Evolution Question About Dinosaurs

[ARGOSY]

12 hours ago, one.opinion said:

I think I mentioned earlier that there are many of these genes, but that may be an understatement. Here is a link to an article that studies these sequences in more detail:

https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1005721

This is a common misconception about the experiment. It is not designed to generate novel phenotypes, but to observe adaptations to a single set of highly consistent growth conditions. The bacteria have been grown in the exact same growth medium, at the exact same temperature, and at the same starting concentration (I may be missing other constant parameters) for each new culture, for decades. Why would anyone expect novel phenotypes to arise? The bacteria have adapted to these consistent growth conditions by actually losing a lot of unnecessary genetic coding information, including genes for DNA repair. One interesting event in one of the cultures is a mutation that allows the E. coli to use the carbohydrate citrate as a fuel source. E. coli will ordinarily only use citrate under anaerobic conditions. A random shuffling event place a new promoter in just the right position to lead to activate the gene under aerobic conditions. Sometimes, random changes in genomes really do interesting things without a requirement for increased fitness (ie, de novo genes).

In any case, the LTEE has never been about trying to force E. coli to develop new phenotypes, so it is a poor model for something like the Cambrian Explosion.

Reading that link, the whole process is so theoretical. Originally it was thought that novel de novo genes are primarily formed through duplication then novelty introduced in the duplicate. (a theory yet to be proven or observed). Yet in the link it is established that primates have genes that have no similarity at all to other mammals, showing zero signs of "duplication" from an original genome.   So how did these genes form after the lineages separated from their common ancestor? They claim that it is possible that the novel de novo genes come from non transcribed regions that have then begun to express itself in coding DNA genes.  

If they can prove it, rather than surmise it, then you would have a point that multiple de novo genes can form over a limited period. But the theory is ridiculous in practice because even a single point mutation can disrupt a gene's expression. How then can a beneficial gene of thousands of base pairs actually function without a chance to develop that function?  How did all this  pre-programmed data get into the non transcribed sections of DNA in the first place, before expressing itself? 

"We have found thousands of transcripts that are human and/or chimpanzee-specific and which are likely to have originated de novo from previously non-transcribed regions of the genome. "  That could occur under creationist assumptions, it cannot occur under evolutionist assumptions.

Edited April 6, 2019 by ARGOSY

[ARGOSY]

9 hours ago, one.opinion said:

 

This is a common misconception about the experiment. It is not designed to generate novel phenotypes, but to observe adaptations to a single set of highly consistent growth conditions. The bacteria have been grown in the exact same growth medium, at the exact same temperature, and at the same starting concentration (I may be missing other constant parameters) for each new culture, for decades. Why would anyone expect novel phenotypes to arise? The bacteria have adapted to these consistent growth conditions by actually losing a lot of unnecessary genetic coding information, including genes for DNA repair. One interesting event in one of the cultures is a mutation that allows the E. coli to use the carbohydrate citrate as a fuel source. E. coli will ordinarily only use citrate under anaerobic conditions. A random shuffling event place a new promoter in just the right position to lead to activate the gene under aerobic conditions. Sometimes, random changes in genomes really do interesting things without a requirement for increased fitness (ie, de novo genes).

In any case, the LTEE has never been about trying to force E. coli to develop new phenotypes, so it is a poor model for something like the Cambrian Explosion.

Regarding the E-coli, sure that was never their intention to prove de novo genes.  My only point is that this theory of duplication leading to novel de novo genes is just a theory.  There is no evidence to support it even in the longest studies. Normally if you double up on proteins this damages an organism, only in certain circumstances in certain specialised parts of the genome does the duplication add to fitness. Even then no novelty is ever observed in those cases because the duplicate gene is needed as is,  without a new novel function.  

Anyway this E-coli chat is just a distraction, I was just saying that novel de novo genes that add to fitness are never observed in reality. 

 

[one.opinion]

3 hours ago, ARGOSY said:

Reading that link, the whole process is so theoretical. Originally it was thought that novel de novo genes are primarily formed through duplication then novelty introduced in the duplicate. (a theory yet to be proven or observed).

DNA duplications are frequent and often include entire genes. A good example is the gene for green color perception in humans. We have either 1, 2, or even 3 copies of this gene. There are many other examples in the literature.

 

3 hours ago, ARGOSY said:

But the theory is ridiculous in practice because even a single point mutation can disrupt a gene's expression.

Not really. A single point mutation can disrupt a gene function, but not its expression. A protein is still made, but with an error in it.

 

3 hours ago, ARGOSY said:

How then can a beneficial gene of thousands of base pairs actually function without a chance to develop that function?

It is well-known that non-specific transcription occurs. The transcription complex has high affinity for DNA and often transcribes little bits from normally non-coding regions. The hypothesis suspects that random changes in DNA can occasionally improve the specific affinity of certain regions for an RNA polymerase and lead to consistently transcribed regions over time and every so often, those transcripts could even begin to be translated into proteins.

An alternative is that hundreds to thousands of genes were active in humans and other primates, but they all “broke” in the lineages of the other primates and only remained active in humans. Although mutations frequently disrupt the final product, selection of functional genes prevents too many mutations from accumulating because they would lead to overall loss of fitness for the population. The gain of function in a single species is a much more probable event than the coordinated loss of function in many species over the last 6000 or so years (if you believe living organisms have only been on the planet for that long).

[ARGOSY]

1 hour ago, one.opinion said:

DNA duplications are frequent and often include entire genes. A good example is the gene for green color perception in humans. We have either 1, 2, or even 3 copies of this gene. There are many other examples in the literature.

 

Not really. A single point mutation can disrupt a gene function, but not its expression. A protein is still made, but with an error in it.

You can see from my last post that I was aware that duplication can add to fitness. I was specifically referring to NOVEL genes which add fitness. Have you any examples of a duplication event resulting in a novel gene that adds fitness?

Regarding a single point mutation, I'm surprised that you are distracting this chat through semantics. I feel it would be more constructive if we get to the core issues. I was looking forward to a long constructive chat. 

If healthy proteins were produced, then unhealthy proteins are produced, then the expression has changed. (Been disrupted)

I don't think discussions on these side issues are that necessary or in good faith, we will get no where like this.

Edited April 6, 2019 by ARGOSY

[one.opinion]

12 minutes ago, ARGOSY said:

Have you any examples of a duplication event resulting in a novel gene that adds fitness?

We have evidence of past events. Evidence strongly indicates that entire gene families have arisen by duplication and divergence. However, I’m guessing you want to see a major duplication/divergence event that has happened in the last 30 years that has clearly contributed to increased fitness. But the time scales involved simply don’t work that way.

16 minutes ago, ARGOSY said:

I don't think discussions on these side issues are that necessary or in good faith, we will get no where like this.

I am giving you an opportunity to clear up misconceptions and refine your arguments with accuracy. If you are unwilling to learn and become unnecessarily defensive by corrections to fundamental understanding, then I will be happy to let this conversation drop. 

[ARGOSY]

On 4/6/2019 at 2:59 PM, one.opinion said:

We have evidence of past events. Evidence strongly indicates that entire gene families have arisen by duplication and divergence. However, I’m guessing you want to see a major duplication/divergence event that has happened in the last 30 years that has clearly contributed to increased fitness. But the time scales involved simply don’t work that way.

I am giving you an opportunity to clear up misconceptions and refine your arguments with accuracy. If you are unwilling to learn and become unnecessarily defensive by corrections to fundamental understanding, then I will be happy to let this conversation drop. 

Please fault my "fundamental misunderstanding":

 If healthy proteins were produced, then unhealthy proteins are produced, then the expression has changed. (Been disrupted)

 

https://www.thoughtco.com/dna-mutations-1224595

"The changes at the nucleotide level then influence the transcription and translation from gene to protein expression. Changing even just one nitrogen base in a sequence can change the amino acid that is expressed by that DNA codon which can lead to a completely different protein being expressed. These mutations range from being non-harmful all the way up to causing death."

In what manner is a "completely different protein being expressed" NOT a disruption to the expression of proteins ???

 

 

Edited April 8, 2019 by ARGOSY

[ARGOSY]

14 minutes ago, one.opinion said:

However, I’m guessing you want to see a major duplication/divergence event that has happened in the last 30 years that has clearly contributed to increased fitness. But the time scales involved simply don’t work that way.

Exactly, the theory behind novel genes is unfalsifiable, impossible to prove, neither does the fossil record point to evolution, so there's nothing really behind the theory. The explanation of the Cambrian Explosion is weak, and the exponents of evolution often revert to cheap semantics. No wonder the theory hasn't gained universal acceptance

[one.opinion]

2 hours ago, ARGOSY said:

Please fault my "fundamental misunderstanding":

If you are under the impression that a single mutation is going to nullify the entire process, then you have a fundamental misunderstanding. Expression still occurs and is population-wide, rather than only in single individuals where a single mutation could possibly represent a roadblock.

[one.opinion]

2 hours ago, ARGOSY said:

The explanation of the Cambrian Explosion is weak

Why do you think the explanation is weak. Can you provide evidence that refutes it?

2 hours ago, ARGOSY said:

No wonder the theory hasn't gained universal acceptance

Acceptance of a near-spherical earth hasn’t gained universal acceptance, either. Does that mean it isn’t true?

[ARGOSY]

6 hours ago, one.opinion said:

If you are under the impression that a single mutation is going to nullify the entire process, then you have a fundamental misunderstanding. Expression still occurs and is population-wide, rather than only in single individuals where a single mutation could possibly represent a roadblock.

Love you buddy. Don't want a battle of wills. I just thought we could have a decent chat.