do not! They have to do an entire genome scan to see if it is there! Why is that? Because of what I have been saying all along - a gene which is not intricately connected to the rest of the genome will do nothing. So essentially to get a new working gene, just one, you need what amounts to a miracle. You need:

1. a mutation which produces a duplicate gene.
2. that the duplicate gene does not hurt a vital part of the genome.
3. that the duplicate gene gets spread through the species at chances of 50% survival at each generation (note no selective advantage since the gene is just a duplicate at this point).
4. that the new gene acquires a mutation and then goes through 3 above to spread itself throughout the species again (again no selective advantage yet).
5. that it hits upon the correct helpful mutation by pure chance while going through 3 above after each try.

(Now the above alone should be enough to dissuade a reasonable person, one not blinded by faith in materialistic evolution, to say such a thing is impossible. The above is where we were some 50 years ago when DNA was discovered. Now we know more and the problem is worse.)

6. After all the above though, we still do not have a working gene! Now we need another miracle, we need the gene to:
a) be expressed in the cells where the new function, ability or whatever should go. Since there are some 3 billion cells in the human body finding which ones it should be expressed in is quite a task.
b. be connected to other processes in the organism that will tell it when to do its thing and when to stop doing it.
c. become part of the developmental program of the organism which tells the organism in what sequence each of the cell divisions is to take place. (we start with one cell and the program at each division has to determine what kind of cells to produce until we get a fully formed human being, the program does not stop there though, it continues running and telling the cells what to do until death).

Evolutionists believe however that all the above have happened - and not just once, but millions of times since the first single-celled organisms arose. Now who says that evolutionists do not believe in miracles?

1,605 posted on 06/22/2002 5:44:23 AM PDT by gore3000
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To: gore3000; Godel; longshadow
1. a mutation which produces a duplicate gene.
2. that the duplicate gene does not hurt a vital part of the genome.
3. that the duplicate gene gets spread through the species at chances of 50% survival at each generation (note no selective advantage since the gene is just a duplicate at this point).
4. that the new gene acquires a mutation and then goes through 3 above to spread itself throughout the species again (again no selective advantage yet).
5. that it hits upon the correct helpful mutation by pure chance while going through 3 above after each try.

First off, #2 touches on why the presence of junk DNA helps facilitate macroevolution: If the 73% of our genome that isn't coding nor introns really is junk - in the sense that the specific sequences don't affect the cell's metabolism - then that gives a random gene insertion a 73% chance of not clobbering an existing gene, & therefore not harming the organism in any way.

I think I tried to explain to you before why your #3 is all wrong. Let me quickly try again. (And godel or longshadow or some other mathematician will have to put some real math to my assertions here:)

The chance of any one allele (new mutation in this context) being passed on to a specific child is 1/2. The chance of the same allele being passed on to the second child is also 1/2.

The chance of at least one of these two children getting the mutation is 3/4. With 3 children, it's 7/8. With 8 children it's 255/256.

Put another way: The number of children that will have this new mutation will be (on average) 1/2 the number of children! If the mutated parent has 6 children over its lifetime, then the mutation will spread to three individuals. If the parent has 50 children, then this mutation will spread to 25 individuals, where before there was only one! There is no problem spreading a neutral mutation from one to several individuals.

So your #3, which you think is such a daunting barrier, is no such thing. This makes your #4 & #5 evaporate as well.

1,616 posted on 06/22/2002 12:02:17 PM PDT by jennyp
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To: gore3000
So essentially to get a new working gene, just one, you need what amounts to a miracle. You need: 1. a mutation which produces a duplicate gene. ...

This is generally how new genes are made. I gave several examples before of gene duplication. From the Nature report cited often here:

"Another approach to genomic history is to study segmental duplications within the human genome. Earlier, we discussed examples of recent duplications of genomic segments to pericentromeric and subtelomeric regions. Most of these events appear to be evolutionary dead-ends resulting in nonfunctional pseudogenes; however, segmental duplication is also an important mode of evolutionary innovation: a duplication permits one copy of each gene to drift and potentially to acquire a new function. Segmental duplications can occur through unequal crossing over to create gene families in specific chromosomal regions. This mechanism can create both small families, such as the five related genes of the -globin cluster on chromosome 11, and large ones, such as the olfactory receptor gene clusters, which together contain nearly 1,000 genes and pseudogenes."

How else do you explain these clusters of very closely related genes all adjacent to each other on the chromosome? The authors who sequenced the genome do not doubt for a second that these arose from gene duplication and then subsequently acquired more distinct functions via mutation and selection. Are you arguing that they were “created” that way right off the bat? How do explain pseudogenes? Did the creator purposely put those in there too?

Basically your entire point about the survival value of duplicated genes is pure speculation on your part. Sometimes overexpression of a gene is beneficial to an organism. This has actually been observed in the laboratory:

From here :

“Some early molecular biology experiments concerned how bacterial cells evolve in response to various changes in conditions. These experiments used chemostats - fermentation vessels in which the conditions could be varied. One of the interesting experiments concerned depriving cells which normally required glucose of glucose and providing them instead with another sugar, xylose. Cells from the chemostat were analysed and found to have gained multiple copies of genes responsible for an early stage in glucose metabolism. These additional genes occurred as tandem repeats, a section of DNA repeated a number of times over in sequence. In this situation multiple copies were advantageous because the gene responsible for glucose break down was not 100% specific for glucose. The enzyme had a weak side specificity for xylose. By amplifying the gene, that is having multiple copies, enough of the enzyme was produced to metabolise xylose. The repetition of a section of DNA is believed to occur through an error in copying DNA. A loop can form from a stretch of one strand of DNA and rather than copying this loop once as it should, DNA polymerase may traverse this loop two or more times. Multiple copies also have an indirect advantage. They increase rapidity of subsequent evolution. With multiple copies: The genome makes more experiments with changes to that gene per generation. Mutations that damage one copy only of the duplicated gene are not lethal. It makes possible evolution of a new option. In this example it makes possible the evolution of a xylose metabolism option without destruction of a previous option, glucose metabolism.”

Now it doesnt take much of an imagination to see those extra glucose metabolism genes aqcuiring mutations which make the enzyme more specific to xylose. Run for the hills everyone, we just observed how new "information" is made without a need for intelligent design!

But even if there is no initial beneficial effect in the case of higher organisms, these duplicates are very likely to make it to future generations by virtue of their proximity to the critical genes (the parental gene which gave rise to the duplicates for example) In time some will gain valuable function.

Good recent evidence for duplication of genes evolving into distinct functions in higher organisms:

Here and here

Also you are too hung up on assigning value to every bit of DNA. Maybe much of that "junk" does have a yet to be discovered beneficial purpose, but there certainly looks like a lot of genetic "accidents" which have become trapped in the genome. How in the world do you explain proccesed pseudogenes? Unitary pseudogenes (ex L-GLO)? Whoever "designed" the genome purposely put errors in there? The point is DNA doesn’t have to be “important” to stay. Our chromosomes are so large it would be a trifle to carry around unimportant/non-functional sequences especially if they segregate with pieces of chromosome which DO contain vital genes. Generally you tear the page out of the newspaper that has an interesting story on it. For higher eukaryotic organisms it is completely unnecessary evolve a costly pair of scissors.

6. After all the above though, we still do not have a working gene! Now we need another miracle, we need the gene to: a) be expressed in the cells where the new function, ability or whatever should go.

You are still greatly underestimating the ability of the genome to respond to change! Who are you to say that when new genes arise naturally that they will not be tolerated by the genome? The effects are for the most part are unpredictable; you must think of the genome as more of a recipe book than a blueprint. Adding brown sugar just gives you a different kind of cake. Nature makes sure the recipes which encode for good cakes persist.

I will give you Gore that most changes are likely to be deleterious but surely in the millions of years in the history of life on Earth some of these mutations initially conferred a slight advantage initially and after many of rounds of selection were further improved upon both in regards to their specific function and how they fit into the overall context of the developing organism. Think in terms of tiny, gradual steps.

1,654 posted on 06/23/2002 6:35:21 PM PDT by RightWingNilla
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