Evolution's False Doctrines: i.e. Punctuated Equilibrium Etc.

mark kennedy

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If there were no precursors, how could it be just "60 de novo genes"? Wouldn't it require an entirely new genome?

We had been told for decades that the genomes of chimpanzees and humans were so close the explanation had to be gene expression, constantly pretending they couldn't find any differences. After the publication of the Human Genome paper they began comparing the DNA of humans and chimpanzees and the divergence was a lot more then previously thought. They began arguing that the genes were still nearly identical but there were some 40,000 divergent amino acids, only about 30% were actually identical. No explanation offered as to how all that happened.

If we don't have DNA from an ancestor, how do you know it required "60 de novo genes"?

Selection can explain the survival of the fittest but the arrival of the fittest requires a cause:

The de novo origin of a new protein-coding gene from non-coding DNA is considered to be a very rare occurrence in genomes. Here we identify 60 new protein-coding genes that originated de novo on the human lineage since divergence from the chimpanzee. The functionality of these genes is supported by both transcriptional and proteomic evidence. RNA– seq data indicate that these genes have their highest expression levels in the cerebral cortex and testes, which might suggest that these genes contribute to phenotypic traits that are unique to humans, such as improved cognitive ability. Our results are inconsistent with the traditional view that the de novo origin of new genes is very rare, thus there should be greater appreciation of the importance of the de novo origination of genes…(De Novo Origin of Human Protein-Coding Genes PLoS 2011)​

Whatever you think happened one thing is for sure, random mutations are the worst explanation possible. They cannot produce de novo genes and invariably disrupt functional genes. You can forget about gradual accumulation of, 'slow and gradual accumulation of numerous, slight, yet profitable, variations' (Darwin). That would require virtually no cost and extreme benefit with the molecular cause fabricated from vain imagination and suspended by pure faith. The only available explanation would have to be punctuated equilibrium on a scale not seen since the Cambrian explosion.

You really aren't very good at this, are you?

A little better then you might have guessed.

Have a nice day :)
Mark
 
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Justatruthseeker

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We had been told for decades that the genomes of chimpanzees and humans were so close the explanation had to be gene expression, constantly pretending they couldn't find any differences. After the publication of the Human Genome paper they began comparing the DNA of humans and chimpanzees and the divergence was a lot more then previously thought. They began arguing that the genes were still nearly identical but there were some 40,000 divergent amino acids, only about 30% were actually identical. No explanation offered as to how all that happened.



Selection can explain the survival of the fittest but the arrival of the fittest requires a cause:

The de novo origin of a new protein-coding gene from non-coding DNA is considered to be a very rare occurrence in genomes. Here we identify 60 new protein-coding genes that originated de novo on the human lineage since divergence from the chimpanzee. The functionality of these genes is supported by both transcriptional and proteomic evidence. RNA– seq data indicate that these genes have their highest expression levels in the cerebral cortex and testes, which might suggest that these genes contribute to phenotypic traits that are unique to humans, such as improved cognitive ability. Our results are inconsistent with the traditional view that the de novo origin of new genes is very rare, thus there should be greater appreciation of the importance of the de novo origination of genes…(De Novo Origin of Human Protein-Coding Genes PLoS 2011)​

Whatever you think happened one thing is for sure, random mutations are the worst explanation possible. They cannot produce de novo genes and invariably disrupt functional genes. You can forget about gradual accumulation of, 'slow and gradual accumulation of numerous, slight, yet profitable, variations' (Darwin). That would require virtually no cost and extreme benefit with the molecular cause fabricated from vain imagination and suspended by pure faith. The only available explanation would have to be punctuated equilibrium on a scale not seen since the Cambrian explosion.



A little better then you might have guessed.

Have a nice day :)
Mark

It is there comparison method. They use BLAST...

The process requires that they cut the genome up into little snipets that they then sequence. They then match that sequence to any part in the human genome, regardless if it is in a completely different part of the genome and may have a completely different function.... This is how they arrived at their almost identical claim.

Now if you were to try doing that in a court of law to show someone's DNA matched that at a crime scene, it would be thrown out of court so quickly you wouldn't have time to blink....

This is what they call evidence...
 
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mark kennedy

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It is there comparison method. They use BLAST...

The process requires that they cut the genome up into little snipets that they then sequence. They then match that sequence to any part in the human genome, regardless if it is in a completely different part of the genome and may have a completely different function.... This is how they arrived at their almost identical claim.

Now if you were to try doing that in a court of law to show someone's DNA matched that at a crime scene, it would be thrown out of court so quickly you wouldn't have time to blink....

This is what they call evidence...
Sure, DNA is one of the best evidential arguments you can get in court. When you are talking millions of years gradual of accumulated mutaions makes sense on the surface. But when your talking vital organs like the human brain the probability statistics are off the charts. The evolution of the human brain from apes arguments I have made on here remain unanswered. Speculation abounds but the means of such an evolutionary giant leap simply don't exist. The rest is silence which speaks volumns to the fallacy of the Darwinian tree of life. Evolution happens, just not on that scale.
 
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Justatruthseeker

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Sure, DNA is one of the best evidential arguments you can get in court. When you are talking millions of years gradual of accumulated mutaions makes sense on the surface. But when your talking vital organs like the human brain the probability statistics are off the charts. The evolution of the human brain from apes arguments I have made on here remain unanswered. Speculation abounds but the means of such an evolutionary giant leap simply don't exist. The rest is silence which speaks volumns to the fallacy of the Darwinian tree of life. Evolution happens, just not on that scale.

I protest your use of words. Evolution doesn't happen.

Adaptation happens. Variation happens...

Black rabbits placed near the arctic may over time become fat white rabbits, but they will always be rabbits.... The wolf may vary in appearance from a Mastiff to the Pug, but it remains the same species....

This is not evolution on any scale. It is adaptation and variation. The word evolution need not even be mentioned.....

I know how you mean it, but not all can make that distinction....
 
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mark kennedy

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I protest your use of words. Evolution doesn't happen.

Adaptation happens. Variation happens...

Black rabbits placed near the arctic may over time become fat white rabbits, but they will always be rabbits.... The wolf may vary in appearance from a Mastiff to the Pug, but it remains the same species....

This is not evolution on any scale. It is adaptation and variation. The word evolution need not even be mentioned.....

I know how you mean it, but not all can make that distinction....
The distincton comes down to evolution as adaptation and the natural history known as Darwinisn. They are not the same thing but are used synonomously. I share your frustration, I don't appreciate how any change in DNA is called a mutation, even when the alternate allele requires no change.
 
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Heissonear

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Are you worried if evolution with whatever characteristics was shown to happen it would somehow be evidence against God? No, it would only be evidence about some theories. God can create in any manner He wishes, and His interventions can appear even to look like what we call evolution, etc., and none of it can ever one way or another mean anything for or against God.

No one ever knows God because they believe in some creationism theories instead of other creationism theories.

People only ever come to know of God by responding to the pull to seek Him, with all of their heart.
Jeremiah 29:13 You will seek Me and find Me when you search for Me with all your heart.

Saving faith only ever comes only by hearing the word of Christ --
17 So faith comes from hearing, and hearing through the word of Christ. (Romans 10:17)

There are other kinds of faith of course, faith in this or that. Faith in a football team, or a car, or free market capitalism.

Even faith in one creationist theory over another.

But none of those various faiths are saving.

Only faith in Christ is saving.
You are correct in the details you list.

Creation happening as per Genesis 1 and 2 show a young Creation.

Evolution evidence shows evolution never happened.

Does this save a person? No.

Does this put a person front of the Creator, no other position. Yes.

But as you say God know what He has done.

God bless, brother.
 
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Gene2memE

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Whatever you think happened one thing is for sure, random mutations are the worst explanation possible. They cannot produce de novo genes and invariably disrupt functional genes. You can forget about gradual accumulation of, 'slow and gradual accumulation of numerous, slight, yet profitable, variations' (Darwin). That would require virtually no cost and extreme benefit with the molecular cause fabricated from vain imagination and suspended by pure faith. The only available explanation would have to be punctuated equilibrium on a scale not seen since the Cambrian explosion.

A little better then you might have guessed.

Have a nice day :)
Mark

The bolded part is simply untrue. [1] [2] [3]

It has been demonstrated, repeatedly, that mutations are sufficient for de novo gene origination, in large mammals generally and in humans specifically. It has also been demonstrated that natural selection is sufficient to conserve these de novo genes in populations.

Study one:

Mutation of the DNA molecule is one of the most fundamental processes in biology. In this study, we use 283 parent-offspring trios to estimate the rate of mutation for both single nucleotide variants (SNVs) and short length variants (indels) in humans and examine the mutation process. We found 17812 SNVs, corresponding to a mutation rate of 1.29 × 10−8 per position per generation (PPPG) and 1282 indels corresponding to a rate of 9.29 × 10−10 PPPG. We estimate that around 3% of human de novo SNVs are part of a multi-nucleotide mutation (MNM), with 558 (3.1%) of mutations positioned less than 20kb from another mutation in the same individual (median distance of 525bp). The rate of de novo mutations is greater in late replicating regions (p = 8.29 × 10−19) and nearer recombination events (p = 0.0038) than elsewhere in the genome.

...

In each generation new genetic variants are introduced by mutations. In this study we use whole genome sequence data from Icelandic families to directly observe such new mutations. Our estimate of the mutation rate implies that a newborn with 30-year-old parents will on average carry 75 new SNV mutations and 6 new short indel mutations. We observe that some of the found mutations occur much closer together than would be expected by chance. Our analysis shows that mutational hotspots cannot explain this clustering, instead the clustering mutations are likely created by a single mutational event.
Study two:

The emerging picture across different species is that de novo genes emerge at high rates [4,6,12]. The birth of de novo genes encoding functional proteins involves two important steps: the acquisition of an ORF and the addition of regulatory signals needed for transcription. The sequence of events is not clear, however, and evidence for both models can be found in the literature.
Study three:

The birth of new genes is an important motor of evolutionary innovation. Whereas many new genes arise by gene duplication, others originate at genomic regions that do not contain any gene or gene copy. Some of these newly expressed genes may acquire coding or non-coding functions and be preserved by natural selection. However, it is yet unclear which is the prevalence and underlying mechanisms of de novo gene emergence. In order to obtain a comprehensive view of this process we have performed in-depth sequencing of the transcriptomes of four mammalian species, human, chimpanzee, macaque and mouse, and subsequently compared the assembled transcripts and the corresponding syntenic genomic regions. This has resulted in the identification of over five thousand new transcriptional multiexonic events in human and/or chimpanzee that are not observed in the rest of species. By comparative genomics we show that the expression of these transcripts is associated with the gain of regulatory motifs upstream of the transcription start site (TSS) and of U1 snRNP sites downstream of the TSS. We also find that the coding potential of the new genes is higher than expected by chance, consistent with the presence of protein-coding genes in the dataset. Using available human tissue proteomics and ribosome profiling data we identify several de novo genes with translation evidence. These genes show significant purifying selection signatures, indicating that they are probably functional. Taken together, the data supports a model in which frequently-occurring new transcriptional events in the genome provide the raw material for the evolution of new proteins.
Have a nice day Mark.
 
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Bungle_Bear

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We had been told for decades that the genomes of chimpanzees and humans were so close the explanation had to be gene expression, constantly pretending they couldn't find any differences. After the publication of the Human Genome paper they began comparing the DNA of humans and chimpanzees and the divergence was a lot more then previously thought. They began arguing that the genes were still nearly identical but there were some 40,000 divergent amino acids, only about 30% were actually identical. No explanation offered as to how all that happened.



Selection can explain the survival of the fittest but the arrival of the fittest requires a cause:

The de novo origin of a new protein-coding gene from non-coding DNA is considered to be a very rare occurrence in genomes. Here we identify 60 new protein-coding genes that originated de novo on the human lineage since divergence from the chimpanzee. The functionality of these genes is supported by both transcriptional and proteomic evidence. RNA– seq data indicate that these genes have their highest expression levels in the cerebral cortex and testes, which might suggest that these genes contribute to phenotypic traits that are unique to humans, such as improved cognitive ability. Our results are inconsistent with the traditional view that the de novo origin of new genes is very rare, thus there should be greater appreciation of the importance of the de novo origination of genes…(De Novo Origin of Human Protein-Coding Genes PLoS 2011)​

Whatever you think happened one thing is for sure, random mutations are the worst explanation possible. They cannot produce de novo genes and invariably disrupt functional genes. You can forget about gradual accumulation of, 'slow and gradual accumulation of numerous, slight, yet profitable, variations' (Darwin). That would require virtually no cost and extreme benefit with the molecular cause fabricated from vain imagination and suspended by pure faith. The only available explanation would have to be punctuated equilibrium on a scale not seen since the Cambrian explosion.



A little better then you might have guessed.

Have a nice day :)
Mark
Firstly, you didn't answer either of my questions.

Secondly, the evidence you are quoting does not support your assertion.

Conclusion: you are no better at this than I thought :oldthumbsup:
 
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mark kennedy

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The bolded part is simply untrue. [1] [2] [3]

It has been demonstrated, repeatedly, that mutations are sufficient for de novo gene origination, in large mammals generally and in humans specifically. It has also been demonstrated that natural selection is sufficient to conserve these de novo genes in populations.

Study one:

Mutation of the DNA molecule is one of the most fundamental processes in biology. In this study, we use 283 parent-offspring trios to estimate the rate of mutation for both single nucleotide variants (SNVs) and short length variants (indels) in humans and examine the mutation process. We found 17812 SNVs, corresponding to a mutation rate of 1.29 × 10−8 per position per generation (PPPG) and 1282 indels corresponding to a rate of 9.29 × 10−10 PPPG. We estimate that around 3% of human de novo SNVs are part of a multi-nucleotide mutation (MNM), with 558 (3.1%) of mutations positioned less than 20kb from another mutation in the same individual (median distance of 525bp). The rate of de novo mutations is greater in late replicating regions (p = 8.29 × 10−19) and nearer recombination events (p = 0.0038) than elsewhere in the genome.

...

In each generation new genetic variants are introduced by mutations. In this study we use whole genome sequence data from Icelandic families to directly observe such new mutations. Our estimate of the mutation rate implies that a newborn with 30-year-old parents will on average carry 75 new SNV mutations and 6 new short indel mutations. We observe that some of the found mutations occur much closer together than would be expected by chance. Our analysis shows that mutational hotspots cannot explain this clustering, instead the clustering mutations are likely created by a single mutational event.
Study two:

The emerging picture across different species is that de novo genes emerge at high rates [4,6,12]. The birth of de novo genes encoding functional proteins involves two important steps: the acquisition of an ORF and the addition of regulatory signals needed for transcription. The sequence of events is not clear, however, and evidence for both models can be found in the literature.
Study three:

The birth of new genes is an important motor of evolutionary innovation. Whereas many new genes arise by gene duplication, others originate at genomic regions that do not contain any gene or gene copy. Some of these newly expressed genes may acquire coding or non-coding functions and be preserved by natural selection. However, it is yet unclear which is the prevalence and underlying mechanisms of de novo gene emergence. In order to obtain a comprehensive view of this process we have performed in-depth sequencing of the transcriptomes of four mammalian species, human, chimpanzee, macaque and mouse, and subsequently compared the assembled transcripts and the corresponding syntenic genomic regions. This has resulted in the identification of over five thousand new transcriptional multiexonic events in human and/or chimpanzee that are not observed in the rest of species. By comparative genomics we show that the expression of these transcripts is associated with the gain of regulatory motifs upstream of the transcription start site (TSS) and of U1 snRNP sites downstream of the TSS. We also find that the coding potential of the new genes is higher than expected by chance, consistent with the presence of protein-coding genes in the dataset. Using available human tissue proteomics and ribosome profiling data we identify several de novo genes with translation evidence. These genes show significant purifying selection signatures, indicating that they are probably functional. Taken together, the data supports a model in which frequently-occurring new transcriptional events in the genome provide the raw material for the evolution of new proteins.
Have a nice day Mark.
That does not descibe a de novo gene produced even once. Certainly not one as highly conserved as a brain related gene. You at least bothered to read it but a mutation resulting in such highly conserved gene is ridiculous at best.
 
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Bungle_Bear

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That d o es not descibebabde novo gene produced even once. Certainly not onebas highly conserved as a brain related gene. You at least bothered to read it but mutation resulting in such highly conserved gens is ridiculous.
Hahahaha. I love the way you compliment somebody for reading something then demonstrate that you didn't read it yourself! Priceless! You should have read the part that says "However, it is yet unclear which is the prevalence and underlying mechanisms of de novo gene emergence. In order to obtain a comprehensive view of this process we have performed in-depth sequencing of the transcriptomes of four mammalian species, human, chimpanzee, macaque and mouse, and subsequently compared the assembled transcripts and the corresponding syntenic genomic regions."
 
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mark kennedy

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Firstly, you didn't answer either of my questions.

Secondly, the evidence you are quoting does not support your assertion.

Conclusion: you are no better at this than I thought :oldthumbsup:
The word is trolling. A random quote and no connection to the discussion is an obvious attempt to detail the thread.
 
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mark kennedy

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Hahahaha. I love the way you compliment somebody for reading something then demonstrate that you didn't read it yourself! Priceless! You should have read the part that says "However, it is yet unclear which is the prevalence and underlying mechanisms of de novo gene emergence. In order to obtain a comprehensive view of this process we have performed in-depth sequencing of the transcriptomes of four mammalian species, human, chimpanzee, macaque and mouse, and subsequently compared the assembled transcripts and the corresponding syntenic genomic regions."
Yes, they looked at the transcriptones which is exactly where you would look. They found nothing and reported exactly that.
 
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Gene2memE

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That does not descibe a de novo gene produced even once.

Yes it does, multiple times...

Sigh, fine. Want to get REALLY specific:

Hominoid-Specific De Novo Protein-Coding Genes Originating from Long Non-Coding RNAs

Here we identified 24 hominoid-specific de novo protein-coding genes with precise origination timing in vertebrate phylogeny. Strand-specific RNA–Seq analyses were performed in five rhesus macaque tissues (liver, prefrontal cortex, skeletal muscle, adipose, and testis), which were then integrated with public transcriptome data from human, chimpanzee, and rhesus macaque. On the basis of comparing the RNA expression profiles in the three species, we found that most of the hominoid-specific de novo protein-coding genes encoded polyadenylated non-coding RNAs in rhesus macaque or chimpanzee with a similar transcript structure and correlated tissue expression profile.

....

We found that most of the hominoid-specific de novo protein-coding genes encoded long non-coding RNAs in rhesus macaque or chimpanzee, with similar transcript structure and correlated tissue expression profile, but the protein-coding genes often had higher transcriptional abundance. According to the rule of parsimony, we conclude that at least a portion of long non-coding RNAs, especially those with active and regulated transcription, may serve as a birth pool for protein-coding genes that are then further optimized at the transcriptional level, a pattern insensitive to the parameters used in the identification and analysis of de novo genes.
...

We analyzed the characteristics of these de novo protein-coding genes. Consistent with previous reports [4], we found that the gene products were smaller, with a median length of 150.5 amino-acids, compared with 416 amino-acids in the human genome, suggesting the difficulty in de novo origination of long ORFs [reference omitted]. The transcripts were generally expressed at lower levels compared with the human genome background [reference omitted]. Nineteen of the 24 de novo genes (79.2%) showed evidence to co-opt the transcriptional context, including seventeen (70.8%) that overlapped with another gene (nine anti-sense and nine at the same strand) and five (20.8%) located downstream of bi-directional promoters [table reference omitted]. Consistent with the case of FLJ33706 or C20orf203 [8], Alu elements contributed to eight exons in eight genes (33.3%), and to three splicing junction sites in two genes [table reference omitted], further supporting the previous observation that repeat elements might be involved in the origination of some de novo genes [11]

...

Brain and testis may be favorable locations for newly created de novo genes


The out-of-testis hypothesis states that the testis is a hotbed of new gene origination, given its permissive chromatin state allowing widespread transcription [13], [29]. We analyzed the expression profiles of the de novo protein-coding genes we identified and tested the out-of-testis pattern by following the idea described in [29]. First, we investigated the relative abundance of each de novo gene across testis, skeletal muscle, liver, heart, adipose, prefrontal cortex and cerebellum in terms of RNA-Seq read counts. As shown in [table reference omitted], the de novo genes were most often transcribed in cerebellum. Testis ranked number two or three, depending on the species. Second, we tested whether class I (human-specific) de novo genes are more often biased to testis compared to class II (human/chimpanzee shared) de novo genes. As discussed in [29], Class I should be more often expressed in testis if the out-of-testis hypothesis stands. As shown in [table reference omitted], different from this prediction, class II de novo genes had a much higher proportion of reads expressed in testis. Thus, de novo genes may not generally conform to the out-of-testis hypothesis. Testis-biased expression of de novo genes had been reported so far in the fruit fly [9], [12]. By contrast, none of the previously reported human-specific de novo genes appeared to have such a pattern:
i) the three de novo genes identified in [7] are broadly transcribed;
ii) higher expression levels of FLJ33706 [8] were observed in several brain regions such as cerebellum or cerebral cortex compared to testis (relative expression levels, 2.4–4.9 versus 1.5);
iii) sixty de novo genes identified in [5] are most often transcribed in cerebral cortex with testis following as the second top tissue. In summary, testis may still be the location of some de novo genes, but brain appears to be a favorable location for the origination of many human de novo genes.
....

And another study

Tracing the De Novo Origin of Protein-Coding Genes in Yeast

Here, we identified 84 de novo genes in S. cerevisiae S288C since the divergence with their sister groups. Transcriptome and ribosome profiling data revealed at least 8 (10%) and 28 (33%) de novo genes being expressed and translated only under specific conditions, respectively. DNA microarray data, based on 2-fold change, showed that 87% of the de novo genes are regulated during various biological processes, such as nutrient utilization and sporulation. Our comparative and evolutionary analyses further revealed that some factors, including single nucleotide polymorphism (SNP)/indel mutation, high GC content, and DNA shuffling, contribute to the birth of de novo genes, while domestication and natural selection drive the spread and fixation of these genes.

 
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Bungle_Bear

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The word is trolling. A random quote and no connection to the discussion is an obvious attempt to detail the thread.
I specifically addressed your posts. You, on the other hand, did not address mine - and you then accuse me of being at fault? :scratch:
 
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DogmaHunter

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In your case for PE, you explain the details well.

Thank you. Too bad it won't stick in your head though.

But you cannot prove one event much less the course of life over time experienced PE.

I can easily prove that PE occurs like I explained it.

BoxCar2D

Leave the site open for 2 to 3 hours.
By then, the "cars" in that program will have reached a local optimum.
If you leave it open for another hour, you'll notice that the cars will barely continue to change, if at all, since they've reached their local optimum.

Now, change the track by clicking the button "Input see / change terrain".
You'll get a dropdownlist where you can choose another terrain.
Now have the program continue. You'll already notice notable change within several generations

There, done: PE in action.


The way YOU would want it proved can't be done.
Why? Well, because we don't have time machines and because we don't have a fossil of every single generation of every single lineage for the entire 3.8 billion year history of life on earth.

In short: because your demands are beyond ridiculously unreasonable. In ultra-short: because you are dishonest.

I'm not gonna bother with the rest of your post, since it's the same delusional PRATT stuff as always.
 
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DogmaHunter

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Yes you present "PE in a nutshell", in good details.

But let us read from the chaps who originated it, from their words as was an intoduction overview as follows:

View attachment 243166

Ah, just what I thought. To understand the science of why there are periods of rapid evolution then near stasis gaps in the fossil record.

In other words presented by the authors, evolution is finicky. AV may call it consistently finicky.

Another quote mine, another lie.
And curiously, the quoted part doesn't call into question evolution at all. That's just you again, lying about what it actually says.
 
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DogmaHunter

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Sure, DNA is one of the best evidential arguments you can get in court. When you are talking millions of years gradual of accumulated mutaions makes sense on the surface. But when your talking vital organs like the human brain the probability statistics are off the charts. The evolution of the human brain from apes arguments I have made on here remain unanswered. Speculation abounds but the means of such an evolutionary giant leap simply don't exist. The rest is silence which speaks volumns to the fallacy of the Darwinian tree of life. Evolution happens, just not on that scale.

Ow look, another appeal to ignorance based on an argument from incredulity.



Greeeeaaaat.....
 
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Jimmy D

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If you believe in man descending from ape you must believe in punctuated equilibrium. The hominid line starts 2 mya without precursors and requires at least 60 de novo genes. Impossible by any strech of the imagination but that conclusion would require actually reading something. You obviously cant be bothered with such things.

I was referring to your unusual description of PE in post 6.

"Punctuated equilibrium is the idea that a 'hoprfull monster' can emerge in one generation"

"Adaptive evolution has to happen in a couple of generations for it the happen at all. What we have in the fossil record is new species with high developed traits emerging suddenly without precursors."
 
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mark kennedy

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The bolded part is simply untrue. [1] [2] [3]

It has been demonstrated, repeatedly, that mutations are sufficient for de novo gene origination, in large mammals generally and in humans specifically. It has also been demonstrated that natural selection is sufficient to conserve these de novo genes in populations.

Study one:

Mutation of the DNA molecule is one of the most fundamental processes in biology. In this study, we use 283 parent-offspring trios to estimate the rate of mutation for both single nucleotide variants (SNVs) and short length variants (indels) in humans and examine the mutation process. We found 17812 SNVs, corresponding to a mutation rate of 1.29 × 10−8 per position per generation (PPPG) and 1282 indels corresponding to a rate of 9.29 × 10−10 PPPG. We estimate that around 3% of human de novo SNVs are part of a multi-nucleotide mutation (MNM), with 558 (3.1%) of mutations positioned less than 20kb from another mutation in the same individual (median distance of 525bp). The rate of de novo mutations is greater in late replicating regions (p = 8.29 × 10−19) and nearer recombination events (p = 0.0038) than elsewhere in the genome.

...

In each generation new genetic variants are introduced by mutations. In this study we use whole genome sequence data from Icelandic families to directly observe such new mutations. Our estimate of the mutation rate implies that a newborn with 30-year-old parents will on average carry 75 new SNV mutations and 6 new short indel mutations. We observe that some of the found mutations occur much closer together than would be expected by chance. Our analysis shows that mutational hotspots cannot explain this clustering, instead the clustering mutations are likely created by a single mutational event.
Study two:

The emerging picture across different species is that de novo genes emerge at high rates [4,6,12]. The birth of de novo genes encoding functional proteins involves two important steps: the acquisition of an ORF and the addition of regulatory signals needed for transcription. The sequence of events is not clear, however, and evidence for both models can be found in the literature.
Study three:

The birth of new genes is an important motor of evolutionary innovation. Whereas many new genes arise by gene duplication, others originate at genomic regions that do not contain any gene or gene copy. Some of these newly expressed genes may acquire coding or non-coding functions and be preserved by natural selection. However, it is yet unclear which is the prevalence and underlying mechanisms of de novo gene emergence. In order to obtain a comprehensive view of this process we have performed in-depth sequencing of the transcriptomes of four mammalian species, human, chimpanzee, macaque and mouse, and subsequently compared the assembled transcripts and the corresponding syntenic genomic regions. This has resulted in the identification of over five thousand new transcriptional multiexonic events in human and/or chimpanzee that are not observed in the rest of species. By comparative genomics we show that the expression of these transcripts is associated with the gain of regulatory motifs upstream of the transcription start site (TSS) and of U1 snRNP sites downstream of the TSS. We also find that the coding potential of the new genes is higher than expected by chance, consistent with the presence of protein-coding genes in the dataset. Using available human tissue proteomics and ribosome profiling data we identify several de novo genes with translation evidence. These genes show significant purifying selection signatures, indicating that they are probably functional. Taken together, the data supports a model in which frequently-occurring new transcriptional events in the genome provide the raw material for the evolution of new proteins.
Have a nice day Mark.
I've never said there can't be de novo genes, on the contrary, I have odten pointed out the arctic cod has done it at least four times. Vut a protien coding gene from simple repeats is not the same thing as a brain related gene. These 60 de novo genes would have had to originate 2 mya along with the other major molecular overhauls. This is supposed to have happened 2 mya, without precursors, and no viable cause. This obsession with mutations is self deprecating, you cant identify a single unique de novo gene originating in the human genome. All this come from comparisin and idke speculation.
 
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I've never said there can't be de novo genes, on the contrary, I have odten pointed out the arctic cod has done it at least four times.

I never said you did.

What I said was that your claim that random mutations can't produce de novo genes was a lie. I then supported this with multiple studies that provide evidence for mutations producing de novo genes.

Here's an excerpt from the Schlotterer paper:

"Interestingly, a considerable fraction of these RNAs are also associated with ribosomes, suggesting they are actively translated. Such short peptides form proto genes, which can be subject to selection. Through the acquisition of new mutations, proto genes can grow and result in functional de novo genes"

I don't think it can be made much clearer....

Vut a protien coding gene from simple repeats is not the same thing as a brain related gene.

Except that's not what studies argued. Transactional co-option in genes is not just 'simple repeats'. The Besenbacher paper highlights that there are insertions/deletions, transitions, transversions and tandem mutations all in de novo gene production in humans.

These 60 de novo genes would have had to originate 2 mya along with the other major molecular overhauls. This is supposed to have happened 2 mya, without precursors, and no viable cause. This obsession with mutations is self deprecating, you cant identify a single unique de novo gene originating in the human genome. All this come from comparisin and idke speculation.

This, along with your line from earlier in the thread - that "The hominid line starts 2 mya without precursors and requires at least 60 de novo genes" - is completely unsupported. To support that, here's that Wu et al 2011 paper you're so fond of misconstruing:

Our finding of 60 de novo genes, 59 of which are fixed in the human population, suggests that the de novo origin of protein coding genes on the human lineage is not a rare event. Since the chimpanzees and humans shared a common ancestor ∼5–6 million years ago, this indicates that the rate of origin of de novo genes is ∼9.83–11.8 genes per million years, an estimate that is much higher than previously reported.​

Where does that 2mya figure come from, by the way?

Even some of the papers the Wu study references (in this case Knowles and McLysaght A, 2009) indicate there are genetic precursors to de novo genes:

This is the first evidence for entirely novel human-specific protein-coding genes originating from ancestrally noncoding sequences. We estimate that 0.075% of human genes may have originated through this mechanism leading to a total expectation of 18 such cases in a genome of 24,000 protein-coding genes.​

To support my case further, here's yet another paper - on de novo genes nonetheless - showing that there ARE precursors present in hominidae de novo gens prior to fixation.

De Novo Genes Arise at a Slow but Steady Rate along the Primate Lineage and Have Been Subject to Incomplete Lineage Sorting


Here, we describe a rigorous search for cases of de novo gene origination in the great apes. We analyzed annotated proteomes as well as full genomic DNA and transcriptional and translational evidence. It is notable that results vary between database updates due to the fluctuating annotation of these genes. Nonetheless we identified 35 de novo genes: 16 human-specific; 5 human and chimpanzee specific; and 14 that originated prior to the divergence of human, chimpanzee, and gorilla and are found in all three genomes. The taxonomically restricted distribution of these genes cannot be explained by loss in other lineages. Each gene is supported by an open reading frame-creating mutation that occurred within the primate lineage, and which is not polymorphic in any species. Similarly to previous studies we find that the de novo genes identified are short and frequently located near pre-existing genes. Also, they may be associated with Alu elements and prior transcription and RNA-splicing at the locus. Additionally, we report the first case of apparent independent lineage sorting of a de novo gene. The gene is present in human and gorilla, whereas chimpanzee has the ancestral noncoding sequence. This indicates a long period of polymorphism prior to fixation and thus supports a model where de novo genes may, at least initially, have a neutral effect on fitness..​

It's like I say "Look, water" and you reply "Where?", all while standing knee deep in a puddle.
 
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