Of interest to the 'non-random' types...

It is often claimed - including by some that post on this board - that transposition events are non-random and therefore evidence of design, or at least evidence that non-random events occur and therefore 'RM&NS' is disproven.The argument goes something like this(and is usually accompanied by quotes describing insertion):-Inserting elements in the genome requires proteins
-these proteins are often encoded on the inserting element itself
-the event occurs at specific loci
-therefore, the insertion event itself is non-random, i.e., directed, and therefore, the notion of random mutation ismoot.I cited this in another thread, but it is important in a stand-alone thread on the topic of randomness (any emphases mine):Genome Res 2001 Dec;11(12):2050-8
Genomic characterization of recent human LINE-1 insertions: evidence supporting random insertion.Ovchinnikov I, Troxel AB, Swergold GD.LINE-1 (L1) elements play an important creative role in genomic evolution by distributing both L1 and non-L1 DNA in a process called retrotransposition. A large percentage of the human genome consists of DNA that has been dispersed by the L1 transposition machinery. L1 elements are not randomly distributed in genomic DNA but are concentrated in regions with lower GC content*. In an effort to understand the consequences of L1 insertions, we have begun an investigation of their genomic characteristics and the changes that occur to them over time. We compare human L1 insertions that were created either during recent human evolution or during the primate radiation. We report that L1 insertions are an important source for the creation of new microsatellites. We provide evidence that L1 first strand cDNA synthesis can occur from an internal priming event. We note that in contrast to older L1 insertions, recent L1s are distributed randomly in genomic DNA,and the shift in the L1 genomic distribution occurs relatively rapidly. Taken together, our data indicate that strong forces act on newly inserted L1 retrotransposons to alter their structure and distribution.*The creationist will doubtless use this to reassert their claim of non-randomness. But to do so will be an exercise in sophism.

Lets even give ourselves the ability to strech and bend space as in some sense in the cosomology discussions THEN it seems to me that this specific issue in acutal TRASPOSON knowledge does not mitigate AGAINST there being some GENERATIONAL randomness (in WOlfram's sense) aka ( I agree with you).When I was reading the story of Barbara MClintock I was rather dismayed as this spanned the time frame that my grandfather was teaching evolution and making students "disssY" counting fruit flies. It seems to me that the whole notion of randomness (not chance)(in biology here) is caught up the incidental -)overlap(- of chromosomes and genes as factors and that we would be so discussing chance significances within this (phenomenology) of the overlap.But rather what traspired historically is that people began to get to bacteria etc and work conceptually with introns, codons etc that whatever statistcally unclear atomic varations involved physical chemically were already materially in part in the discussion (which was not in the same when discussed by types such ar McClintock and Mayr etc). There is a scaling problem in addition to the conceptual one of said Shift with respect to transposons, position effect, unity of genotypes, genome molecular biology etc. I hop and hope this helps.

Dear Page,P: The creationist will doubtless use this to reassert their claim of non-randomness. But to do so will be an exercise in sophism.The 'creationist' (recently converted, thanks to you ) says:"Thanks a lot and I will spell it out".Best wishes,
Peter

Do tell....

The argument goes something like this(and is usually accompanied by quotes describing insertion):-Inserting elements in the genome requires proteins
-these proteins are often encoded on the inserting element itself
-the event occurs at specific loci
-therefore, the insertion event itself is non-random, i.e., directed, and therefore, the notion of random mutation ismoot.I cited this in another thread, but it is important in a stand-alone thread on the topic of randomness (any emphases mine):Genome Res 2001 Dec;11(12):2050-8
Genomic characterization of recent human LINE-1 insertions: evidence supporting random insertion.------all of the above is a quote from within this thread-------------The important thing that I noticed whether in bold or not is as to (as if) KNOWN supporting evidence from random insertion. It would be fun to chrip up the argument in detail but I am rather thinking likely not in line with the majority here.I have recently been reading TOPOBIOLOGY by Endelman and I find that Richard Lewontin's commnetary rather even obsfucates the thing even more. I was struck particularly by a sentence that stated to the paraphrase that 'development is nonlinear with respect to any mutational change' which seems to me relevant if I may have another go in this rope to the topic of it some design is being had on the insertion being "non-random". The question wholly comes down the specific plotting of whatever this "non-linear" CORRELATION would be if the data was there...but that is not all since the argument details remand that the insertion is at a particular loci so what the thread says to my reading is that there is TRANSPARENCY in the evolution and developemtal question where Lewontin sought to use language to answer in the (in my language-- syntactics of map perceptive communication---) but to each his words own....

but what of the RANDOM base shifting caused by some chemicals and inorganic compounds....they float about and simply get stuck where they get stuck...moving all the pairs on one of the helix's along on base thus screwwing up the entire genome after that event, mostly leading to direct cell detah...sometimes (rarely) leading to freaky mutant characteristics..this is a completely random event and is not effected by anything that the cell/body can do against it...does that fuel any ones arguments?Bread

Thread moved here from the The Great Debate forum.

SLP:
It is often claimed - including by some that post on this board - that transposition events are non-random and therefore evidence of design, or at least evidence that non-random events occur and therefore 'RM&NS' is disproven.judge:
It seemed from my reading of the various posts that the problems (in part at least) depended on different definitions of random.
Even though mutations are described in everyday language as being "non random"...in that they don't appear to happen "randomly", if they contain any random element at all they are still technically random, and so NDT holds.Does NDT need to be changed to accomodate the same sequences arising again and again in seperately created genomes?Again and again I have been assured (not primarily on this forum) that the chances of say, the sequences shared by apes and humans arising independently are "laughably improbable".But I am still not sure how we can say this.
Apparently when we look at mutations occuring in life forms with far shorter generations than ourselves today we see random mutations becoming fixed in different lines.How do we know these assumptions apply to previous generations of man and apes.
Is there a simple way to demonstrate this to a layman like myself?
(apologies for any obvious errors in this post...I am pushing the boundaries of my own knowledge)

Hi judge,

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Does NDT need to be changed to accomodate the same sequences arising again and again in seperately created genomes?

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The flaw here is that the genomes are not separately created but share a common ancestor. I could be misunderstanding your question. Do you mean that if a similar or the same mutation occurs in clearly unrelated organisms how does one account for it?If the latter is more relevant to your question, there are mutational hotspots i.e. though where a mutation will occur is random not all mutations are equiprobable. For example, of the four bases in DNA (ACGT) transitions C to T are more likely than say A to C. Some specific DNA sequences can be more exposed than others..after all, DNA is a structure.

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But I am still not sure how we can say this.
Apparently when we look at mutations occuring in life forms with far shorter generations than ourselves today we see random mutations becoming fixed in different lines.

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How do we know these assumptions apply to previous generations of man and apes.
Is there a simple way to demonstrate this to a layman like myself?
(apologies for any obvious errors in this post...I am pushing the boundaries of my own knowledge)

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We know these assumptions apply to humans and other mammals from studies of population genetics. Also (to a limited extent) from the study of DNA from fossils.cheers,
M

Hi Judge, Maybe I can help by explaining it in a different way then M. People often say random when what they really mean is equiprobable, and by that I mean that the probability of a singel event is the same across all possibilities (ie mutation at a single nucleotide accross a long string of nucleotides in a gene). Mutations accross a chromosome or a long stretch of DNA is not equiprobable for any given site, the probability of a mutation at a site varies based on the sequence at that site and relative to teh surrounding sites. Add in the fact that mutations are not equiprobable w.r.t. time, ie mutations can increase during times of cellular stress, and you begin to get an idea of what "random" mutation really is.That said, the probabilities can be roughly calculated for a specific mutation in a specific sequence. The same holds true for transposon insertion, differences between transposons and aspects of sequence specificity can also play a role. It is from these calculations that statements such as

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the sequences shared by apes and humans arising independently are "laughably improbable".

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properly arrise.Hope that this helps and does not increase the confusion. ------------------
"Chance favors the prepared mind." L. Pasteur
Taz

Thanks mammuthus and tazimus!If you could indulge me a little further? If for example we all went to the casino and you two wandered off to try your hand at blackjack whilst I opted for roulette. Then after some time we met up again whereupon it was revealed that sadly you two had "done your dough", while I had turned my meagre initial ammount into a staggering fortune. (now I'll show them all) }(
When you enquired how i had done this I merely stated that I always bet on the number 12 and then in the following spin bet all my winings on 12 again.
You would then say no doubt...that is laughingly improbable!!You could say this because we know that the odds of 12 coming up are 1 in 37 (I think).
So my question is...Is it possible to see the maths that shows the improbabilty of common sequences occurring between men and apes?[This message has been edited by judge, 05-23-2003][This message has been edited by judge, 05-23-2003]

judge writes:

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So my question is...Is it possible to see the maths that shows the improbabilty of common sequences occurring between men and apes?

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Given our current knowledge, no. We have no idea what the constraints are. To take your roulette example, the reason we know that there is a 1 in 38 (most Vegas casino roulette wheels have both a 0 and a 00 slot) probability is because we know what all the possible outcomes are and that each one is equally likely.For something like what mutations are required to differentiate humans and the other apes from the common ancestor, we would have to know the specific environmental factors which are myriad.And it isn't just a simple question of which mutations show up in individuals...we need to know which ones make it to reproduction which is not always a factor of the mutations being "more beneficial." That is, if the tree falls on you before you make it to reproduction, it doesn't matter if your genes would have made you a generally sturdier creature than your fellows...the tree fell on you and not them.And on top of all of that, we need to make sure that we don't confuse the probability of getting a specific outcome with the probability of getting any outcome at all.Suppose I have a standard deck of 52 cards and I draw one.What is the probability of drawing the Ace of Spades?
What is the probability of drawing an Ace?
What is the probability of drawing a Spade?
What is the probability of drawing a black card?
What is the probability of drawing a card?The first probability is not the same as the last one...and yet it just might be that in the last instance, I drew the Ace of Spades.In other words, was it unlikely to get humans from the primate ancestor? Yes, it was.Was it unlikely to get an organism from the primate ancestor? Not at all.------------------
Rrhain
WWJD? JWRTFM!

I think the point being made is that IF the changes are NOT random then they could occur with a higer probability in the same place without there being a common ancestor.So you can't say "share a common ancestor" in this case until you can demonstarte the improbability of the same flaw occuring.It now seems that that depends on the type of mutation. I think we've all agreed that some sites are more subject to mutation than others. Or is it that the other sites, that appear to be LESS subject are being weeded out by a selection process?Now can it be demonstrated that the particular type of changes in a pair of genomes are in sites subject to mutation and the mutations are the kind that are, in some sense, "random"?[This message has been edited by NosyNed, 05-24-2003]

I think Taz has phrased the argument the best by addressing equiprobability of mutation as opposed to the randomness.I think mutation is random. You never know which base is going to get nailed by ionizing radiation. You don't know which provirus will recombine and leave a solo LTR behind. However, as Rhrain and Taz have pointed out, mutations are not equiprobable. Not all the reasons for this are clear yet. But some are more obvious. DNA is wrapped around histones..that means some sequences are more exposed than others. There are types of sequences like long stretches of homopolymers that are just lousy templates for accurate replication by DNA polymerase..they have a higher probability of mutation. There are chemicial reasons i.e. it is easier to change from a C to a T by demethylation than to change a pyrimidine to a purine...however, if there was an intrinsic "non-random" mechanism governing mutation in the genome, one would with great accuracy be able to a priori determine where mutations will occur in a given sequence. Even knowing what some of the factors are that make muations non-equiprobable, does not allow one to accurately make such a determination.Think of the way mouse mutants are generated for the most part for large screens of genetic defects...you basically bomb them with mutagens and then screen after the fact for the mice that do strange things like run in circles endlessley (twirler mutants which ironically are very fertile...though I wonder when they find the time to stop spinning and actually mate...but I digress).Regarding the types of different mutations being used to evaluate identity by descent...hypermutable regions are used to address very different questions...and some loci are completely useless as they mutate too quickly. But if I want to know the difference between two individuals in a population i.e. the same species..I need a locus that mutates a lot. If I want to compare sea anemones to primates however, using a fast evolving locus would be very uninformative because you would have hit what is called saturation whereby any individual site has probably mutated so many times in the hundreds of millions of years since the two lineages split that you have no idea what the ancestral state could have been..you have no way to make a comparative analysis since you don't know what the original differences between the lineages were having been erased by mulitple mutation hits at the same sites....in such cases you need very conserved loci that tolerate only very limited mutation and hence evolve slowly in order to determine any kind of relationship....sorry for the overerly long winded postcheers,
M

Mammuthus:
..however, if there was an intrinsic "non-random" mechanism governing mutation in the genome, one would with great accuracy be able to a priori determine where mutations will occur in a given sequence.Judge:
Perhaps as the notorious PB (yikes...hi PB ) seemed to say some mutations are much more "non random".
Thus the ones shared by chimps and humans would have occurred due to a "mechanism".How could we weigh up whether this was a possibilty with regard to a particular mutation shared by chimps and humans?
How can we say that with regard to a particular shared mutation this is highly unlikely?mammuthus:
..sorry for the overerly long winded postcheers,
Mjudge:
Naaa! carn mate...don't be so hard on yourself! You should see some of the posts on other forums here [This message has been edited by judge, 05-27-2003]