When I say functional sequences, Iâm talking about those that produce a functional rna or protein. In this case, though, I didnât qualify âsequencesâ.
So âallâ, without qualification, isnât correct. I do think that a random process can produce a functional sequence, but only a very short sequence. For example, if you were to randomly arrange Scrabble tiles, I have no doubt that you would get short (2, 3 or 4 letters) words now and then. But not a coherent sentence.
I also think that, since it a created system, not only can the cell repair errors in DNA sequence, the cell can modify itâs own DNA when necessary. This is what I said in an earlier post:
I actually think that the cell is able to modify DNA as needed. Lenskiâs cit+ mutation is a perfect example. I think that that mutation is a case of an intentional, adaptive modification.
In the case of the cit+ mutation, the cell apparently knows where the CitT gene is and can copy it and place it downstream from an active promoter. Follow-up experiments to the original Cit+ mutation shows that the mutation can happen rapidly and repeatedly targets the CitT gene.
So, what does your paper actually show? Does it show random mutation creating a lengthy functional sequence or a very short one? Does it show random mutation or the same mutation in each strain?
From your paper:
The different replicates acquired the same mutations, yet sometimes in a different order (Supplementary Data 1)
Also, the active sequence in the promoter which is needed for transcription is the TATA*T box which is very short. The 2nd short sequence, TTGACA, doesnât appear to be a requirement, although it appears to improve expression.
So, while I concede that random mutations can produce very short sequences, I think what your paper actually shows is closer to the Cit+ mutation rather than just a random mutation.
Iâm not questioning the testing of predictions. Why would you think so?
Iâm simply saying that a successful prediction does not mean that the underlying hypothesis is true.
Not sure why you think so, and besides, the word âsupposeâ indicates a hypothetical.
Iâm not sure how you think Iâm questioning the existence of ribozymes.
I didnât say that the testing of predictions was inconclusive. You seem to be having a lot of difficulty in understanding what Iâm saying.
Disagree completely. And your claim doesnât deal with the idea that truth can only come from science. Do you believe that?
Iâm not making a prediction about what God would have or should have done. Iâm saying that the system was created by God arranging the sequences of the various parts of the machinery.
Because Iâm talking about the information flow from DNA through protein expression. I didnât say that it was the only information flow.
What does that have to do with what I said?
They are two separate things. The Genetic code existed and was operating long before humans were able to discover it.
The instructions are machine instructions, not communication between people.
The mechanism (supernatural) is beyond the scope of science. Surely you know that.
We have overwhelming evidence that functional protein sequences have evolved de novo from non-coding DNA, so this belief of yours is in contradiction with the evidence. Look up the various threads on this very forum on the protein t-URF13 that evolved in maize during domestication of the species. Itâs 89 amino acids long (so the coding region would be 267 basepairs in DNA sequence), which is within the length range of average english sentences.
Or you can look up this recent paper:
The de novo gene GSE9 codes for a 107 amino acid long protein (324 DNA basepairs coding region) with an experimentally demonstrated function in affecting rice grain shape, which has evolved during the domestication of rice.
So we have direct observational falsification of your intuition here, which means your intuition is not a reliable guide to truth on matters of the evolvability of functional sequences.
First of all the aerobic Cit+ trait is a trait, not a single mutation. The trait is the product of multiple mutations that work together to produce the function.
Nevertheless, your claim is completely inconsistent with the results of the Lenski experiment, where the Cit+ function only evolved once in one of 12 replicate populations, and it took over 31000 generations. The other 11 populations (each an independent but identical experiment started from the same ancestor, evolving in an identical environment) have yet to evolve the Cit+ function. One has to wonder why, if the cell somehow magically knows what mutations will be beneficial to it and can cause them to occur intentionally, it didnât evolve instantly in the very first generation, and why it has only happened in one population out of 12?
Your claim here is completely unable to explain this result.
However, the function being the product of blind and random mutation accumulation that only gets beneficial in the particular selection protocol used in the experiment after multiple potentiating mutations have already occurred, perfectly well explains why it has only happened once and after 31000 generations: because it is fundamentally a chance process that is blind to the future, and cells donât magically know the combinations of mutations that will produce beneficial effects. If they did, it should reliably and repeatedly happen under any environmental circumstance within the very first day of culturing. But this just isnât what happens. In ANY experiment.
Those experiments involve a radically altered selection protocol that much more strongly favor the Cit+ function, which also has implications for the favorability of the multiple potentiation mutations that leads to the Cit+ trait. And still, in those experiments it still took several hundred generations for the trait to emerge. Which again demonstrates the mutations have to accumulate by chance and get favored enough by selection to rise high enough in population frequency for additional mutations to be likely to occur in the potentiated background.
The paper that Venema is referring to is talking about riboswitches which (as far as I understand it) has an amino acid bound to an rna strand. Some amino acids are often bound to its codon within the riboswitch..
There are several questions that need answered when saying that this preference is good evidence of the Genetic code passing through a stereochemical era. One is: what is the pathway that leads from an amino acid binding directly to its codon to a process where the codon and amino acid are entirely separated, never coming into contact with each other in the translation process? Another is: are riboswitches produced by machinery within the cell, or do amino acids and rna strand find each other and bind without any assistance? I think that the answer is the former, not the latter.
Lastly, I think that Venema (and many in this thread) are using the wrong meaning of âarbitraryâ. At least theyâre using a different one than I am (and I think that Meyer is using). The meaning isnât ârandomâ or âby chanceâ, itâs âby choice rather than necessityâ.
1b: based on or determined by individual preference or convenience rather than by necessity or the intrinsic nature of something.
This meaning is entirely consistent with what Iâve been saying (God chose the mappings) and it is also consistent with how codes like Morse code or ASCII were developed.
It would still be a code in my view. The mapping (grouping to effect) is still there, even if it wasnât being used.
If there is a mapping (grouping of tree rings to a particular effect and a different effect will result with a reordering of the grouping), then I would agree that it is a code, even if we donât know about it.
It shows that functional promoter sequences are highly abundant in DNA sequence space. This was tested by replacing the canonical LAC promoter with completely random 100bp DNA sequences and recording how many of them result in activation of the downstream genes. It turns out about 10% of those random sequences can function as promoters already, and that a further 60% could turn into a functional promoter with a single mutation.
From your paper:
The different replicates acquired the same mutations, yet sometimes in a different order (Supplementary Data 1)
Yeah that just shows those specific mutations are strongly favored over others as they independently converged on similarly strong promoter sequences(the promoters were highly similar but not identical, which you can see in Supplementary Data 1) over the course of the experimental evolution:
Minimal mutations turn random sequences into promoters. To determine the molecular nature of the evolutionary adaptation, we sequenced the region upstream to the lac genes (from the beginning of the lac genes through the random sequence and up to the neighboring gene upstream). Within each of the evolved random sequences, a single mutation was found to confer the ability to utilize lactose. Continued evolution yielded additional mutations within the random sequences that further increased expression from the emerging promoters. The different replicates acquired the same mutations, yet sometimes in a different order (Supplementary Data 1). Each mutation was inserted back into its relevant ancestral strain, thus confirming that the evolved ability to utilize lactose is due to the observed mutations.
But it still took several dozen generations for those mutations to emerge in the evolving populations:
Lactose-utilizing mutants isolated on lactose only plates. To isolate lactose-utilizing mutants, we routinely plated the samples from the evolving populations on plates with lactose as the sole carbon source (M9+Lac) (Fig. 1b). Remarkably, within 1â2 weeks of evolution (less than 100 generations), all populations acquired lactose-utilizing abilities, except for the ÎLacOperon population. These lab evolution results therefore argue that the populations carrying random sequences, instead of promoters, can rapidly evolve the de novo expression. Next, we addressed the question of whether the solutions found during evolution were mutations in the random sequences or simply copying of existing promoters from elsewhere in the genome.
If the cell somehow knew in advance which mutations would produce the best promoter thereâs no reason why it required weeks of evolution (<100 bacterial generations) for the function to evolve. Why didnât it happen instantly in the very first generation to all cells in the population?
Itâs because the cells obviously donât know what mutations create the function of interest. The mutations happen randomly, most individuals that get a mutation get the wrong one and so are out-competed, and the few âwinnersâ of the lucky mutation quickly rise to higher frequency, and then within this new emerging variant, further enhancing mutations arise and are subject to selection. Eventually the different lineages converge on similar promoter sequences because they are simply superior promoters.
Itâs not TATA-box, which is a feature of eukaryotic promoters. The bacterial one (this experiment was with E coli, a bacterium) is similar but distinct.
Information can transfer between completely inanimate objects.
You keep attempting to equate biochemistry to symbolic abstractions, and therefore requiring a mind to initiate; that is what is not true, and no amount of wordsmithing can make it true.
What is the obvious and visible difference between the Genetic code and a code like ASCII? Something that everyone can plainly see or understand, like the difference between a white and black swan.
You are basing your argument on a philosophic assumption:
Every intelligent being that can create a code requires the genetic code to exist.
You donât have any scientific evidence to support this statement.
Also, I donât think Iâve been shown any empirical evidence that the Genetic code originated through evolution. Please give an example.
Okay. But you do realize, of course, that with that remark, it becomes evident that there is no point in anything youâve said, and that you are engaged in nothing but navel-gazing speculation about things unknowable.
I totally agree the base is irrelevant - that is the point I am making.
AND thatâs also why you are blowing smoke when you claim the genetic code is special because it is digital.
ANY chemical reaction.
But we can make this simpler: Name a chemical reaction that requires intelligence to occur.
Which is a silly bit of rhetoric - no chemical reaction requires an intelligence - it just happens. Therefore âŚ
The laws of chemistry act on atoms and molecules regardless of any intelligent interpretation. Given the proper ingredients and energy a chemical reaction WILL happen, no intelligence required. It is irrelevant to impose the human concepts of Information to chemical reactions for the purpose of inferring the supernatural.
Perhaps we could set a counter for how many times this obviously correct point, so troublesome to the argument, has been made, without its even being answered. We must be approaching triple digits.
No. Riboswitches are triggered by many different types of small molecules, not simply amino acids. Would it be too much to expect a Wikipedia-level dive?
No, riboswitches do not have codons.
Venema, specifically on p. 190, is referring to many papers published before the time he wrote it; many more relevant to your claim have been published since then. He is explicitly referring to Meyerâs (and your) objectively false claim that the mapping (a metaphor) of amino acids to codons in translation, with no reference to riboswitches, is arbitrary.