My thoughts on an Evolution News post on ERVs

I think scd is actually asking how the creature survived before infection with the retrovirus that has evolved to provide a function.

I concede that this is equivalent to asking how Devonian fish survived before bats evolved sonar.

We have plenty of evidence that the Loch Ness monster isn’t real. We have plenty of evidence that evolution happens and has happened for a very long time. We have evidence that earlier ancestors of the species with these funcitonal retroviral insertions didn’t have them. You just ignore all the evidence.

I don’t. The probability isn’t even over the genome. If I recall, insertions are more probable in regions of the genome that are often uncoiled.

That doesn’t cast their origin in doubt. An ERV could be the result from a retroviral insertion and still protect against viral infections after insertion.

That doesn’t cast their origin in doubt. An ERV can be produced through retroviral insertion and function as a gene regulator for genes around the insertion site.

The Muller two step. A change is beneficial, then made necessary.

We are talking about the same base, not within 100 kbp. I would put those odds at around 1 in 50,000 at best for a specific sequence motif for a specific virus, and much more rare in the vast majority of cases.

Prove it. Show that a significant portion of all LTRs have adaptive functions in gene regulation. Don’t just sit there and make stuff up.

Sal? Scd is Salvador Cordova? That almost makes sense.

By the function not being necessary to survival, but merely useful should it evolve.

An organism living in a colder climate might benefit from gaining a thicker coat of fur than it currently has, but it might still be able to survive without it’s fur becoming thicker. But should some organism in that population be born with a thicker coat of fur because some mutation created a regulatory function that caused the fur to become thicker, it might be at an advantage compared to those organisms without this.

Oops! fixed.

Sal Cordova and SCD have different IPs. I don’t think they are the same person.

such as? remember that scientists said something similar in the past about finding a living coelacanth.

if we can explain all these evidence without evolution (depend also what kind of evolution you refer to)- we cant consider it as evidence for evolution.

if so you accept that viral insertions are very specific. up to 1\30,000 of the genome.

i didnt said otherwise. i just give you an alternative explanation under the design scenario.

hard to prove. its like saying that in theory a cell-phone can function with only 1-2 parts. we know that any cell-phone need more than 1-2 parts. so what make you think that a cell phone can function with 1-2 parts?

but i do talking about 100 kbp. so under your scenario can you show what is the chance to get 2 such insertions?

see here:

The design scenario doesn’t explain the three layers of phylogenetic evidence.

Then you are talking nonsense. The insertions are found at the same base, not within 100,000 base pairs. Therefore, we need to know the probability of two independent insertions happening at the same base. Any other calculation is irrelevant.

You would need to show that the initiated transcription is functional. Transcription alone is not function.

Also, there are only 1743 that initiate transcription of genes. That’s less than 1% of ERVs.

Read:

That just shows transcription can be initiated by sequences found in LTRs (which nobody denies), not that they have any biological function.

So no, that did not provide any evidence that a significant portion of LTRs are functional.

Not that I know of. What are you talking about? The evidence against the Loch Ness monster is similar to the evidence that there is no elephant in your living room. You look in your living room, and you don’t find one. This assumes that you would have found the elephant if it had been there, and given the intensiveness of the search, it seems clear that there are neither elephants nor monsters in Loch Ness.

True. If you can explain the evidence, and explain it equally well, by some other phenomenon, then it isn’t evidence for evolution. However, you have no alternative explanation. Right?

I wouldn’t call that very specific. What I’d say is that the probability of an insertion is not uniform over the genome. The more highly transcribed a region, the greater the probability for an insertion there.

Then the size and temperature of Loch Ness. eDNA studies have been done at Loch Ness. It suggests no Nessie as well.

irrelevant. there is a reason why im talking about 100kbp. so do you agree that the chance to get 2 insertions in a chunk of 100kbp is something like 1/30,000?

see also here:

https://www.spandidos-publications.com/10.3892/ijmm.2013.1460

“Although most HERV genes are partially deleted and not intact, HERV LTRs comprise features including promoters, enhancers, selective splicer sites and polyadenylation sites in order to regulate the expression of neighboring genes.”

“accumulating evidence has revealed that LTR sequences derived from distantly related ERVs have been exapted as regulatory sequences for many host genes in a wide range of cell types”

the same with the coelacanth fish. in the past everyone thought it doesnt exist since we had no evidence that it exist. till we find one in 1938.

i do actually. here for instance we can see that ERVs can be explained well even without evolution.

That’s not an explanation.

It isn’t. Loch Ness is quite different from the whole world. It’s much easier to say what is or isn’t in a small area.

Go ahead. Explain them.

so we can compare it to someone who claim that plesiosaurus still exist somewere on earth.

one explanation is that these ERVs are integral part of the genome, and not the result of viral insertions. its at least one possible explanation. its also explain why a retrovirus need a host and why it has so few genes.

That is the same as the previous one, it just shows that there CAN BE functional sequences in LTRs. It doesn’t show any significant proportion of them are. Heck, it mostly just shows that there is transcriptional activity associated with some of these LTRs, which still doesn’t entail a useful or adaptive function derives from it.

A locus is some times expressed by some sort of promoter-activity from another sequence =/= it must have a biological function. It just doesn’t follow. This is the same problem as we saw with the whole ENCODE fiasco and their poor reasoning surrounding “biochemical activity”.

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