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Examples of beneficial mutations?

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Xaero

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These snails are also interesting:
http://www.don-lindsay-archive.org/creation/snails.html
snails_work.gif

The picture shows 10 samples from a sequence of snail shells, oldest on the left, youngest on the right.
If there had been gaps in the fossil sequence, we would have thought that these were fossils from several different species. If we look at snails alive today, we can find separate species which differ by less than the difference shown in the picture.
The shells are from a freshwater deposit in Yugoslavia, laid down from 10 million years ago to 3 million years ago.
 
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laptoppop

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I don't understand the significance of the snails. If I read it right, these are all from the same strata, and vary more from each other than we see currently in different species of snails. What does this show -- that similar species were living at the same time?
 
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gluadys

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I don't understand the significance of the snails. If I read it right, these are all from the same strata, and vary more from each other than we see currently in different species of snails. What does this show -- that similar species were living at the same time?

No these are not different species living at the same time. It is a single species sequence laid down over a period of seven million years. This shows the morphological change in the species over that time period. (And these are only some representative samples in the full series).

Go to the link and you will also see examples of a species diverging into two groups of descendants.
 
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Mallon

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That's because this appears to me to be more of a malformity rather than something that we look at as clearly beneficial. Negative or neutral examples abound. This one is "iffy" at best.
Apparently, ectrodactyly enables the Vadoman people to climb trees more swiftly. That's a benefit. There's no need to pretend otherwise.
IF the fossil record was covering as long of a period as postulated, including as many areas as it covers, it strains credibility that it never captures the essence of the changes.
I just showed you that it does. If you want another example, just look at the development of branched feathers among theropod dinosaurs.
Are there ANY clear examples of the kinds of beneficial postulated morphological changes represented in each of these steps?
lalala.gif
 
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Deamiter

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I don't understand the significance of the snails. If I read it right, these are all from the same strata, and vary more from each other than we see currently in different species of snails. What does this show -- that similar species were living at the same time?
You seem to be confused by the fact that they are found in strata that's all called "Plioscene." This can be hundreds of meters deep and the different shells were not found all jumbled together but one type on top of another.
 
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Gwenyfur

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Again, it depends on the environment. Pre anti-malaria drugs, having a copy of the sickle cell allele allowed people to survive malaria. Without it, they'd die (and with 2 copies, they'd also end up dying). This is a beneficial mutation without any drugs, and now a harmful mutation with the drugs. You must take environment into account.

Here's another hypothetical example on why the environment must be in account. Suppose it takes energy to manufacture vitamin C. If you end up with a broken copy of the gene, and you have a diet without vitamin C, then it would be a harmful mutation. If you have a diet that's rich in vitamin C, and it's easy to get the vitamin from your food source, it's a good mutation. Without the environment, you'd have a hard time figuring out if it's good or bad.



New structures come from modifying existing structures, usually through gene duplication. For example, (someone correct me if I'm wrong), but several clotting factors in blood are coded from duplicated genes from other genes.


I'm not sure if this counts as your new structure (since it's very hard to actually observe the structure in the lab due to time scale constraints), but scientists believe that the anti-freeze gene developed from duplicating a gene involved in the pancreas. There's a lot of evidence to back this theory up. An overview can be found here, but read the sources for a more indepth overview.

http://www.pnas.org/cgi/content/full/94/8/3485

Source above.
And this is considered a "beneficial" mutation?
The disease is chronic and lifelong. Individuals are most often well, but their lives are punctuated by periodic painful attacks. In addition to periodic pain, there may be damage of internal organs, such as stroke. Lifespan is often shortened with sufferers living to an average of 40 years.
Source
 
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random_guy

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And this is considered a "beneficial" mutation?
Source

That's if they have full blown sickle cell anemia. One copy of the allele (from either the mother or father) is enough to protect from malaria. Two copies or no copies usually results in death. That's why the allele is prevalent not only in Africa, but in other areas that have malaria (such as India).

Harvard Site said:
Sickle hemoglobin provides the best example of a change in the hemoglobin molecule that impairs malaria growth and development. The initial hints of a relationship between the two came with the realization that the geographical distribution of the gene for hemoglobin S and the distribution of malaria in Africa virtually overlap. A further hint came with the observation that peoples indigenous to the highland regions of the continent did not display the high expression of the sickle hemoglobin gene like their lowland neighbors in the malaria belts. Malaria does not occur in the cooler, drier climates of the highlands in the tropical and subtropical regions of the world. Neither does the gene for sickle hemoglobin.
Sickle trait provides a survival advantage over people with normal hemoglobin in regions where malaria is endemic. Sickle cell trait provides neither absolute protection nor invulnerability to the disease. Rather, people (and particularly children) infected with P. falciparum are more likely to survive the acute illness if they have sickle cell trait. When these people with sickle cell trait procreate, both the gene for normal hemoglobin and that for sickle hemoglobin are transmitted into the next generation.
....
In the center are people with sickle cell trait who possess one gene for normal hemoglobin and one gene for sickle hemoglobin. These children are more likely to survive their initial acute malarial attacks than are people with two genes for normal hemoglobin. Also, they suffer none of the morbidity and mortality of sickle cell disease. Therefore, the people with sickle cell trait are more likely to reach reproductive age and pass their genes on to the next generation
(Ringelhann, et al., 1976).
Key parts bolded. People with one copy of the sickle cell gene suffer very little from sickle cell, and gain a resistance to Malaria. I'd say the sickle cell hemoglobin is a great mutation before the advent of anti-malaria drugs. Now, the neat thing is, even if having one sickle cell allele meant death at 40, I would predict that this would still be selected for if it meant not having the disease meant death at 12. Passing on of genes is what matters, not the age you die at.

Anyway, I hope this clears up any misconceptions you had. Key points is, it's beneficial if you're hetrozygeous, it's detrimental if you're homozygeous for the disease.

EDIT:

Harvard has a great site that explains why sickle cell anemia is selected for. Check it out here:

http://sickle.bwh.harvard.edu/malaria_sickle.html
 
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random_guy

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BTW, does the Sickle Hemoglobin count as positive new structure, or since scientists didn't observe the actual mutation, it doesn't count? If it doesn't count, that means Adam or Eve had to be a carrier (before malaria existed) and that also means that 1/4 of their subsequent children might've died from the disease.
 
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random_guy

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I found another example via the Panda's Thumb.

Labbe P, Berthomieu A, Berticat C, Alout H, Raymond M, Lenormand T, Weill M. (2007) Independent Duplications of the Acetylcholinesterase Gene Conferring Insecticide Resistance in the Mosquito Culex pipiens. Mol Biol Evol. [Epub ahead of print]
Gene duplication is thought to be the main potential source of material for the evolution of new gene functions. Several models have been proposed for the evolution of new functions through duplication, most based on ancient events (My). We provide molecular evidence for the occurrence of several (at least 3) independent duplications of the ace-1 locus in the mosquito Culex pipiens, selected in response to insecticide pressure that probably occurred very recently (< 40 years ago). This locus encodes the main target of several insecticides, the acetylcholinesterase. The duplications described consist of two alleles of ace-1, one susceptible and one resistant to insecticide, located on the same chromosome. These events were detected in different parts of the world and probably resulted from distinct mechanisms. We propose that duplications were selected because they reduce the fitness cost associated with the resistant ace-1 allele through the generation of persistent, advantageous heterozygosis. The rate of duplication of ace-1 in C. pipiens is probably underestimated, but seems to be rather high.​
So here's an example of gene duplication resulting in the duplicated gene creating a resistance to pesticide. Again, we didn't observed it, but we inferred that it happened, very recently, because there are mosquitos that have the duplicated gene and those that don't (plus different versions). So unless you're suggesting the original mosquito kind started off with all these genes and all the allele versions of the genes, and the only thing that has been occurring is gene lost (and reappearing, I guess), this would be another example of a positive mutation since it results in a protein that isn't targetted by pesticides.

EDIT:
This is very recent research, too. I suspect as time goes on, this challenge will become much easier since we'll have a lot more data to work with.
 
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