First genetic evidence for early animal evolution

Remember the lactose intolerance mutation? Also, tetrochromats.

I forgot about that! Here's the FR thread on the mutation that conferred lactose tolerance on adults:

... The researchers drew blood samples in order to study the DNA of a Finnish group of 196 lactose-intolerant adults of African, Asian and European descent. Each of them showed the genetic mutation for lactose intolerance in their DNA.
"That we found the same DNA variant in all lactose-intolerant people across distant ethnic groups indicates to us that it is very old," Peltonen said. "We believe that the variant we identified in patients is the original form of the gene — which mutated to tolerate milk products when early humans adopted dairy farming.
"This suggests that everyone was originally lactose intolerant," she added. "It's an excellent example of a useful mutation in human history. ..."

There was a FR thread several months ago re: tetrachromats (people with 4 color receptors instead of just RGB), but I can't find them.

NAME ONE MUTATION that has PROVEN to be beneficial. Show me the previous version of a creature that mutated, then show me the better version that had more complexity and became another species. You cannot use theory, either, you must use evidence.

Wow! A tall order! I don't know if I can fulfill all of your requests but..................

NAME ONE MUTATION that has PROVEN to be beneficial. Show me the previous version of a creature that mutated, then show me the better version that had more complexity...........You cannot use theory, either, you must use evidence.

I know of a single mutation (base pair change) in a single gene in HUMAN BEINGS that is beneficial: A "point" mutation in which valine replaces glutamate at position 6 of the hemoglobin beta-chain results in the syndrome known as SICKLE CELL ANEMIA.

The malarial parasite is an obligatory parasite for one part of it's life cycle..........it reproduces in human Red Blood Cells. The "sickling" of cells does not allow this parasite to reproduce.

A benefit of having this mutation is that IF you live in an environment that also is conducive to the malarial parasite (Africa) this mutation would be beneficial. Many people of African descent "carry" this mutation and it IS benefical for those living in Africa since they are not "easy" hosts for the malarial parasite.

I believe this fulfills all of the above challenges, except for............and became another species.

I don't mean to be picky, but given how contentious this subject can be, shouldn't we be more careful in our phrasing?

Of course, one can never be too careful. But, don't get carried away. The multisegmented body plan (brine shrimp) is ancestral to the tri-segmented body plan (fruit fly). I don't insist on the exact phylogenetic ancestry of the shrimp to the fly, but, make no mistake, there is strong scientific support for the theory that crustaceans are ancestral to insects.

I don't insist on the exact phylogenetic ancestry of the shrimp to the fly, but, make no mistake, there is strong scientific support for the theory that crustaceans are ancestral to insects.

Nor do I dispute it. Think of lobsters as ocean roaches.
Thanks for the clarification.

Some mutations are pretty obviously "beneficial" or "harmful", but the interesting thing is, beneficial is only meaningful in the context of the organism's environment. So there's no absolute measure of beneficial-ness, outside of actually putting the organisms into a specific environment.

Exactly. We don't have ways to measure fitness, especially not of single mutations. It's enough to show that enormous populations of healthy humans exist and they differ by 2%, 3%, and maybe more, in their genetic makeup. So there we have a ton of mutational differences which are not detrimental.

Oh Thanks a lot. No more lobster for me!

To my evo buddies: But isn't this still a case of pre-existing genes being turned OFF? I except the validity of the experiment as something that could happen in nature, but disagree with the idea that it makes shrimp to fly evolution more likely.

What you need is a way to show that new genes can evolve to create complex structures that were not there before. This only explains that genes for previously exisiting structures can be turned off. Unless you want to take the position that the original life form(s) had all the genes for all the potential animals in the Earth's history in it (them) from the git-go. This position strikes me at least as most improbable, though Behe has suggested it.

Even, as has been suggested, if you could get a T-rex from an ostrich by turning on genes, it does not mean that the latter evolved from the former. How did the T-rex "know" that someday it may need to evolve into the imrobable ostrich? How did it organize itself in advance with that kind of flexiblity, with all of those 'ostrich' genes turned off? Were they just waiting around in the T-rex for 60 million years?

To confirm evolution you must show how it can ADD NEW INFO in genes, not turn on or off swithces for previously existing info- unless that 1st cell had all that potential in it from the start. If that is the case, and it may be, it would support Theistic Evolution much more than the naturalistic kind.

Oh Thanks a lot. No more lobster for me!

Would it help to know that locusts are kosher?

New info is good and necessary, but don't discount the importance of losing your training wheels.

To my evo buddies: But isn't this still a case of pre-existing genes being turned OFF?

Take a look at that mosquito article I mentioned. It talks about two new genes, B1 & B2, which they didn't even have before 1984. Then the new pesticide resistant mosquitos have since duplicated them, "as many as 250 copies of the B1 allele and 60 copies of B2."

It'd be interesting to trace the study back from The Beak of the Finch (where Lindsay got the reference) & see if it's true that mosquitos didn't even have B1 & B2 before 1984. But even if they had, the duplications themselves represent an increase in information! You need a few more bits to specify that the B1 & B2 genes are duplicated instead of there being just a single copy of each.

To my evo buddies: But isn't this still a case of pre-existing genes being turned OFF?

It's a little more sophisticated than that. The mutations set up a gradient of expression from the existing gene, such that its expression ensures limb development in the thorax but not in the abdominal region of the fly. Fine-tuning and exact specification of genetic expression of this type is a gain of function, not a loss of function. Such gradients control the development of all organisms.

You may have missed the greater sequence homology at the level where evolutionary distance is less.

I merely look at the evidence presented and make judgements on the things I see, not on the things someone else has privy to. You have the great opportunity to present elucidation, presently you are not. My question was fairly simple, are not the insects I mentioned at the same level according to diagram B as presented. Another question from someone who relies on good answers from others who should know, what is considered the repressor region in the sequences shown? Is it the red region? The Blue? or the whole sequence as given? Or is it one of the lined regions?

A legend would probably be helpful. Referring to this figure :

A repression domain containing poly-alanine evolved in the insect lineage. a, An alignment of part of helix 3 of the homeodomains and C-terminal amino-acid sequences from several Ubx orthologues. Red shading indicates residues conserved among the homeodomains and Ubd-A peptides. Identical amino acids are designated by black letters within the shading, whereas those similar in function are indicated by white letters. Amino acids identical to those in DUbx C-terminal to the Ubd-A peptide and shared by at least three sequences are shaded blue; those similar in function are shaded green. Sequence gaps are shown as dashes, and translation stops are asterisks. An ellipsis (...) indicates additional amino acids not shown. Note the presence of the poly-alanine motif in all insects but not in collembolan or other arthropod Ubx orthologues. b, The distribution of the poly-alanine domain is mapped onto an arthropod phylogeny (taken from ref. 30). The repression domain arose in the insect lineage after its split from the more basal hexapods. In a, the two-letter species designations used to name Ubx orthologues designate the following animals: Dm, Drosophila melanogaster (Diptera); Ag, Anopholes gambiae (Diptera); Jc, Junonia coenia (Lepidoptera); Ms, Manduca sexta (Lepidoptera); Tc, Tribolium castaneum (Coleoptera); Fc, Folsomia candida (Collembola); Er, Ethmostigmus rubripes (Myriapoda); Cs, Cupiennius salei (a chelicerate with two Ubx orthologues); Af, Artemia franciscana (Crustacea); Ak, Acanthokara kaputensis (Onychophora).

No, I am just pointing out the absurdity of the idea that this proves it could happen in nature. This was a complex series of things done here, done in a sterile atmosphere, done in a guided way, performed over a series of tests until they got it right...and yet, that is supposed to show it could happen by chance?? Pul-Eaze!!

This whole event is something spectacular for DESIGN, because THAT'S WHAT IT IS, INTELLIGENT DESIGN, not chance/evolution/survival of the fittest.

How do you know it is a geneti mutation, and just something that those outside of that area had bred out through time? Creationists believe in genetic change through geographic isolation, but not a change from one life to another form of life. This change you mention certainly sounds unique, I would like to hear more, but it is not a symbol of evolution across phylum boundries.

This was a complex series of things done here, done in a sterile atmosphere, done in a guided way, performed over a series of tests until they got it right...and yet, that is supposed to show it could happen by chance??

Nobody is suggesting that the complex series of events in the lab were performed in nature.

Take another look at the figure I posted at #33. At the very top you can see a sequence of blue highlighted amino acids labeled 'DmUbx'. Thats the sequence in the fly, the one with the repressor fully functional. Now, move down that list until you see the one labeled 'AfUbx'. That's the sequence in the shrimp, the one that has no repressor function. Can you count how many amino acids are different in that region? I count 17.

You are saying that natural mutations, over the course of millions of years, could not account for these 17 changes.

Can you tell us why not?

Yes, it was a complex series of things, but its purpose was to find a set of 'simple' genetic changes that lead to the change in body plan.
You may have to perform a complex series of steps to open a combination lock but a million monkeys playing with it long enough will open it 'by chance'.
Regards.

This whole event is something spectacular for DESIGN, because THAT'S WHAT IT IS, INTELLIGENT DESIGN, not chance/evolution/survival of the fittest.

IOW: "No experiment can provide a valid explanation of anything that happens in nature, because all experiments are designed." It's so simple, & so obvious. You want to protect your particular religious interpretation in the face of a specific theory of biology, and you just don't care if it destroys the validity of each & every experiment ever performed in the history of science in the process. For shame.

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