Classic example of the Creationist NUH-UH Fallacy. People show a Creationist metric tons of scientific evidence crushing YEC claims, the Creationist goes NUH-UH! and runs off declaring victory without addressing the evidence even once.
These findings are all consistent with what science has concluded for a while now, that the vast majority of many genomes is non-functional. You seem to think that humans canât be the product of just 5-10% of our genome, for whatever reason, but that conclusion doesnât seem to be based on any evidence. We observe that the vast majority of vertebrate genomes accumulate mutations at a rate consistent with neutral drift which means there is a lack of sequence specific function in those regions.
Itâs a chemical reaction that is catalyzed by an enzyme that is coded by a piece of DNA in the genome, right? So if the enzyme is perfect in the sense that it catalyzes a chemical reaction with 100% efficiency, it means that the sequence that codes for the enzyme is the best you can get.
But anyway, were you not trying to refute the following statement by @PDPrice? itâs much more easy to cause damage to a machine (or to the information that codes for it), than it is to improve upon it.
Yeah, it was debunked. It is not just wrong, it is incoherent.
You have not even dealt with the debunking on THIS thread. How did H1N1 resist GE over millennia? What âstabilization and control mechanisms no longer functionâ? This IS your claim, and it is a vital one, so back it up.
If you take a sledge hammer to the stuff in your trash can, how much damage does it do to functioning machines? Does your house lose function if you take your trash outside and light it on fire?
The vast majority of mutations occur in the genomeâs trash. If mutations do cause deleterious effects in the functional part of the genome then they are selected out by natural selection. They donât accumulate because of selection.
Apparently you canât figure it out either, since you didnât say how they are more complicated - which should have taken less time to type than the gratuitous insult you added.
Also, you ignored blue whales completely.
P.S. Apparently redwoods arenât just much larger than humans in size, they also have much larger genomes.
This is a good way of framing the question. Why is 300Mb apparently ânot enoughâ to produce a human, but 3000Mb is? There is only a difference of one order of magnitude there, so show your work as to how the other 2700Mb is all as essential as the 300Mb. Or is it the mere presence of 3000Mb in our genomes, and your theological views, that makes you lean towards the conclusion that itâs all function, as though you donât believe itâs possible for non-functional sequences to accumulate over time?
The Moderately Efficient Enzyme: Evolutionary and Physicochemical Trends Shaping Enzyme Parameters
Abstract
The kinetic parameters of enzymes are key to understanding the rate and specificity of most biological processes. Although specific trends are frequently studied for individual enzymes, global trends are rarely addressed. We performed an analysis of k cat and K M values of several thousand enzymes collected from the literature. We found that the âaverage enzymeâ exhibits a k cat of âź10 sâ1 and a k cat/ K M of âź105 sâ1 Mâ1, much below the diffusion limit and the characteristic textbook portrayal of kinetically superior enzymes. Why do most enzymes exhibit moderate catalytic efficiencies? Maximal rates may not evolve in cases where weaker selection pressures are expected. We find, for example, that enzymes operating in secondary metabolism are, on average, âź30-fold slower than those of central metabolism. We also find indications that the physicochemical properties of substrates affect the kinetic parameters. Specifically, low molecular mass and hydrophobicity appear to limit K M optimization. In accordance, substitution with phosphate, CoA, or other large modifiers considerably lowers the K M values of enzymes utilizing the substituted substrates. It therefore appears that both evolutionary selection pressures and physicochemical constraints shape the kinetic parameters of enzymes. It also seems likely that the catalytic efficiency of some enzymes toward their natural substrates could be increased in many cases by natural or laboratory evolution.
Generally enzymes with longer histories, and which are rate-limiting for growth(sit in central metabolism with the rates of many other reactions being determined by them), are more efficient. Which makes perfect sense as the product of longer periods of optimization by natural selection. There is no in principle difficulty with finding an enzyme that has a rate of substrate turnover at the diffusion limit. Particularly for enzymes that catalyze reactions with small (low mass and size) substrates.
Now if what you appear to think, that life must have once been perfect(and that catalytic rates for enzymes is an indication of this), is true, then that leads to testable predictions: We should generally be able to find that more ancient nodes in reconstructed enzyme histories, have higher fitness/or higher catalytic rates, than their descendants. Do we in fact find that, Gil?
I donât think either figure is sufficient. I believe that DNA will turn out to be only the tip of the iceberg for information stored in life. But I canât prove that as of now. Even if DNA is the primary storage medium, we now know that DNAâs information is not stored in a merely linear fashion, which means all these âmbâ designations are way off.
Iâm sorry Gil but thatâs just not true. The âefficiencyâ you speak about is the speed with which the enzyme catalyzes a reaction, and if that rate is equal to the rate at which the substrate can diffuse to the active site, then it is said to be âperfectâ, in the sense that it would not matter if it could work even faster since the substrate couldnât move through the medium and enter the active site faster anyway.
But catalytic rate is not the only measure of the fitness effects of enzymes. Another factor that affects enzyme fitness are their kinetic and thermodynamic stability. If the enzyme is extremely fast, but breaks apart quickly and often, it might actually be a less fit enzyme than a slightly slower one that has a lower metabolic cost associated with itâs expression, as an unstable one that falls apart quickly will have to be replaced. The effect of enzyme catalytic rate on organismal fitness is more complicated than just âfaster means fitterâ.
And in any case, there is no problem from the standpoint of evolution, in principle, with finding an enzyme that catalyzes some reaction at the diffusion limit.
The first thing you would need to consider is how this supposed information is heritable.
We already know that DNA function can be due to 2D and 3D structures through enhancer binding or binding between complementary bases. All of that function is due to specific DNA sequences. Change the sequence and you can change the function. That does nothing to change the number of bases in the genome.
Yet another example of the damage done by ENCODE to public understanding of science. Here we see all the classic tropes: the conflation of junk and non-coding DNA, the assumption that if a deleterious mutation is possible in some sequence, it must be functional, the notion that if some sequences of a type are functional, they all must be, the assumption that human beings are so complex that known functional sequences canât account for development, apparent ignorance of the c-value paradox and the onion test. Did I miss any?
Not nearly. For instance, it would be an even better enzyme if it catalyzed a chemical reaction with 100% efficiency and gave every child on earth a free pony.
The point being that it is ridiculous to describe a DNA sequence âperfect.â Never mind that the claim you are supposed to be defending is that there are perfect genomes. Did you forget?
To a certain degree, the functionality of a genome is independent of its size. This is due to junk DNA. There are species of amoeba that have 670 billion base genomes, fish that have 0.4 billion base genomes, salamanders that have 30 billion base genomes, and plants with genomes many times the 3 billion base human genome.
You seriously need to get away from lecturing others as a professional apologist, and take some basic classes in biology if you want to gain some understanding in the field.
As John asked, just how would you suggest such information is inherited, and how would it be translated into protein, redwoods and blue whales? What do you feel is inadequate in DNA being the repository of information?
BTW, just state that you have no intention of ever supporting your statement that âstabilization and control mechanisms no longer functionâ for the H1N1 virus, and I will stop asking you to do so.