quote:
Have you actually looked at anything about gene duplication and neo-functionalisation? These seem to simply be assumptions with absoloutely nothing to support them other than your preconcieved notions of how mutations work.
As a hypothetical would you consider the sort of frame shift mutation which is thought to have produced at least one of a number of proteins allowing nylon digestion to be creating new information. If a long stretch of DNA which does not code for a protein or have any apparent regulatory function undergoes a frameshift and suddenly produces a coding region for a protein with some metabolic activity would you consider this an example of a gain of 'new' information?
By the way have you actually suggested anything which you would consider to be a gain of information for your 'Every Bird has wings' example yet?
What aspects of gene complexity were you thinking of, it is a pretty broad subject. There are complex elements in regulatory , structural, genetic and functional areas, was there anything specific you were interested in?
TTFN,
Mutations are copying errors that occur.
About the nylon:
" Thwaites claimed that the new enzyme arose through a frame shift mutation. He based this on a research paper published the previous year where this was suggested.5 If this were the case, the production of an enzyme would indeed be a fortuitous result, attributable to ‘pure chance’. However, there are good reasons to doubt the claim that this is an example of random mutations and natural selection generating new enzymes, quite aside from the extreme improbability of such coming about by chance.6
Evidence against the evolutionary explanation includes:
1.
There are five transposable elements on the pOAD2 plasmid. When activated, transposase enzymes coded therein cause genetic recombination. Externally imposed stress such as high temperature, exposure to a poison, or starvation can activate transposases. The presence of the transposases in such numbers on the plasmid suggests that the plasmid is designed to adapt when the bacterium is under stress.
2.
All five transposable elements are identical, with 764 base pairs (bp) each. This comprises over eight percent of the plasmid. How could random mutations produce three new catalytic/degradative genes (coding for EI, EII and EIII) without at least some changes being made to the transposable elements? Negoro speculated that the transposable elements must have been a ‘late addition’ to the plasmids to not have changed. But there is no evidence for this, other than the circular reasoning that supposedly random mutations generated the three enzymes and so they would have changed the transposase genes if they had been in the plasmid all along. Furthermore, the adaptation to nylon digestion does not take very long (see point 5 below), so the addition of the transposable elements afterwards cannot be seriously entertained.
3.
All three types of nylon degrading genes appear on plasmids and only on plasmids. None appear on the main bacterial chromosomes of either Flavobacterium or Pseudomonas. This does not look like some random origin of these genesthe chance of this happening is low. If the genome of Flavobacterium is about two million bp,7 and the pOAD2 plasmid comprises 45,519 bp, and if there were say 5 pOAD2 plasmids per cell (~10% of the total chromosomal DNA), then the chance of getting all three of the genes on the pOAD2 plasmid would be about 0.0015. If we add the probability of the nylon degrading genes of Pseudomonas also only being on plasmids, the probability falls to 2.3 x 10-6. If the enzymes developed in the independent laboratory-controlled adaptation experiments (see point 5, below) also resulted in enzyme activity on plasmids (almost certainly, but not yet determined), then attributing the development of the adaptive enzymes purely to chance mutations becomes even more implausible.
4.
The antisense DNA strand of the four nylon genes investigated in Flavobacterium and Pseudomonas lacks any stop codons.8 This is most remarkable in a total of 1,535 bases. The probability of this happening by chance in all four antisense sequences is about 1 in 1012. Furthermore, the EIII gene in Pseudomonas is clearly not phylogenetically related to the EII genes of Flavobacterium, so the lack of stop codons in the antisense strands of all genes cannot be due to any commonality in the genes themselves (or in their ancestry). Also, the wild-type pOAD2 plasmid is not necessary for the normal growth of Flavobacterium, so functionality in the wild-type parent DNA sequences would appear not to be a factor in keeping the reading frames open in the genes themselves, let alone the antisense strands.
Some statements by Yomo et al., express their consternation:
‘These results imply that there may be some unknown mechanism behind the evolution of these genes for nylon oligomer-degrading enzymes.
‘The presence of a long NSF (non-stop frame) in the antisense strand seems to be a rare case, but it may be due to the unusual characteristics of the genes or plasmids for nylon oligomer degradation.
‘Accordingly, the actual existence of these NSFs leads us to speculate that some special mechanism exists in the regions of these genes.’
It looks like recombination of codons (base pair triplets), not single base pairs, has occurred between the start and stop codons for each sequence. This would be about the simplest way that the antisense strand could be protected from stop codon generation. The mechanism for such a recombination is unknown, but it is highly likely that the transposase genes are involved.
Interestingly, Yomo et al. also show that it is highly unlikely that any of these genes arose through a frame shift mutation, because such mutations (forward or reverse) would have generated lots of stop codons. This nullifies the claim of Thwaites that a functional gene arose from a purely random process (an accident).
5.
The Japanese researchers demonstrated that nylon degrading ability can be obtained de novo in laboratory cultures of Pseudomonas aeruginosa [strain] POA, which initially had no enzymes capable of degrading nylon oligomers.9 This was achieved in a mere nine days! The rapidity of this adaptation suggests a special mechanism for such adaptation, not something as haphazard as random mutations and selection.
6.
The researchers have not been able to ascertain any putative ancestral gene to the nylon-degrading genes. They represent a new gene family. This seems to rule out gene duplications as a source of the raw material for the new genes.8
P. aeruginosa is renowned for its ability to adapt to unusual food sourcessuch as toluene, naphthalene, camphor, salicylates and alkanes. These abilities reside on plasmids known as TOL, NAH, CAM, SAL and OCT respectively.2 Significantly, they do not reside on the chromosome (many examples of antibiotic resistance also reside on plasmids).
The chromosome of P. aeruginosa has 6.3 million base pairs, which makes it one of the largest bacterial genomes sequenced. Being a large genome means that only a relatively low mutation rate can be tolerated within the actual chromosome, otherwise error catastrophe would result. There is no way that normal mutations in the chromosome could generate a new enzyme in nine days and hypermutation of the chromosome itself would result in non-viable bacteria. Plasmids seem to be adaptive elements designed to make bacteria capable of adaptation to new situations while maintaining the integrity of the main chromosome."
I made a new sentence as a new example. It can be found on one of my previous posts. It isn't "Every bird has wings" but it is the same principle. Only thing is that the sentece itself represents a gene, unlike the bird sentence that wong was added to. I am guessing that you were thinking of each word being a gene and thats why you only duplicatied wing instead of the whole sentece.
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