... but men are by far much more savage killing many many more men, women, and babies every day.
Random variations over large populations with selection only maintaining the functional versions.
Each change from the simpler not reproducing monomer chemicals doesn't need to occur in a particular chain of events for a single chain. It's important to remember that each successful variation will multiply to fill the environment massively increasing the sample space for a successful variant.
A particular genetic make up is vanishingly unlikely, but the task of survival doesn't require a particular technique.
It's like the old playing cards analogy... the chance of a single specific hand is very, very low, but the chance of a winning hand is significantly higher.
"A gene can emerge from scratch" tell us about this in detail.Well, the Rugged landscape experiment, described in post n° 617 shows this statement wrong. A gene can emerge from scratch in 20 generations.
When hard empirical evidence contradicts a theory, it's the theory that is wrong.
The annoying thing is that reality - god's creation, if you like - shows you wrong.
Just a few examples:
Here is a link to a site that lists more than 700 variations of the human haemoglobin gene - all viable.
A very cool experiment, performed by Yuuki Hayashi et al. proves you also wrong.
Before the actual gene there is a genetic "switch" in the DNA before the DNA part that codes for a protein. This switch can be activated by a hormone, a the metabolic starting material or any other signal molecule. Yuuki Hayashi et al. performed a cool experiment: they stripped the coding part of the DNA of a virus that codes for the protein that grants access to a E. coli batcteria and replaced it with a random stretch of DNA. After 20 generations the virus had increased its infectivity by 1.7*10^7 compared with the starting generation.
The funny thing is that despite doing exactly the same function (allowing the virus to enter a cell) the sequence was completely different from the wild type.
source to the original papers:
Experimental Rugged Fitness Landscape in Protein Sequence Space
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 ...
www.ncbi.nlm.nih.gov
https://www.sciencedirect.com/science/article/abs/pii/S0022519306005984
Another simple and elegant way to show multiple variations can perform the same function, was set up by professor Kishony and his team. A gigantic petri dish was divided in lanes with increasing concentration of antibiotics, from (0 , no antibiotics: 1 just enough to kill all bacteria, gradually up to 1000 x the concentration of 1). Different strains of Escherichia Coli were spotted in the 0 lane. As this lane got filled and the places for new bacteria got depleted the bacteria were pushing against the boundary of the 10 lane. Only those bacteria and their descendants that got the suitable mutations for surviving in a higher concentration of antibiotics made it to the next lane. The experiment filmed over 11 days shows clearly that bacteria can evolve a resistance to a 1000 fold stronger concentration of antibiotics than the wild type bacteria.
Here you have the same experiment, but with professor Kishony explaining the experiment
It shows that evolution is cumulative. Each mutation increases the resistance to the antibiotics in an incremental way (see how the growth of the culture pauses at every boundary and how the growth always start at one tiny spot). But it also shows that different lineages with different DNA sequences can make it to the next concentration.
a technical paper published by the team
Spatiotemporal microbial evolution on antibiotic landscapes
the website of Roy Kishony's research institue:
Home - Kishony lab
The problem with statistical "arguments" of that kind is that it assumes all possible compounds are equally likely to form under all conditions, which is not the case.For a typical protein length of about 300 amino acids, more than 10^390 different polypeptide chains could theoretically be made. This is such an enormous number that to produce just one molecule of each kind would require many more atoms than exist in the universe.
So the sequence (code) was created by nature? Code's NEVER get created w out intelligent design, we know this.
"Before the actual gene there is a genetic "switch" in the DNA before the DNA part that codes for a protein."
Where did the DNA come from? How about the machinery to interpret DNA? did they evolve at the same time? If so, what luck!!!!
You start with a random DNA sequence that is expressed as a protein and if it does something useful it is selected for. Otherwise it is just some random protein running about the cell."A gene can emerge from scratch" tell us about this in detail.
It is explained in post #617, as is referenced in the post Thurston-howell III quoted. But Thurston-howell III deleted that part "by coincidence" deleted that part."A gene can emerge from scratch" tell us about this in detail.
Thurston-howell III is committing the fallacy of moving the goal posts. His original challenge was"Before the actual gene there is a genetic "switch" in the DNA before the DNA part that codes for a protein."
Where did the DNA come from? How about the machinery to interpret DNA? did they evolve at the same time? If so, what luck!!!!
Post n° 617 gives three real life examples that his statement is wrong.The sequence is VERY SPECIFIC, it is a code that gets translated. Tell us how the sequence became arranged.
So if you limit the conditions, the chance is even less that a useful protein will emergeThe problem with statistical "arguments" of that kind is that it assumes all possible compounds are equally likely to form under all conditions, which is not the case.
It is a fact of biochemical synthesis that the compounds which are produced will depend on the starting conditions. Given the starting materials, not all possible combinations of them will be equally likely to form under any given set of conditions.So if you limit the conditions, the chance is even less that a useful protein will emerge
I think you have your logic backwards.So if you limit the conditions, the chance is even less that a useful protein will emerge
The opposite is true. That’s what takes care of the randomness. It’s the difference between getting six sixes on 6d6 with or without keeping the sixes.So if you limit the conditions, the chance is even less that a useful protein will emerge
A human cell contains about 10000 different proteins, do you want to play this numbers game?The opposite is true. That’s what takes care of the randomness. It’s the difference between getting six sixes on 6d6 with or without keeping the sixes.
Not following you, what goal post??????Thurston-howell III is committing the fallacy of moving the goal posts. His original challenge was
Post n° 617 gives three real life examples that his statement is wrong.
Instead of having the integrity of admitting as such, he isn't addressing not a single point tat is made, but deflects to a side question.
How are you measuring them?A human cell contains about 10000 different proteins, do you want to play this numbers game?
How ate you measuring them?
luckily, point mutations are reversible.Oh look -- a mutation!
We following Jesus do not need any models for development.Because those don't make for reasonable models for development.