bernd writes:
I hope you don’t mind when I step in.
I ALWAYS welcome sincere feedback by bios, docs, laymen and/or tactful trollers, as long as they stay on topic and cough-up some 'credible' motives and/or evidences for their position. Your abstract on duplicated genes is of belated interest (my apologies). Let's break it down a bit:
Although the complete genome sequences of over 50 representative species have revealed the many duplicated genes in all three domains of life, the roles of gene duplication in organismal adaptation and biodiversity are poorly understood.
"Poorly understood" ... is the bottom line.
Poorly understood speculations on mutation mechanisms? Of course they're poorly understood! Beneficial (advantageous) mutations don't ever occur (unless one unscrupulously perverts the defintion of mutation into mere "change", "NS", "adaptation", or the like fallacy)
In addition, the evolutionary forces behind the functional divergence of duplicated genes are often unknown, leading to disagreement on the relative importance of positive Darwinian selection versus relaxation of functional constraints in this process.
Of course ToE forces of mutation are unknown! Even if a serious genetic programmer (human or divine) altered a given gene pool program to make artifical mutation somehow beneficial for survival, he'd risk ultimate extinction for that organism. HOW MUCH MORE would random mutations seem to expedite extinction of any gene pool program.
The methodology of earlier studies relied largely on DNA sequence analysis but lacked functional assays of duplicated genes, frequently generating contentious results.
Admittedly,
duplicated genes are the only real commencing mechanism of evolution, were beneficial (advantageous) mutations *hopefully* viable.
Here we use both computational and experimental approaches to address these questions in a study of the pancreatic ribonuclease gene (RNASE1) and its duplicate gene (RNASE1B) in a ... monkey
Ah, those computational approaches to the gene-pool-enzyme mutation, and their *complete* genomic sequences (notwithstanding the cascading eukaryotic protein factors of this monkey's complex gene-pool-app)
We show that RNASE1B has evolved rapidly under positive selection for enhanced ribonucleolytic activity in an altered microenvironment, a response to increased demands for the enzyme for digesting bacterial RNA.
Whoa cowboy! Is this REALLY mutation? ... or is it merely natural adaptation (pre-built genome variability or such)?
At the same time, the ability to degrade double-stranded RNA, a non-digestive activity characteristic of primate RNASE1, has been lost in RNASE1B, indicating functional specialization and relaxation of purifying selection.
"relaxation of purifying selection" ...Ouch, that babbling effeminate ToE syntax, again. This supports nothing concerning 'brand new genes', 'advantageous gene-pool-mutations', etc. Just bad grammar.
Our findings demonstrate the contribution of gene duplication to organismal adaptation and show the power of combining sequence analysis and functional assays in delineating the molecular basis of adaptive evolution.
Ah! so it is merely "
adaptive" selection after all; this is not evolution. The monkey's gene-pool program never changed via this code-duplication. (... Any more than my C++ program changed when it passes 2 [vs. 1] parameters into a sub-routine function).
Obviously, there is much flexibility of adaptive codon-parameters passing (unscathed) in programs and functions throughout eukaryotic gene pool programs and apps. Again, this is not evolution proper, just program 'design' with finite flexible parameters of adaptation.
... Or did the gene REALLY duplicate into some 'freak' new code-function for the monkey's gene-pool-program? NOT!
In sum: These studies in
no way support: random "brand-new advantageous mutations" of new genes, just "hot-spot mutations" and other
fallacious misnomers of beneficial mutation (i.e., having been pre-coded into that gene-pool program)
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