Mutations and new morphological features

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otseng
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Mutations and new morphological features

Post #1

Post by otseng »

In my understanding of biological evolution, new morphological features are explained by random genetic mutations.

So, for debate:

What causes these mutations?
What evidence are there that random mutations can cause new morphological features?
What is the process in which new morphological features arise?

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Jose
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Post #2

Post by Jose »

I'll bite.

Let's look at the first (and easiest) one: what causes mutations.

As a practicing geneticist who has induced mutations in many a fruit fly and yeast cell, I can tell you that X-rays, hydroxylamine, and ethyl-methanesulfonate do so very effectively. So does UV light, which is why it is impossible to get a "safe tan."

X-rays typically break DNA. Repairs are usually imperfect, and often involve chromosomal rearrangements--translocations, inversions, etc--in which pieces of broken chromosomes are put back together wrong.

Chemicals often attack DNA chemically. In the case of hydroxylamine, it causes the base C to look like a different base T, so that when the DNA is replicated, the polymerase inserts an A (to pair with T) rather than inserting the proper G. This changes G:C base pairs to A:T base pairs.

Other chemicals do DNA damage that is repaired by having an enzyme remove the damaged DNA strand, and then having a polymerase copy the undamaged strand. Unfortunately, the repair polymerase (Pol 1) isn't as careful as the replication polymerase (Pol 3), so mistakes often occur.

UV induces DNA damage that is repaired in this last, sloppy way. It increases the mutation frequency from around 1/million to 1/thousand.

Natural chemicals (plant defense compounds, for example) and natural radiation (cosmic rays, radioactivity, etc) account for the mutation rate that we see normally (in humans, about 1 mutation per billion base pairs per year).

Because DNA damage cannot be targeted to any particular gene, and cannot be kept away from any particular gene, DNA damage occurs at random (as near as we can tell--maybe God or Coyote is directing the mutations so they just look random to us mere mortals).

Mutations in gene sequences can change the gene product so that it functions differently. Usually, it is inactivated, but sometimes it is changed only subtly.

Mutations in the DNA sequences that control gene expression can change the time or place that a protein is produced.

Mutations in DNA that has no function other than as "spacer" usually have no effect.

Mutations in genes for enzymes can change the way the enzymes function.

Mutations in genes for regulatory proteins can change the way these proteins regulate the expression of other genes. It is these kinds of mutations that are most likely to cause morphological effects on the organism, since many of these proteins are intimately involved in embryonic development.

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Post #3

Post by Jose »

I'm not really sure if this is the right place for this, but in a number of threads, creationists have asked for evidence that "mutations can add up." The general claim is that they cannot--but I think that claim is based on a non-standard definition of "mutation." The true definition is "a change in DNA."

This is relevant for the issue of morphological change because we know that evolution proceeds by sequential modifications of existing structures--that is, one mutation causes a change, and then a later mutation causes another change. It is necessary to know that mutations can, indeed, "add up."

The following image is remarkably clear evidence that they do. It's a little big, and I don't know how to shrink it (any ideas, otseng?). It shows the relationships of the Hawaiian Drosophila (fruit flies), most of which are unlike any other species in the world. In the center of the diagram is a box marked "STANDARD." It contains the symbols, X, 2, 3, 4, 5, and 6. These are the "standard" chromosomes. The rest of the diagram identifies each fly species, with the name of the island on which it is found, and a box that indicates the mutation(s) that occurred between this species and its ancestor--in each case, identifying chromosomal changes. The nomenclature of the chromosomal changes actually means something to people who worry about these things.
Image
The point is this: we have a very well documented series of mutations that relate a whole bunch of species to each other. These are mutations that occurred (a) at random and (b) one after another. For example, follow the diagram straight down from STANDARD, to the box containing XiK Xo /. Then go to the left to mutation Xj 3d and then up. From Xu2/. go to the left, and then go up again. Eventually, you come to the sister species, D. sylvestris and D. heteroneura. That's a whole lot of mutations that occurred one after the other between the ancestor and the current species.

There are other mutations that have occurred, but that don't show up as changes in the appearance of the chromosomes. These account for species that have the same chromosomal arrangement, but are nonetheless different.

Mutations "add up."
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Post #4

Post by YEC »

Who really knows what a mutation does? typically they are harmfull.

Anyway, for the sake of the discussion lets say a benificial mutation occurs....how big will the change be?

What allows "nature" to notice it and then select this teeny weeny morphological change?

But lets say this happens and the teeny weeney change is selected and passed on to the generations that follows...

What ate the odds of a similar mutation happening again? Producing another teeny weeney change to the same portion of the species undergoing this morphological change?

BUT, lets say even this happens......"quite a stretch".....What are the odds of it happening millions of times, over and over again in the same DNA strand responsible for the morphological change?

Suddenly evolution stops dead in it's tracks.

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Post #5

Post by juliod »

What evidence are there that random mutations can cause new morphological features?
I don't understand what your problem is. Morpholigical features were among the first recognized genetic variables. Many examples are known in plants, insects, animals, etc.

One example I know of from my graduate lab is a mutation in a single gere of yeast that results in the spores being grouped in 16s rather than tetrads (4). Consequently, there is a morphological change in the shape of the asci.

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Post #6

Post by MagusYanam »

I would just like to say that I have a bit of a problem with the use of the word 'mutation' as it is meant when it gets bandied about in discussions of evolution. Mutation is too often meant in the colloquial sense to mean an abnormal variance in the genetic structure, and this inevitably leads to equivocation over what comprises a 'mutation'. For example,
YEC wrote:Who really knows what a mutation does? typically they are harmfull.
Classical Darwinian theory only asserts that there is natural variation among offspring of any species. This is self-evident, because I don't have blue eyes like my dad's while my sister does. Is having or not having blue eyes a 'harmfull [sic]' variation, as it were? Of course not.

Classical Darwinian theory also asserts that over many generations, members of species with an inherited variation that is beneficial to their ecological niche tend to occur more frequently in the population over time because they are more likely to survive to reproduce. This is an observed phenomenon - Darwin's finches are proof. Is a heavier beak for crushing seeds a 'mutation' in the sense that it is harmful? Likewise, no. More likely, it was simply a natural variation that helped a subset of the species acculturate to a particular ecological niche.

That's why I don't like the word 'mutation' - the colloquial connotations too often lead the uneducated to equivocate in their arguments against evolution.

A second point. Logically, the variation can be as large as meiosis in the parents' DNA and the combination of the corresponding gametes will allow. We can see variations among offspring of cats, for example, in coat colour, length and pattern, in build, in eye colour, et cetera. Two solid-coat cats can give birth to a litter consisting mostly of tabbies. Moggies come in all builds and coat lengths. Artificial selection and cross-breeding have led to the development of new breeds of cat (an extreme example would be the Bengal, which was the result of a mating between a Persian and a different species, the Asian Leopard Cat).

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Post #7

Post by Jose »

YEC wrote:Who really knows what a mutation does? typically they are harmfull.
Yes, many are harmful. Many are not. we've had this discussion before, but I'll again mention the mutation that a lot of us carry, and that we think is beneficial: adult persistence of lactase. This mutation allows us to consume milk (and its lactose) after weaning, without getting sick.
YEC wrote:Anyway, for the sake of the discussion lets say a benificial mutation occurs....how big will the change be?
I guess I have to agree with MagusYanam, that the term "mutation" has been misused in colloquial English, to the point that gross misunderstandings result. A mutation doesn't have a size, in the sense that you are considering. It's a change in DNA sequence. A single base change can cause a dramatic change in the development of the organism (is this a "big" mutation because there's a "big" change in development, or a "small" mutation because it's only a change in one base pair?). Or, a chromosomal rearrangement can occur, with no effect on the organism. In any event, it is meaningless to ask what a change will be, because there are too many possibiities. We have to look at mutations that have occurred, and determine what their effect is.
YEC wrote:What allows "nature" to notice it and then select this teeny weeny morphological change?
Well, let's think about lactose tolerance. If you drink milk, you don't get sick. Consequently, you have a good source of dietary protein for yourself and your kids (if they carry the mutation also). Your kids are healthier than they would be without this protein source. This allows you to develop a culture that includes cows and dairy products. Over the years, people with this teeny weeny change are healthier than those without it, because they can take advantage of the dairy-based culture. The result is what we see today: most Europeans carry the mutation, which first occurred (as near as we can tell so far) in eastern Europe. A lot of Americans also carry the mutation, due to the colonization of the Americas by Europeans. Many Americans do not carry the mutation, if they are descended from peoples from other parts of the world.

In other words, nature "notices" the mutation, as it does with any characteristic by letting the individual animals or plants live their lives. If they are successful, they have lots of offspring. If they are less successful, they have fewer offspring. It's so simple that anti-evolutionists try to make up more complicated stories, so that they can claim that evolution can't happen. The real story is so obvious that many people don't even recognize it.
YEC wrote:But lets say this happens and the teeny weeney change is selected and passed on to the generations that follows...

What ate the odds of a similar mutation happening again? Producing another teeny weeney change to the same portion of the species undergoing this morphological change?
The odds of a similar mutation happening again are pretty low, but so what? The mutation happened, and was selected for and passed on to the next generation. It doesn't ever have to happen again--it just gets inherited.
YEC wrote:BUT, lets say even this happens......"quite a stretch".....What are the odds of it happening millions of times, over and over again in the same DNA strand responsible for the morphological change?
I've asked you before, and I'll ask again: why do you think the mutation has to happen millions of times? I agree with you fully that it won't. This is, I think, an example of what I just said--that people seem to invent complex stories about what "has to happen" because the obvious, true story is just too simple and obvious.

Once a mutation occurs, and is passed on to offspring, it becomes part of the species' genetic diversity. Over time, that particular genetic variant may be lost (if it is not helpful), or it may become common (if it is helpful).

You've said numerous times that you accept microevolution. That's what this is. Why make it more complicated by invoking some impossible requirement for the same mutation happening over and over and over?
YEC wrote:Suddenly evolution stops dead in it's tracks.
Yes, it sure would, if your scenario were actually required. Since it isn't, and since it is not a part of evolution, there's no problem. Evolution proceeds perfectly fine.

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juliod wrote:
What evidence are there that random mutations can cause new morphological features?
I don't understand what your problem is. Morpholigical features were among the first recognized genetic variables. Many examples are known in plants, insects, animals, etc.
It might be worthwhile, juliod, providing a bit of history to this question. In some other thread, the discussion moved toward the issue of mutations and selection. Otseng noted that many people don't know the details of how mutations--changes in DNA sequence--can cause morphological changes. Hence, he started this thread to explore those details.

I see this as not only a valid point, but an illustration of a Big Hole in science teaching. We typically lament the fact that our students never seem to understand how genotype dictates phenotype. At best, they memorize the terms for the exam, and promptly forget them. What can we really expect, if we never actually provide the information they need to understand the problem? We can talk about eye color and lactose tolerance all we want, and provide a glimmer of the relationship between genes and traits, but these examples fail utterly to communicate the genetic basis of morphological characterisitics. There's a big gap here.

I suspect that the thing to do is provide a bunch of examples. The tetrad-to-octad mutation is good, but is only one example. There are lots of other examples also, like the 4-winged fly:
Image
It's interesting, however, that the anti-evolution folks jump on the bx,pbx fly and say that "it's still a fly, and therefore doesn't show evolution" when the fact is that it is a superb example of how genes control morphological features.

I've tried to put together some other, general information on this issue here, in an effort to give teachers some additional help with the genotype/phenotype problem and its role in understanding evolution. We'll see if it helps...
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Post #8

Post by TQWcS »

I suspect that the thing to do is provide a bunch of examples. The tetrad-to-octad mutation is good, but is only one example. There are lots of other examples also, like the 4-winged fly:

It's interesting, however, that the anti-evolution folks jump on the bx,pbx fly and say that "it's still a fly, and therefore doesn't show evolution" when the fact is that it is a superb example of how genes control morphological features.
The mutations in the fly you provided were due to artificial changes made by geneticists. You also failed to show that this change is not beneficial to the creature. It does not have muscles in the second pair of wings...

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Post #9

Post by juliod »

The mutations in the fly you provided were due to artificial changes made by geneticists.
But the artificial changes were made randomly, which was the question asked.
You also failed to show that this change is not beneficial to the creature.
This isn't relevant. The question was about morphological changes, not benefits.
It does not have muscles in the second pair of wings...
Right! Since these wings are not functional, they are free to evolve into something else.

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Post #10

Post by Jose »

TQWcS wrote:
I suspect that the thing to do is provide a bunch of examples. The tetrad-to-octad mutation is good, but is only one example. There are lots of other examples also, like the 4-winged fly:

It's interesting, however, that the anti-evolution folks jump on the bx,pbx fly and say that "it's still a fly, and therefore doesn't show evolution" when the fact is that it is a superb example of how genes control morphological features.
The mutations in the fly you provided were due to artificial changes made by geneticists. You also failed to show that this change is not beneficial to the creature. It does not have muscles in the second pair of wings...
Thank you for making my point so eloquently! We provide a perfect demonstration of an essential point, and the response is to criticize things that are irrelevant to the issue at hand. The bx, pbx double mutant (actually with a third mutation that isn't mentioned) illustrates the genetic control of morphology. These mutations affect the expression of the Ubx gene, which is a Master Control gene that affects the expression of other genes, which bring about the development of particular body parts. Genes control development. Illustration complete.

Now, I haven't actually dissected one of these flies to check the muscles, but since the mutations affect the development of the body segment, and not just the integument, I'd be really surprised if there are not indirect flight muscles there. The leg muscles will also be those of the second segment, not those of the third segment. You're right that there are problems moving the new wings adequately for flight, but that's partly a result of the fact that other body segments are required to collaborate in the neural wiring and the segmental connections that make everything work correctly.

Uhh...what's an "artificial change," by the way? The first bx mutation that Ed Lewis found was spontaneous, but he was clever enough to spot it and follow it up. I think pbx was also spontaneous. We've made many more alleles in mutagenesis projects, but all of these mutations are real changes in the DNA, just like any other mutation. Does "artificial" mean that the mutation occurred indoors, rather than outdoors?

Uhh....why does it have to be beneficial to demonstrate the fact that genes control morphology? The 4-winged fly illustrates that the Ubx gene is expressed at a certain level in body segment T2, and that this turns on the T2 pattern of development. If a mutation turns on Ubx expression at that same level in T3, we get the T2 pattern in segment T3. There are mutations that alter Ubx expression that create an entire body of identical segments (except for the head and tail)--essentially a millipede. These die as embryos, but the point remains: the genes determine developmental patterns. That's why Ed, along with Iani Nusslein and Eric Wieshaus, got the Nobel Prize. This is really important stuff, which has had a huge impact on human embryology (because of the evolutionary conservation of the basic mechanisms).

And who cares whether it was done in a lab? It still proves that genes control morphology, which was otseng's question. Maybe you'd prefer something not from a lab--like, say, the mutation that turns cabbage flowers into broccoli. It's another of those "homeotic" mutations, in a gene we know, that determines the pattern of flower development. No lab involved there. Ah...there was human intervention, though, in that someone found the mutant and saved the seeds. Does that make this example irrelevant also?
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