You seem to think that your interpretation of an article published in a major science journal constitutes the downfall of NDT. May I ask why it is you think that no other scientist who has read these articles thinks they falsify NDT?
It reminds me of someone who thinks they've invented a perpetual motion device
you haven't done anything of the sort borger, and if you think you have then you don't understand science very well
you cannot falsify random mutation unless you can isolate mutation as one of the variables. When you look at the fly genome you cannot seperate the variables mutation and selection. You can only assume that selection has no affect (based on what little you actually know about the gene, which is in effect, nothing)
so until you can isolate mutation from selection in an experimental setting, you cannot possibly "falsify" random mutation
pehaps the worst thing about it is that you seem to think that your interpretation of this article is the only correct one, despite the fact that it has been read by many other scientists and peer reviewed by experts who don't seem to think it falsifies NDT. Thats nothing but arrogance
EXAMPLE 1) The problem with this is that it doesn't even consider that these traits may be byproducts of genes which do serve functions which aid survival.
An analogy to demonstrate why I think this is ridiculous.
A person can use their hands to clap. Clearly being able to clap can have no survival advantages. So are hands redundant?
EXAMPLE 2) It isn't hard at all to imagine why the ability to regenerate has been turned off in some human tissues. It's because once development has occured, regenerating functional tissue in complex organs is extremely problematic. I'll give the example of brain tissue, as I have some knowlege of developmental neurobiology. Cell differentiation in the developing brain depends both on temporal and spatial cues. Its an extremely complex cascade which involves crosstalk between cells as they are developing. Regeneration of FUNCTIONAl adult brain tissue is therefore extremely problematic, because the complex interactions of cells in development can't be "reset", because cells in an adult brain are terminally differentiated. Temporal and spacial cues relied upon in the development of brain are no longer there. They cant be reset without compromising the function of adult brain cells. The reason lower organisms have the ability to regenerate is primarily most likely because they don't have the problem of regenerating the complexity which higher animals have to.
EXAMPLE 3) I don't know anything about botany, but remember that you are merely assuming that the trait is redundant, and that it doesn't offer any survival advantage. You can't really show that its redundant, until you can compare fitness of liana with and without this trait.
"In humans, ACTN2 is expressed in all muscle fibres, while ACTN3 expression is restricted to a subset of type 2 fibres." My possible explanation for why ACTN3 is still present in the genome (i'm not as certain of my opinions as peter seems to be) is that act-3 offers a performance advantage. Difference in fibre composition in muscle is known to affect endurance/power, due to differences in metabolism/morphology between fibre types. The fact that act-3 is only expressed in a subset of fibre types indicates that it may have some role in the differences between those fibres. Loss of the gene doesn't show any obvious myopathy for the same reason that differences in muscle fibre composition are not treated as myopathies.
"Maybe we simply do not know the mechanisms of de-differentiation, yet."
Not only do cells have to de-differentiate, they then have to read temporal and spatial cues from their environments, and their axons have to read chemotaxic cues to synapse with the correct dendrites. These temporal and spatial cues are specific to the developmental period, they aren't present in adult brain.
And: "The reason lower organisms have the ability to regenerate is primarily most likely because they don't have the problem of regenerating the complexity which higher animals have to."
"I notice a bit of a contradiction here. Since higher organisms are able to regenerate bones and liver it is not restricted to lower organisms. So, this is not an argument, let alone a reason."
Liver and bone are made out of fairly simple (in comparison to other organs, appendages etc.) arrangements of relatively few cell types, arms and legs are not. (an arm requires epidermal, muscle, blood vessels, nerve etc. to regenerate in precise locations.)
"That experiment is not that hard to carry out. One only needs to compare the fitness of far-soared offspring and direct-neighborhood-of-the-parent-tree offspring. I predict that there will no difference in fitness."
This doesn't test fitness, because you've assumed the only purpose of the flaps is to carry them long distances. Gene knockout is the only way to be certain.
And, finally: "Loss of the gene doesn't show any obvious myopathy for the same reason that differences in muscle fibre composition are not treated as myopathies."
... and that makes it a redundant gene, isn't it?
No, because it can give the organism an advantage, muscle fibre compositions between sprinters and endurance runners are usually different, they do different tasks. If the gene in question affects muscle fibre types then it has a function and will be subject to selection.
Furthermore, you did not respond to my reply in the previous letter, where you say that: "you haven't done anything of the sort borger (about the falsification of NDT), and if you think you have then you don't understand science very well"
The reason I don't think you have is because the gene is the result of Mutation and Selection. You've assumed something about the selection pressure on certain base pairs to deduce that mutation is non-random. You actually don't know the value of the variable "selection" for any of the bases. So its an assumption, and assumptions do not falsify scientific paradigms. Your assumption might be reasonable, but until you can actually isolate the variable of mutation in the absence of selection pressure, you can't "falsify" random mutation.
like I said pete, you're assuming that they're neutral because they don't code for amino acids.
There are many examples of conserved nucleotide sequences which do not code for amino acids, most of which are regulatory regions. Introns themselves neccessarily must have some selection pressure on their sequence in order for them to be recognised as introns, and not as exons.
If you are going to claim that all nucleotides which don't encode for amino acids are selectively neutral then you've got big problems when it comes time to explain homology in junk DNA and pseudogenes.
borger, you are right in that regions previously described as junk have been found to have function. You must remember that in order for this DNA to be evidence of design, the function has to depend on the sequence. You also have to explain the function of certain pseudogenes. I suggest you look at the thread "what is design" in the intelligent design forum. What function can you attribute to the urate oxidase pseudogene that indicates it was "intelligently designed"?
[This message has been edited by monkenstick, 08-09-2002]