So weird that
@Rise stopped replying in this thread on July 21 when his many bluffs were called...
To suggest that shows you don't understand the new genetic code introductions that are needed to go from a single cell into mankind.
That you keep writing (argument by repetition) this nonsense about "new genetic code" proves that you do not understand genetics.
As I have explained to you before:
THAT is the 'genetic code.' There is nothing new to be made from it.
That you still use this middle-schoolish 'needs new genetic code blah blah blah' explains why you rely so much on bare assertion and hiding behind your logical fallacy boogeymen - you don't understand the science.
New code [sic] which adaptation alone as a mechanism can't account for...
Argument by assertion fallacy. Merely asserting that this is the case doesn't prove it's true just because you assert it is.
You are required to provide specific evidence of this to prove your claim is true.
You still think adaptation is just epigenetics?
That's why you can get different colors of fur on a cat but you can't get scales instead of fur just by natural selection alone.
Argument by assertion and strawman fallacy. Merely asserting that this is the case doesn't prove it's true just because you assert it is.
You are required to provide specific evidence of this to prove your claim is true.
The genetic code already has the information needed to express different colors of fur.
False claim, the Genetic Code is not genes.
It doesn't have the genetic code to express scales instead of fur.
" genetic code"...
Logical fallacy, argument by assertion.
Oh, sweet irony...
I gave you the example of the folding of a new protein and the genetic code required for that to happen.
"Genetic code". Middle-school science.
You can't get a new function in a cell unless you can get genetic code that will fold a new type of protein.
Ignoring your repetitious naiveté for now, I do suggest you read
a post in a thread I made that regards, in part, your claims such as this 'new code' silliness, and what you claim is not in evidence.
...this needs to a protein that will change something so significantly in the organism that it confers a survival/reproductive advantage ...
How significantly? How do you measure that? Please explain.
I can shuffle the lines of a code in a computer program around but that's not going to create a new function.
Argument by assertion and a poor analogy.
All I need is one example to prove your mere assertion incorrect. As you do not seem very competent in the area of actual (as opposed to the simplistic 'genetics via analogy' that people like you tend to employ) genetics, I have bolded the relevant parts:
Group II Introns Generate Functional Chimeric Relaxase Enzymes with Modified Specificities through Exon Shuffling at Both the RNA and DNA Level
Abstract
...In contrast to their eukaryotic derivatives, bacterial group II introns have largely been considered as harmful selfish mobile retroelements that parasitize the genome of their host.
As a challenge to this view, we recently uncovered a new intergenic trans-splicing pathway that generates an assortment of mRNA chimeras. The ability of group II introns to combine disparate mRNA fragments was proposed to increase the genetic diversity of the bacterial host by shuffling coding sequences. ...
We demonstrated that some of these compound relaxase enzymes yield gain-of-function phenotypes, being significantly more efficient than their precursor wild-type enzymes at supporting bacterial conjugation. We also found that relaxase enzymes with shuffled functional domains are produced in biologically relevant settings under natural expression levels.
Finally, we uncovered examples of lactococcal chimeric relaxase genes with junctions exactly at the intron insertion site. Overall, our work demonstrates that the genetic diversity generated by group II introns,
at the RNA level by intergenic trans-splicing and at the DNA level by recombination, can yield new functional enzymes with shuffled exons, which can lead to gain-of-function phenotypes.
That was just in the first 3 or 4 returns I got with a 30-second Google search.[/QUOTE]
...you don't see to understand the distinction between a functional line of code and the alphabet that code uses.[/quote]
Why do you insist on using such silly analogies? 'Code' and 'alphabet'? We are grown ups here, just use the grown up words.
The genetic code has only four letters in it's alphabet.
No, the genetic code is what I explained to you before. It has nucleotides, not letters. Unlike letters in the alphabet, different combinations of those nucleotides can 'write' the same 'words' - look, you've got me using your 8th grade jargon!
But a genetic function requires those four letters to be in a precise coded sequence.
Bare assertions replied to with one:
No, it really doesn't.
If that is not done then there will be no function. Such as the function of folding a protein into a specific shape so that it can achieve a specific purpose.
Argument via assertion, Logical fallacy.
You don't get a new protein by simply changing one letter in the long string of code. The most that would do is just give you a failed protein.
You are making the argument of a child that took no more than 9th grade biology.
That is my assertion. My evidence is the things you keep writing as 'arguments.'
You are using the language analogy way too literally. Look at this gene that makes a functional protein - all those red bars? Repeated identical or nearly-identical sequences:
How does your 'logical fallacy' shield and language analogy deal with that?
The amount of letters you would have to change in that string of code to get a functional new protein is so numerous that it's basically writing a new line of code.
Argument via assertion. Logical fallacy.
Provide some evidence for that straight-up assertion.
The biggest problem for that idea is then that fact that all these changes would have to happen at once...
LOL!
Wow, OK... How much new information do you pretend there is in that gene map I pasted above?
Let's see your work, superstar.
If all you do is change one letter by chance, with no change in function, then natural selection has nothing to select. So that random mutation can't become the dominant one.
Please explain how a mutation becomes dominant, with your amazing genetics knowledge. It is true that I have not taught Genetics for 2 years, but I have taught it about 8 times, so I think I can remember the gist of it all. Use your REAL science words, not this 'new code' nonsense.
So there's no mechanism by which you could have one random letter this generation, one random letter the next, and so on, until you just by chance happen to arrange them into a functional code that folds a new protein that changes the survival rate of the organism.
Logical fallacy. Strawman argument.
And the odds are writing a new piece of code where everything is changed all at once, and ends up in the right sequence, and confers a survival improvement so it can actually become dominant, is a statistical impossibility.
Strawman.
For someone that sees a logical fallacy around every corner, you absolutely rely on some of the most obvious ones to prop up your fantasies.
It would be like suggesting you can let your cat play on your keyboard with a programming software open and, if given enough time, your cat will eventually create the "hello world' program.
You need all characters of the alphabet in place in the right sequence in order to get the program to run. Even one letter out of alignment in the coding portion would cause even such a basic and simple program to fail to function.
With your amazing genetics insights, surely you know what a promoter is, yes?
And surely you've heard of one of the more common ones, the
TATA box, right? OK, now pay attention to the words:
A TATA box is a DNA sequence that indicates where a genetic sequence can be read and decoded. It is a type of promoter sequence, which specifies to other molecules where transcription begins. Transcription is a process that produces an RNA molecule from a DNA sequence. The TATA box is named for its conserved DNA sequence, which is most commonly TATAAA
Not coding sequence, but still pretty important DNA sequences, yes?
And the TATAAA promoter is a consensus sequence. It is not universal. Doesn't bode well for your unsupported assertion, does it?
While it is true that SNPs in exons CAN alter, negatively, the function of a protein, you seem to think it is a universal.
So, let's see your evidence that it is. No more bare assertions.
Even worse if you're talking about something that requires more things than just a single protein to happen simultaneously in order for a new function to be created that confers a survival advantage onto an organism so that new function can become dominant - now you need even more lines of functional code to emerge simultaneously that just happen to be able to pair their function with the other new lines of code that emerged. You're compounding what is already a statistical impossibility with increasingly absurd levels of probability that strain the credulity of logic.
Talk about straining the credulity of logic...
Let's see your EVIDENCE for these bare assertions.
I thought this was a fitting analogy I heard: "Trying to explain DNA by random chance is like saying a tornado can go through a print shop and produce the contents of the library of congress."
Of course you did - you seem to rely on analogy instead of evidence.
Here's one - "Trying to explain DNA by an ancient deity willing it to exist from dust of the ground is like saying even one letter out of alignment in the coding portion would cause even such a basic and simple program to fail to function.'"
No matter how man tornados you send through how many different print shops, you have no reason to believe you could ever produce the library of congress. The number of co-dependant variables for this equation are beyond statistical and logical reason.
Assertion. Fallacy.
Merely asserting that this is the case doesn't prove it's true just because you assert it is.
You are required to provide specific evidence of this to prove your claim is true.
The evidence would never cause you to conclude you could get the code for a protein by random chance unless you had an a priori commitment to materialism that forced you to accept it must have happened simply because you can't accept a designer as a hypothesis - for no other reason than because it conflicts with your a priori belief in materialism.
Major strawman.
And some projection, I'm guessing.
