spinoza99 wrote:
Natural selection would be falsified if there were no advantageous or deleterious mutations that introduced differential survival in environments.
I believe those mutations were done by an intelligence, you believe they were done through randomness. It's as if we saw Stonehenge and you said that it's due to erosion and I say it's due to intelligence
Including all the mutations that cause cancer? I do not "believe" they were caused by randomness, chemical processes such as substitutions and transversions are not uncaused, rather, random means that mutagenic chemistry has an equal probability of acting on genomes, and the evidence for mutations being random includes for instance the paper on the Karst window.
Again, the inference from Universal Common Ancestry is that all organisms share a common ancestor with other organisms, the very closely related ones have more recent common ancestors than those that are more distantly related, and so on and so forth.
We already both agree on this
Your presentation of this was flawed, however.
Is the natural equivalent of that designed? I mean, the intricateness, the ornateness, it is too improbable to come about without a skilled craftsman chipping away, innit?
The intricateness of crystals and a protein, for example, are light years apart. In order to get a protein you have to arrange 20 different amino acids into a specific order roughly 120 sequences long. The odds of which are roughly one in 10^130. To give you idea of how large 10^130 are, there are 10^80 atoms in our Universe and 10^26 Nanoseconds in our Universe's history. Crystals simply obey the laws of physics and consist of a large number of identical molecules packed together in a uniform way. Amino acids when they form protein are not obeying any physical laws. They have to know in what order to get into in order to form. Crystals don't have to know anything, they are just blinding following a physical law.
Proteins are also blindly following translational chemistry. In order to get a protein you only need to have a polypeptide chain of a molecular weight more than 10,000 daltons, which can be achieved by any translatable gene sequence of the corresponding length. A functional protein can be evolved by mutations from random protein sequences, and an example of this follows.
The fitness landscape in sequence space determines the process of biomolecular evolution. To plot the fitness landscape of protein function, we carried out in vitro molecular evolution beginning with a defective fd phage carrying a random polypeptide of 139 amino acids in place of the g3p minor coat protein D2 domain, which is essential for phage infection. After 20 cycles of random substitution at sites 12–130 of the initial random polypeptide and selection for infectivity, the selected phage showed a 1.7×104-fold increase in infectivity, defined as the number of infected cells per ml of phage suspension. Fitness was defined as the logarithm of infectivity, and we analyzed (1) the dependence of stationary fitness on library size, which increased gradually, and (2) the time course of changes in fitness in transitional phases, based on an original theory regarding the evolutionary dynamics in Kauffman's n-k fitness landscape model. In the landscape model, single mutations at single sites among n sites affect the contribution of k other sites to fitness. Based on the results of these analyses, k was estimated to be 18–24. According to the estimated parameters, the landscape was plotted as a smooth surface up to a relative fitness of 0.4 of the global peak, whereas the landscape had a highly rugged surface with many local peaks above this relative fitness value. Based on the landscapes of these two different surfaces, it appears possible for adaptive walks with only random substitutions to climb with relative ease up to the middle region of the fitness landscape from any primordial or random sequence, whereas an enormous range of sequence diversity is required to climb further up the rugged surface above the middle region.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1762315/
Mutation + selection acting on a random 139 amino acid polypeptide encoded by the corresponding genetic sequence (by necessity random too, since random protein sequences require random nucleotide sequences) for 20 cycles resulted in 1.7 x 10
4 times infectivity of the now optimised protein (by mutation and natural selection)
Now are you seriously telling me something was tinkering each base pair so that there was progressive improvement? Why spend 20 cycles to achieve the end result when anyone with any intelligence and the ability to shape genomes would have just popped in the optimal sequence (the original phage coat protein in the non-defective phage) at once? Why does the behaviour of your postulated intelligent designer look exactly like the working of a non-existent one?
Stonehenge - we know said entities are designed because we have evidence of humans building similar structures, and we have evidence for humans having lived in Britain when Stonehenge was built, we also have found the necessary tools. Looks improbable, therefore design is not a valid argument.
You're using logic and inference to make the above determination, not science. You're saying because humans have done this elsewhere, therefore it's reasonable that they've done that.
A. Humans built the Washington Monument
B. Stonehenge is similar to Stonehenge
C. Therefore, it is reasonable that humans built Stonehenge
Nor are odds based on science, next.
You can do the same with the DNA code
A. Intelligence writes code
B. The genome is a code
C. Therefore intelligence wrote the genome.
This particular guff I have seen many times before, and sadly for you, the fact that mutations can produce novel genetic codes and alter the fundamental nature of the genetic code itself brings in parsimony again, and of course I will also present evidence to back the fact up that the code itself is an evolvable entity.
The first important point to note is that there is no code in the genome, the apparent code, or triplet ---->amino acid symmetry that is produced, is a result of the translational machinery, particularly localized to mRNA - tRNA ---->Amino acid acceptor stem chemistry and ribosomal chemistry, and by acting on this, and by mutating this, novel genetic codes have been produced.
Encoding multiple unnatural amino acids via evolution of a quadruplet-decoding ribosome
The in vivo, genetically programmed incorporation of designer amino acids allows the properties of proteins to be tailored with molecular precision1. The Methanococcus jannaschii tyrosyl-transfer-RNA synthetase–tRNACUA (MjTyrRS–tRNACUA)2, 3 and the Methanosarcina barkeri pyrrolysyl-tRNA synthetase–tRNACUA (MbPylRS–tRNACUA)4, 5, 6 orthogonal pairs have been evolved to incorporate a range of unnatural amino acids in response to the amber codon in Escherichia coli1, 6, 7. However, the potential of synthetic genetic code expansion is generally limited to the low efficiency incorporation of a single type of unnatural amino acid at a time, because every triplet codon in the universal genetic code is used in encoding the synthesis of the proteome. To encode efficiently many distinct unnatural amino acids into proteins we require blank codons and mutually orthogonal aminoacyl-tRNA synthetase–tRNA pairs that recognize unnatural amino acids and decode the new codons. Here we synthetically evolve an orthogonal ribosome8, 9 (ribo-Q1) that efficiently decodes a series of quadruplet codons and the amber codon, providing several blank codons on an orthogonal messenger RNA, which it specifically translates8. By creating mutually orthogonal aminoacyl-tRNA synthetase–tRNA pairs and combining them with ribo-Q1 we direct the incorporation of distinct unnatural amino acids in response to two of the new blank codons on the orthogonal mRNA. Using this code, we genetically direct the formation of a specific, redox-insensitive, nanoscale protein cross-link by the bio-orthogonal cycloaddition of encoded azide- and alkyne-containing amino acids10. Because the synthetase–tRNA pairs used have been evolved to incorporate numerous unnatural amino acids1, 6, 7, it will be possible to encode more than 200 unnatural amino acid combinations using this approach. As ribo-Q1 independently decodes a series of quadruplet codons, this work provides foundational technologies for the encoded synthesis and synthetic evolution of unnatural polymers in cells.
http://www.nature.com/nature/journal/v4 ... 08817.html
I have the full paper and they used in-vitro mutagenesis + artificial selection to arrive at a novel code with quadruplet coding and unnatural amino acid assignments, in other words, mutations to translational machinery generates novel genetic codes.
Here is another one...
We investigated directed deviations from the universal genetic code. Mutant tRNAs that incorporate cysteine at positions corresponding to the isoleucine AUU, AUC, and AUA and methionine AUG codons were introduced in Escherichia coli K12. Missense mutations at the cysteine catalytic site of thymidylate synthase were systematically crossed with synthetic suppressor tRNACys genes coexpressed from compatible plasmids. Strains harboring complementary codon/anticodon associations could be stably propagated as thymidine prototrophs. A plasmid-encoded tRNACys reading the codon AUA persisted for more than 500 generations in a strain requiring its suppressor activity for thymidylate biosynthesis, but was eliminated from a strain not requiring it. Cysteine miscoding at the codon AUA was also enforced in the active site of amidase, an enzyme found in Helicobacter pylori and not present in wild-type E. coli. Propagating the amidase missense mutation in E. coli with an aliphatic amide as nitrogen source required the overproduction of Cys-tRNA synthetase together with the complementary suppressor tRNACys. The toxicity of cysteine miscoding was low in all our strains. The small size and amphiphilic character of this amino acid may render it acceptable as a replacement at most protein positions and thus apt to overcome the steric and polar constraints that limit evolution of the genetic code.
Mutate tRNA , change code, in other words, the natural processes that underlie mutations are enough to account for the variations that shape the genetic code, given just two examples.
Of course, let us now come to a brief sampling of the literature on the evolution of the genetic code itself.
Comparative path lengths in amino acid biosynthesis and other molecular indicators of the timing of codon assignment were examined to reconstruct the main stages of code evolution. The codon tree obtained was rooted in the 4 N-fixing amino acids (Asp, Glu, Asn, Gln) and 16 triplets of the NAN set. This small, locally phased (commaless) code evidently arose from ambiguous translation on a poly(A) collector strand, in a surface reaction network. Copolymerisation of these amino acids yields polyanionic peptide chains, which could anchor uncharged amide residues to a positively charged mineral surface. From RNA virus structure and replication in vitro, the first genes seemed to be RNA segments spliced into tRNA. Expansion of the code reduced the risk of mutation to an unreadable codon. This step was conditional on initiation at the 5'-codon of a translated sequence. Incorporation of increasingly hydrophobic amino acids accompanied expansion. As codons of the NUN set were assigned most slowly, they received the most nonpolar amino acids. The origin of ferredoxin and Gln synthetase was traced to mid-expansion phase. Surface metabolism ceased by the end of code expansion, as cells bounded by a proteo-phospholipid membrane, with a protoATPase, had emerged. Incorporation of positively charged and aromatic amino acids followed. They entered the post-expansion code by codon capture. Synthesis of efficient enzymes with acid-base catalysis was then possible. Both types of aminoacyl-tRNA synthetases were attributed to this stage. tRNA sequence diversity and error rates in RNA replication indicate the code evolved within 20 million yr in the preIsuan era. These findings on the genetic code provide empirical evidence, from a contemporaneous source, that a surface reaction network, centred on C-fixing autocatalytic cycles, rapidly led to cellular life on Earth.
http://www.ncbi.nlm.nih.gov/pubmed/10511799
This one is particularly interesting, because they have reconstructed empirically, with mutation and selection as the driving forces, the evolution of the genetic code, in other words, magic man is superfluous to requirements, parsimony wins.
We have devised a phage display system in which an expanded genetic code is available for directed evolution. This system allows selection to yield proteins containing unnatural amino acids should such sequences functionally outperform ones containing only the 20 canonical amino acids. We have optimized this system for use with several unnatural amino acids and provide a demonstration of its utility through the selection of anti-gp120 antibodies. One such phage-displayed antibody, selected from a naïve germline scFv antibody library in which six residues in V(H) CDR3 were randomized, contains sulfotyrosine and binds gp120 more effectively than a similarly displayed known sulfated antibody isolated from human serum. These experiments suggest that an expanded "synthetic" genetic code can confer a selective advantage in the directed evolution of proteins with specific properties.
http://www.ncbi.nlm.nih.gov/pubmed/19004806
Abstract
The discovery of the genetic code was one of the most important advances of modern biology. But there is more to a DNA code than protein sequence; DNA carries signals for splicing, localization, folding, and regulation that are often embedded within the protein-coding sequence. In this issue, Itzkovitz and Alon show that the specific 64-to-20 mapping found in the genetic code may have been optimized for permitting protein-coding regions to carry this extra information and suggest that this property may have evolved as a side benefit of selection to minimize the negative effects of frameshift errors.
http://www.ncbi.nlm.nih.gov/pubmed/17351130
Abstract
Proteins account for the catalytic and structural versatility displayed by all cells, yet they are assembled from a set of only 20 common amino acids. With few exceptions, only 61 nucleotide triplets also direct incorporation of these amino acids. Endeavors to expand the genetic code recently progressed to nucleus-containing cells, after Chin et al.1 transferred Escherichia coli genes for a mutant tyrosine-adaptor molecule and its synthetase into Saccharomyces cerevisiae. Transformed yeast cells were produced that exhibit efficient site-specific incorporation of non-biotic amino acids into proteins. This makes it likely that code complexity can be elevated experimentally in mammals.
http://www.ncbi.nlm.nih.gov/pubmed/14745828
A. I've never seen even the crudest code spontaneously construct due to physical laws, such as a crystal
B. The genome is a code
C. Therefore the genome is not the result of physical laws.
A. The evolution of a genome code is adequately explained by mutation + selection and some of the evidence is presented, the fact that mutant components of the translational chemistry have been used to, in conjunction with artificial selection (not natural selection)this time round have also demonstrated that varying selection conditions can result in the formation of varied genetic codes.
B. We
represent translational chemistry using a code, as Hackenslash would say, the map is not the fucking terrain.
A binds to T, C binds to G , AAA binds to TTT on tRNA, tRNA binds to an amino acid based on the chemistry of aminoacyl tRNA synthetase, again elementary biochemistry where the "code" is a function of the physico-chemical properties of aforementioned components, no intelligence required.
The genetic code is a map of the chemistry of translation, deal with it. The interactions themselves are physical, chemical and more importantly, evolvable, this is demonstrated fact.
Example - based on whether you use naturally occuring ribosomes or the mutant quadruplet encoding ribosome, which IIRC is dependent on a mutant peptidyltransferase ribosomal subunit, the same sequence of DNA, through its mRNA output can result in different protein outputs, in other words,
the DNA itself doesn't contain the code, it emerges from the interactions of DNA, through mRNA, with the translational apparatus.
We have no evidence when Stonehenge was built. It could have been there a million years ago. Humans living in Britain is not evidence. Other animals lived in Britain, why didn't they build it. We know animals didn't build it through the above logical devices outlined.
Tripe. Read this and get back and then assert "we have no evidence"
http://en.wikipedia.org/wiki/Stonehenge
They've also found tools used to make it, by the look of things, so your nonsense is well, nonsense?
You have a penchant for
ex-recto assertions, do you not?
Design by odds is a nonsensical argument,
Quite the contrary, you use the design by odds argument when you determine that Stonehenge is designed. The odds that it was done by erosion are easily greater than one in a googol, that's why we assume humans did it.
Speak for yourself, and if you want to speak for the scientific community, present an apposite peer reviewed citation for this, like I have for my postulates.
Predictions - evasion, obfuscation, and accusations of being a biased scientist who just won't accept design based on ex-recto probability assertions and nothing of substance coming up.
' or 'I don't think my grandfather is a monkey ' (no but he is an ape 
).