That table sort of reminds me of Harun Yahya’s fishing lures prove there is no evolution:

http://forbiddenmusic.wordpress.com/2008/01/09/atlas-of-creation-by-harun-yahya/

I’ve seen creationists make this argument many times. There has been no evolution. Evolutionists say evolution takes place over great periods of time. So then they show several dozen 100 million year old fossils next to photos of ostensibly living modern examples and say “they’re identical! there has been no evolution!”

So, yeah, odd that all these fossils show no evolution. Shouldn’t these fish and plants have evolved? But they haven’t!

The problem with this is two fold.

One, it’s a strawman. Creationists confuse “change happens over time” with “change always happens over time”. Not everything changes. As noted above, if a species is in a stable niche and getting three squares a day, there are no selective pressures.

Two, it’s cherry picking. They are merely cataloging examples of species that haven’t changed much. This is predicted by evolution and not at all fatal to the theory.

To wit, the table is cherry picking. Sure of the many ways bacteria acquire resistance, loss is one way. So it looks impressive, cataloging only the examples of resistance through loss.

Some insects display a remarkable ability to become resistant to pesticides. The mechanisms for such resistance, best as I can tell, are summarized by:

1. Mutations that lead to an over-expression of pre-existing enzymes that hydrolyze the pesticides. A given estrase which already exists inside an insect is over expressed 50-100 fold so that this estrase sequesters and destroys the pesticide.

2. Mutations occur, such that the target protein of the pesticide changes in shape, making the pesticide less efficient. Here, the target protein also becomes less efficient in doing what it was supposed to do in the first place.

3. There is already a pre-selection! I do not pretend to understand this mechanism, but according to this link (http://www.abc.net.au/science/news/stories/s1642457.htm), 70 year old insects, which could not have possibly been exposed to the pesticide nevertheless have the prerequisites of resistance.

4. There is a novel mutation of the estrase gene such that the estrase enzyme becomes more efficient at neutralization of the pesticide. I am still trying to understand this (I do not have subscriptions to the full text articles).

It seems that mechanisms 1 and 2 do not really serve as examples of ‘beneficial’ mutations in that they confer a loss of a mechanism rather than a net gain of information.

Mechanism 3, granted that it is bizarre, actually gives credence to creationist claims.

Mechanism 4 is what I think BlackCat was hinting at. I am trying to get more information about it.

The answer to your question is ‘absolutely’!

I am in the process of reading about BlackCat’s examples. My source of antibiotic resistance being about loss of function rather that developing “novel enzymes” is as follows:

http://www.trueorigin.org/bacteria01.asp

Pay particular attention to table I in the middle of the page.

If the above article and more like it prove to be wrong, then, yes of course I would be more skeptical. If on the other hand, I am unable to verify the presence of these “novel enzymes”, then I would be more skeptical about creationist claims.

I have no agenda here beyond getting at the truth.

Thanks for your explanation of plasmids. College has been a while, and I think I had confused a plasmid with a phage.

Regarding bacteria re-evolving enzymes to digest sugar, I would appreciate some specifics. Which bacteria? What study? I did a google search under “bacteria evolving carbohydrates enzymes” yielded 226,000 hits. I followed some of the links. It is simply amazing to find the details to which the evolution of individual enzymes are worked out.

However, I was not able to find your specific example of re-evolving the sugar digestion enzymes.

As an aside, if BlackCat can explain why there is a big deal made re the plasmid issue, I would be grateful.

Bacteria have many things significantly different from eukaryotes (like us). One of those is how their DNA is partitioned. Our DNA is broken into sections called chromosomes. These are linear regions of DNA that form dense objects during cell duplication. Bacteria, on the other hand, have much of their core DNA contained in usually one, ring-shaped structure of DNA. That is, there are no ends of the DNA strand. However, they also have a large amount of DNA in much smaller ring-shaped DNA fragments called plasmids. These usually only have one or a few genes. What is useful about them is that they can be shared amongst bacteria, even widely different populations. This allows them to spread new and mutated genes rapidly through the population. It serves a similar purpose to sexual reproduction in many plants and animals, that it is it allows for new combinations of genes. Evolution in these genes is still very much evolution, there are no grounds for creationists to complain about it. The advantage, for studying science, is that the genes can be spread very rapidly through a population. I am not aware of a mechanism to actually pick beneficial genes, I think the sharing of plasmid is either random or complete (in that they share all their plasmids). I am not sure about that, however.

As for additional examples, I already provided one: the evolution of novel sugar digesting enzymes after the first ones were intentionally destroyed. I should point out that such examples would not be all that common in modern organisms. Organisms have been living with each other for billions of years. The evolution of novel biochemical pathways would often require the presence of new chemical in the environment that the organism does not presently have the pathways necessary to handle. That is not a common occurrence, the most notable recent one being the evolution of ethyl alcohol synthesis by yeast and even that is an ancient occurrence. Considering this I am a bit surprised by the number of examples I am aware of.

Another example is actually in corn. A specific breed of corn evolved, from scratch, from non-protein coding regions of DNA, a gated ion channel. You could think of a gated ion channel as a door, a very specific door that only lets specific things through. Further, the door is only open when it receives a certain chemical signal. What is more it is made up of several identical proteins that fit together to form the channel. So it really needs 5 things: 2 very specific binding sites that allow instances of the protein to link up, a third very specific binding site that binds to the signaling molecules and when it does so substantially changes the structure of the group of proteins so they can let the ion through, the ion-selective channel that must have a very specific size, shape, and set of electrical properties, and a trans-membrane domain that causes it to embed it itself in a cell membrane. This evolved from scratch within the last hundred years or so, and in an organism with complexity comparable to humans.

Another example is the HIV protein VPU. It has undergone a number of radical changes since HIV first infected humans in the early 1900′s. This includes gaining the ability to form an ion channel (not gated, but it still requires 4 of the 5 parts I listed), additional specific binding sites, large changes in overall structure, and splitting into several different variants that are specialized for different tasks. It appears to be largely responsible for the wide variation in virulence of different HIV strains.

And as for resistance, you are simply incorrect. Resistance, both in bacteria, plants, animals, and fungi, very often involves the evolution of novel enzymes to break down the toxic compound into harmless ones. This is found in bacterial resistance as well as insect resistance (such as blowflies) Other examples, such as in malaria, have the organism develop resistance by developing a mechanism to expel the toxin before it reaches dangerous levels.

Thanks for the comment. Your explanation of dolphin/shark vs. dolphin/bat is compelling.

I also agree with your explanation of the vagueness of classifying a given mutation as ‘beneficial’. Of course, a trait can be either beneficial or harmful given the circumstances. I understand that.

For the purpose of this discussion, I had limited the definition of a ‘beneficial’ evolutionary event to a mutation (or other evolutionary mechanism) that gives rise to a net increase of information in the gene pool. Thus, for example, the Nylonase gene BlackCat and you offered is a perfect in that it meets that definition.

The nylonase gene clearly arose from a region of DNA that made another protein, mutated to produce a gene whose protein product actually had a novel function. This is, unquestionably a mutation that produced a net increase in gene pool information.

The question is whether these kinds of examples are ubiquitous or rare in nature of laboratory. So I would appreciate more examples.

Your question about how many beneficial mutations we should expect is kind of a vague question. There are good estimates of the mutation rate. Sure. How many produce novel mutations that lead to survival is a hard one to answer. Remember, evolution is not about the organism getting better and developing new features all the time. If the niche the organism lives in is unchanging and there is no nearby niche that’s unexploited, novel mutations would have little effect. They are only beneficial if they give the creature a better chance than the rest of the species of passing on genes. If I can produce as many children without wings as you can produce with wings, humans aren’t going to evolve wings.

However if the environment changed, either rapidly or slowly, then novel mutations would come into play. Lets say, for example, rising ocean leaves brought the sea closer to a group of animals that had always been landlocked. The sea is a source of new food. Let’s say a genetic mutation in rats produces bits of webbing between their little claws. The mutation has always been there, it pops up randomly in the population, but was of no survival benefit. These kinds of things are common. Even in humans we’ve noticed some silly differences. Some people can roll their tongue, some can’t. Some people have dangly earlobes, some don’t. Some people have single eyelids, some people have double eyelids. These little differences don’t confer any survival advantage but if suddenly our food source became scarce and a nearby food sourced was easy to exploit by people would could roll their tongues, that odd little mutation is going to go from being a funny thing you can do in a pub to something that lets you live.

Anyway, any rat with the random mutation of the webbing would have a slight advantage in getting at food in the shallow water. A rat without the webbing might miss meals and die. The rat with the webbing would get a meal and live and pass on these gene. The gene would become more common in that population. Other mutations might also occur. Rats with more webbing and less fur would have an advantage. Rats with nostrils pointing more up and back could swim farther…

Think about this. A dolphin looks a lot more like a shark than it looks like a rat. A creationist would make a prediction that a dolphin and shark should be more genetically similar. Both are hairless, both have fins, both have teeth. God would surely re-use the genes. This is their argument for why man and chimps are so genetically similar. God is just making use of what works. But an evolutionist would go, no a dolphin evolved from a mammal and a shark is a fish. A dolphin should actually share more genes with a rat. Ah. A testable hypothesis. And if it didn’t, that would present a very large problem for evolution. Guess what? A dolphin and rat are much more genetically similar than a shark and a dolphin.

Anyway, don’t think evolution has any goal in mind of producing X Men. If a species is getting three squares a day, it’s going to continue being that species. If a new food source appears next door, some of that species might evolve to exploit that new food source and become a whole new species.

With all due respect, I was not able to grok your links. The abstracts you site are too vague.

Your link re nylonase was very interesting, and I accept it as a legitimate example of net info gain by Evolutionary mechanisms.