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ERV FAQ: But how can you rule out design as an explanation?



In science, we apply the principle of parsimony. This means that we go with the simplest hypothesis that accounts for the greatest amount of relevant data, and is contradicted by none of them.

Endogenization fits the bill.

Design does not. 

It fails to explain why ERVs with functional genes should be found in common locations in different species. Their location is not critical to their function.

It fails to explain why long terminal repeats (LTRs) are so configured as to get themselves transcribed by RNA polymerase II

It fails to explain such a scattergun approach as using integrase to insert retroviral genes into host cells' DNA with no regard as to whether or not it will cause damage. 


A common tactic of creationists, writing
 about ERVs, (see this page) is to suggest that ERVs were designed into the genomes of different "kinds" of organisms to provide a means of distributing useful genes by exogenization and re-endogenization. So which were the "original, designed-in" ERVs, and which were the result of exogenization and re-endogenization? How does "design" explain that the latter types are still in orthologous locations in different species? As we know, integrase is incapable of targetting specific DNA loci.

Design also fails to explain all the non-functional LTRs and ERVs. 

Endogenization in common ancestors explains all these things.

If you say, "Ah, well, it could be design, but we just don't know the reasons", then you have made your hypothesis unfalsifiable, and therefore of no interest to science. Under such hypotheses, the actual facts become irrelevant. 

The purpose of science is to explain the actual facts - why they are as they are, and not otherwise.

If anyone thinks that ERVs are designed for a purpose or for several purposes, they must have answers to the following.
a) What is reverse transcriptase designed to do?
b) What is integrase designed to do?
c) Why were ERVs designed with a viral codon bias?
d) What is the design purpose of re-transcribable promoters?
e) What were the HERVs that produced the consensus sequence that generated Phoenix designed for?
f) What is the design purpose of both exogenous and endogenous KoRV
g) If chimps and humans have commonly located ERVs, what is the design purpose of giving these common ERVs common disabling mutations?
h) What is the design purpose of giving some people HERVs and not others?
i) What is the design purpose of creating different syncytins in different placental lineages


Someone attempted to answer these questions. I reply here.


You see, it's no use just waving your arms in the air and saying, "Design". Endogenization explains all these features. How does "design" explain them?


2 comments:

  1. "...therefore of no interest to science." - and therefore no interest to you. If you have a science only worldview, that is sick. We are far more than science can discover. If you are only concerned with what we can know scientifically, I daresay you're going to leave a lot of information, good information, out.

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  2. Whether or not there is more to know than what science can tell us, science tells us a lot. And saying that I am leaving information out does not actually show that I am.

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