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originally posted by: ErosA433
cooperton doesn't understand science
A human on average apparently has 37Trillion cells, so thats 2.03e23 atoms, or 4.05e22 base pairs.
Studies have shown that the mutation rate in humans is about 0.5e-9 mutations per base pair per year.
Thats... 2.03e13 expected changes per year in our DNA... our whole bodies. We deal with it mostly, but, with age obviously we sometimes don't deal with it so well and the chance we get cancer becomes about the 'survival bias' aspect of life, or the longer you live, the higher the chance you get unlucky with the mutations.
Estimated number of bacteria on the earth.... 5e30, which have somewhere between 10-100x more mutations per year... the probabilities like i said, are not in your favour when you actually look at the numbers and have experience with stats. This doesnt include virus or RNA containing things that mutate way way faster and have the ability to add or modify DNA of other organisms. Also your original 1e64 number is
That means it would take 27,000,000,000,000,000,000,000,000,000,000,000,000,000,000 years to make one functional change to an enzyme fold by random chance.
random
Unpredictable in some way. Mutations are “random” in the sense that the sort of mutation that occurs cannot generally be predicted based upon the needs of the organism. However, this does not imply that all mutations are equally likely to occur or that mutations happen without any physical cause. Indeed, some regions of the genome are more likely to sustain mutations than others, and various physical causes (e.g., radiation) are known to cause particular types of mutations.
Abstract
In live cells, protein folding often cannot occur spontaneously, but requires the participation of helper proteins - molecular chaperones and foldases. The mechanisms employed by chaperones markedly increase the effectiveness of protein folding, but have no bearing on the rate of this process,whereas foldases actually accelerate protein folding by exerting a direct influence on the rate-limiting steps of the overall reaction. Two types of foldases are known, using different principles of action. Peptidyl-prolyl cis/trans isomerase and protein-disulfide isomerase catalyze the folding of every protein that needs isomerization of prolyl peptide bonds or formation and isomerization of disulfide bonds for proper folding. By contrast, some foldases operating in the periplasm of bacterial cells are specifically designed to help in the folding of substrate proteins whose primary structure does not contain sufficient information for correct folding. In this review, we discuss recent data on the catalytic mechanisms of both types of foldases, focusing specifically on how a catalyst provides the structural information required for the folding of a target protein. Comparative analysis of the mechanisms employed by two different periplasmic foldases is used to substantiate the notion that combinations of a protein which is unable to fold independently and a specific catalyst delivering the necessary steric information are probably designed to achieve some particular biological purposes. The review also covers the problem of participation of peptidyl-prolyl cis/trans isomerase in different cellular functions, highlighting the role of this enzyme in conformational rearrangements of folded native proteins.
originally posted by: Phantom423
"That means it would take 27,000,000,000,000,000,000,000,000,000,000,000,000,000,000 years to make one functional change to an enzyme fold by random chance."
You don't have a clue what "random chance" means. There isn't a textbook on the planet which says that evolution is random chance.
Your "random" theory just fell flat on its face.
Abstract
In live cells, protein folding often cannot occur spontaneously, but requires the participation of helper proteins - molecular chaperones and foldases. The mechanisms employed by chaperones markedly increase the effectiveness of protein folding, but have no bearing on the rate of this process,whereas foldases actually accelerate protein folding by exerting a direct influence on the rate-limiting steps of the overall reaction. Two types of foldases are known, using different principles of action. Peptidyl-prolyl cis/trans isomerase and protein-disulfide isomerase catalyze the folding of every protein that needs isomerization of prolyl peptide bonds or formation and isomerization of disulfide bonds for proper folding. By contrast, some foldases operating in the periplasm of bacterial cells are specifically designed to help in the folding of substrate proteins whose primary structure does not contain sufficient information for correct folding. In this review, we discuss recent data on the catalytic mechanisms of both types of foldases, focusing specifically on how a catalyst provides the structural information required for the folding of a target protein. Comparative analysis of the mechanisms employed by two different periplasmic foldases is used to substantiate the notion that combinations of a protein which is unable to fold independently and a specific catalyst delivering the necessary steric information are probably designed to achieve some particular biological purposes. The review also covers the problem of participation of peptidyl-prolyl cis/trans isomerase in different cellular functions, highlighting the role of this enzyme in conformational rearrangements of folded native proteins.
originally posted by: Phantom423
a reply to: cooperton
It's' the natural process of self assembly. It happens in nature and can be reproduced in the lab. No magic wand required.
originally posted by: Phantom423
"That is why amino acid polymerization is specifically controlled by enzymes"
And that's exactly what self assembly is - the process of organizing the components to trigger a reaction. No magic wand required.
originally posted by: Ulven
a reply to: cooperton
This is extremely fascinating. And truthfully in the STEM world it has been an exciting two plus weeks! I almost feel like we're on the verge of something big but it's not being talked about, the excitement just isn't there! It makes me scratch my head, because had all this have happened 10 years ago the world would be jumping in joy.
Perhaps we're all just too worn down collectively from Covid, Ukraine, financial stresses to really understand just what we're on the cusp of?
However, this natural fuel cell is new to me, thank you so much for sharing!
originally posted by: Phantom423
a reply to: cooperton
It's' the natural process of self assembly. It happens in nature and can be reproduced in the lab. No magic wand required.
originally posted by: Phantom423
You don't have a clue what "random chance" means. There isn't a textbook on the planet which says that evolution is random chance. You make it up as you go along, typical of your ignorance.
How many times must it be repeated that even if mutations are random (there seems to be some debate about this, but let's assume they are random for this discussion), the selection process is not random so the overall process is not random. I already explained this, here's a source explaining a correction to the "random" misconception:
originally posted by: tanstaafl
You claim these mutations are not random? Then what, pray tell, is driving them? In other words, how can you be so arrogantly certain that there is no intelligent design behind it all?
MISCONCEPTION: Evolutionary theory implies that life evolved (and continues to evolve) randomly, or by chance.
CORRECTION: Chance and randomness do factor into evolution and the history of life in many different ways; however, some important mechanisms of evolution are non-random and these make the overall process non-random.
For example, consider the process of natural selection, which results in adaptations — features of organisms that appear to suit the environment in which the organisms live (e.g., the fit between a flower and its pollinator, the coordinated response of the immune system to pathogens, and the ability of bats to echolocate). Such amazing adaptations clearly did not come about “by chance.” They evolved via a combination of random and non-random processes. The process of mutation, which generates genetic variation, is random, but selection is non-random. Selection favored variants that were better able to survive and reproduce (e.g., to be pollinated, to fend off pathogens, or to navigate in the dark). Over many generations of random mutation and non-random selection, complex adaptations evolved. To say that evolution happens “by chance” ignores half of the picture. To learn more about the process of natural selection, visit our article on this topic. To learn more about random mutation, visit our article on DNA and mutations.
originally posted by: Arbitrageur
a reply to: tanstaafl
How many times must it be repeated that even if mutations are random (there seems to be some debate about this, but let's assume they are random for this discussion), the selection process is not random so the overall process is not random. I already explained thisNA and mutations.
originally posted by: ErosA433
a reply to: tanstaafl
its actually not,
and most of the arrogance comes from those who wish to insert god into everything as a default.
Perfect deflection by someone who arrogantly denies even a remote possibility of some kind of intelligent design.
Life, on the other hand, is negentropic in nature.
originally posted by: Phantom423
There are over 500 peer-reviewed journals and hundreds of thousands of articles on various topics in evolutionary biology.
If you don't agree with any of the content, then it's incumbent on YOU to prove they're wrong. Cooperton has never done that because he can't.
originally posted by: Phantom423
Look up Gibbs free energy in biological systems. If you don't understand it, then do the research.
P.S. This is for your benefit, not mine. I'm not discussing science with you or Cooperton because neither one of you is a trained scientist.