This is based on the inference of common descent and the inference that the ORFans are non functional.
Bald, vacuous assertions, all the way down. 
No, if they’re nonfunctional, it’s not evidence for the origin of new genes. And if the ORFans are functional, its at once evidence for the origin of genes and for common descent. How would you explain it?
Why? Think for a moment. What does the rate of new gene production (and/or loss, don’t forget that) per year have to be in order to produce the observed distribution? How likely are we to have seen one since we’ve been looking?
Secondary source. The claim actually comes from this:
(Deep surveying of alternative splicing complexity in the human transcriptome by high-throughput sequencing | Nature Genetics)
Now, how much of that alternative splicing is functional?
It could simply be common design.
We are likely to see one in a large population that is not yet fixed.
All or most. What is hard to measure is embryo development where it is prevalent.
Could it? What precedent is that conjecture based on? If I say that it could not, would that mean anything to you? If yes, why? If no, then why does your assertion that it could mean anything to you?
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Since anything could be common design, that explanation is useless. Do you really expect common design to produce useless sequences in chimps that closely resemble useful ones in humans?
Show your work.
How do you know? What does your link have to do with that?
Honestly, Bill, how can you participate in forums like this for so many years and pretend to do not know that phylogenetic testing is a mathematical model? It beggars the imagination that you could be exposed to these results so many times yet not understand how these conclusions are reached.
Such statements from you lead me to believe that you are often disingenuous, if not simply trolling. If you ever wonder why I cut off our private discussions, this is the answer.
THERE YOU GO AGAIN. If random deletions can explain it, THAT IS THE MODEL.
Specifically it is the random error term which is part of all statistical models. If some clever ID researcher were to propose a revised or extended model that explain a significant portion of the random error, resulting in a better model fit, then they could be on to something. An ID researcher could easily apply well accepted
methods to ID hypotheses.
Not only has that not happened, but there are articles on ENV specifically denouncing this approach.
BUT then you probably know all this already. How could you not?
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Hi Dan
The phylogenetic testing is testing against the pattern being random. It is not testing against design. The mathematical model that could shows reproduction is connected is a population genetics model.
I do not see direct evidence they are useless sequences.
I am not sure the work you are referring to. I do not see evidence of distinct functional genes in examples like fast breeding mice populations. We do see chromosome variation.
I know because a cause of cancer is the up regulation of embryonic pathways. In cancer cells we see activated alternative splicing.
Bill is either dishonest to an especially disheartening extreme, or intellectually and/or temperamentally unequipped for rational discourse. (“Stupid” is a common term for that.)
Speaking, though, of the word “stupid”: Bill’s behavior is, IMO, dehumanizing. To him, to us, to the forum in general. He forces his readers to either believe him (thereby creating or reinforcing ignorance and disinformation) or to judge him to be a lowlife (by virtue of repeated lying) or judge him to be a typist who suffers from debilitating low intelligence or debilitating lack of comprehension of reasoning and decisionmaking. He forces us to wonder whether he’s a dishonest lowlife or a stupid troll, and then forces us to choose whether to express that or not. It’s all dehumanizing.
No matter how Bill’s pathology is explained, it’s a good choice to manage his “contributions” with the pathology in mind. How to do that while maintaining one’s own sanity? No clue.
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Is it not? How would you know? What does “testing against design” look like, exactly?
John asked how likely we are to have seen an instance of gene production during the timeframe we have been analyzing genetic data. Your response was “likely”, which John charitably interpreted as some vague quantifier of how likely it was. The work John is asking you to show is… well, I doubt they expect an actual mathematical calculation from you, given your track record thus far… but at least some outline of an argument, some sketch, how ever crude, of what ever line of thought it is you followed to arrive at your response. Try to keep up…
Doesn’t matter. Suppose they’re functional. They don’t encide proteins, so must be performing quite a different function than they are in humans. Why would the designer create very similar sequences, in the same place in the genome, for two different purposes? Is that not a truly amazing coincidence, at best?
The work that tells you we are likely to see one in a large population that is not yet fixed.
Neither of these claims shows that all or most alternative splicing is functional.
Interesting that you now mention math when you previously stated there was no math involved. I don’t know what motivates you to be this way, but it is disrespectful to everyone here.
The phylogenetic testing is testing against the pattern being random.
That’s just wrong. Why would you make such a comment to a statistician when you should know better?
It is not testing against design.
Of course not. Design has no hypothesis to be tested*. BUT there are several examples of tests against the multiple origins hypothesis you put forward. Links are available, but I know you have seen them before.
* Here Ewert has taken a wrong turn, attempting to develop his own methods rather than use accepted methods for phylogenetic testing.
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Unless he tried the accepted methods and didn’t get the result he wanted.
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I doubt he tried, but he likely did observe those methods being used, always getting the wrong result. Anyway, Ewert’s method can’t be applied to most phylogenetic data, though I do suppose it could be used for indel or any other binary data. Maybe even RY-coded nucleotides. Probably wouldn’t get the result he wanted, though.
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It occurs to me that Bill has painted himself into a corner here. He believes that ERVs are not actually of viral origin but are designed, functional sequences, and he demands evidence of new genes that are polymorphic in a eukaryote population. So he must accept that polymorphic ERVs in the human population are in fact examples of new genes.
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If I’ve learned anything from all the interactions with Bill, he doesn’t care about getting paint on his clothes. He’ll just pretend it never happened and then paint himself into another corner later.
Bill’s argument has no corners
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True that – they just go round and round and round again.
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Hi John
I believe the whole universe is designed including viruses. Some ERV’s may be from viruses that became fixed in the germ line and others may look like virus sequences but instead be part of the animals original genome.
Nobody cares what you believe, only what you can provide evidence for. And you have just agreed, though of course you don’t know it because you seldome have any idea what you’re saying, that you can have no evdience for anything, because anything can look like anything else. You are only digging a deeper and deeper hole.
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