Evolution

February 25, 2004 9:40 PM

How do evolutionary changes occur in biology? Is there some sort of "intelligence" that helps a species adapt, or does a species have to wait for a random mutation to occur that just happens to confer an advantage (a mutation that might never even happen)? For instance, how do bacteria become resistant? And are there different theories on evolutionary changes?
posted by Tin Man to science & nature (22 comments total)

You really couldn't find anything on Google about this?
posted by Dasein at 10:04 PM on February 25, 2004

This question, it makes my head hurt.

No - really - it's so broad that it could consume of few hundred (nonexistant) gigs of straight text input on Matt's server.

Stephen J. Gould (sadly deceased) is one good populist of evolutionary theory (Punk Eek aside) and Richard Dawkins has a certain severe cachet as well.

"Is there some sort of "intelligence" that helps a species adapt" - none has been observed and none is necessary. Still, I too wonder.....

_____________________________________________

In rather broad terms, "no......yes......random genetic variations which confer resistance.....no"

At the more subtle level - with regards to your last question, look towards the giantess of a biologist who is Lynn Margulis.
posted by troutfishing at 10:09 PM on February 25, 2004

evolution is usually defined as a change in gene (allele) frequency over time, so as something becomes more beneficial it's frequency in the population will increase due to natural selection.

natural selection is the main process by which evolution occurs. this is a very powerful process whose core is very simple; organisms that are best adapted to the environment reproduce more. an even simpler way to see this is organisms that reproduce best become the most numerous. genes that help an organism reproduce best also become prevalent in the population.

This natural selection process can seem like an intelligent process, but it is not. maybe some people would call it emergent.

Often, in a diverse gene pool there will be a lot of differences that confer neither a positive or negative selective pressure. Hair color in humans for example is an easy one. on a molecular level though there are a lot of differences, people might have a slightly different structure of a cell receptor, maybe they both work, so it doesn't matter. If however the environment changes, perhaps monsters come that eat only blond babies, or a virus spreads that enters the cell through the most common form of that receptor there is now a selective advantage for non-blonds, and people with the alternate receptor. There is now said to be a selective advantage associated with those genes, and natural selection will act on them to increase their frequency in the population.

All of this has happened with no mutations yet, but is very much considered evolution. of course you have to ask how that alternate receptor came to be, that is where mutation comes in. Maybe there was a mutation a million years ago in the receptor, and it worked just as well, and so had no associated selective pressure, it could just sit there until the environment changes.

Bacterial resistance follows those patterns as well, but of course with biology it isn't so simple and clean. Scenarios like what's mentioned above certainly occur, for example you can plate out millions of bacteria on antibiotic media and you will get a few scattered colonies, these will reproduce and eventually the plate will be full of restistant bacteria. this is because you exerted a strong negative selection against the bacteria that were not resistant and they all died, maybe one in a million were already resistant, but now they are all that is left.

There are other ways it can happen too though, because biology is never clean :) Many bacteria have the ability to transfer dna from one organism to another even across species so something like staph that grows naturally on your skin can get a resistance gene from a different kind of bacteria that grows in your gut and becomes prevalent when you're on antibiotics. this of course confers a selective advantage to the staph even though the mutation never occurred in its hereditary line.

So mutations occur at a pretty set rate, the machinery that replicates dna makes mistakes at a steady level across the entire genome. Viruses make a lot of mistakes, and so mutate very repidly, the drawback is that a lot of virus particles are completely non-functional. Humans on the other hand make very few errors, estimates are 1 error in about 10⁹ base pairs. The cool thing is people have discovered some bacteria that, when faced with environmental stress, can increase their error rate, and in effect speed up evolution.

Hope that clears everything up! :)

haha, on preview, yea i mean if you're interested you should really read more about it, i skipped, you know, almost everything.
posted by rhyax at 10:36 PM on February 25, 2004

In theory, less resistant bacteria are also appearing all the time. Evolution is a flowering of happy accidents. It's a numbers game. Increase your numbers by adding time, or producing thousands of offspring every time you reproduce (which is why insects are so dominant, ubiquitous, and specialized).
posted by scarabic at 12:41 AM on February 26, 2004

If you are really interested in this I highly recommend The Blind Watchmaker by Richard Dawkins.
posted by furcifer at 1:01 AM on February 26, 2004

Another common means of antibiotic resistance in bacteria is mediated by two types of short DNA molecule, called plasmids and transposons. These molecules often contain genes that confer resistance to particular classes of antibiotic. Two bacteria can get together and "conjugate" (sort of like kissing) and exchange plasmids and transposons, and thus antibiotic resistance, with each other. Transposons can also move around within a given cell between different plasmids and the bacterial genome as well.
posted by shoos at 1:35 AM on February 26, 2004

Second recommendation for Dawkins' TBW. It does carry on a bit, and he's obviously an arsehole with a big chip on his shoulder, but he's also excrutiatingly precise.

Short answer is that natural selection and genetic variation work hand-in-hand to ensure that the odds are -- however exceedingly slim -- always in the favour of the "better" genes. Apply those tiny odds against a suitably long time period and evolution is the logical, natural, and inevitable result. It can't help but be.

Dawkins makes several irrelevent side-arguments, mainly against competing theories which are, of course, fatally flawed in his view. He also likes to snipe and snark about competing evolutionary biologists: blame his editor for not upbraiding him for his childishness.
posted by five fresh fish at 2:25 AM on February 26, 2004

A small caveat, "better" genes mean those which help their host organism survive, not "better" in any more abstract or prescient sense.
posted by signal at 4:53 AM on February 26, 2004

If you by chance really really want to get into the subject, my favorite big gun is Ernst Mayr, though there are other biggies also. Having heard both Mayr and Gould lecture, my impression is that EM was the brains behind SJG, while SJG had the public-speaking skill. Where he drifted away from Mayr he tended to thrash around and tie himself up in compound-complex sentences, as can be seen in his massive and final The Structure of Evolutionary Theory. Too bad the New Yorker review of this is offline; it's worth digging up. (N.b. on preview, this sounds snottier than I intended; obviously my view of both Mayr and Gould is that of a tourist in a deep valley looking up at two immense rocky mountains and trying to decide by eyeball which is the taller.)
posted by jfuller at 5:18 AM on February 26, 2004

I agree that this question is way too broad to be properly answered here--other than the bit about bacteria, perhaps--and that the best we can do is direct you to more complete sources of information. Aside from the books published on the topic, several of which have been mentioned above, I recommend perusing the Talk.Origins archive, which has a number informative articles.
posted by monju_bosatsu at 6:36 AM on February 26, 2004

I agree with much of what has been said. I think it's important to keep track of the notion that evolution is an *outcome* and not a *process* in itself. Organisms do not evolve because they have some drive in them that is making them evolve, but because they are subject to natural selection. Further, natural selection does not create 'better' organisms, but rather more 'fit' ones. By fit, Darwin did not mean 'strong' (this is a later sense of 'fit') but rather 'appropriate,' as in which organism 'fits' into a particular niche in the best way. Such organisms are then naturally selected (as opposed to artificially selected, i.e. bred by humans), and can over a time demonstrate evolution in form.

IANAEB, tho, and so could be wrong on all of this.
posted by carter at 6:52 AM on February 26, 2004

In a nutshell, the four mechanisms of evolution are:

1. Natural Selection: Individual organisms of a species with advantageous traits or combinations of genes are more likely to pass those genes on to the next generation. Essentially, those with disadvantageous traits die before having children, or just don't have children period. This causes a change in the gene frequencies in the population, thus "the species" changes (though it's really an aggregate of individual changes). It doesn't happen in one generation; rather, it takes many generations, and can take from dozens to thousands and millions of years, depending on the average lifespan of a species.

2. Mutation: An error in the genetic development of an individual, which is usually detrimental, but sometimes beneficial. This introduces new alleles into the population, and is considered to be the only way of adding "new" genetic material to a population.

3. Genetic Drift: Random change in the gene frequencies of a population. Individuals only pass on half of their genes to a child, so with each generation, some genetic material is lost. Often those lost alleles are passed on by other individuals bearing the same material, but sometimes alleles are lost from the population if they're rare enough to begin with (this can happen with mutations, if they're not detrimental, because they pop up in an individual, and there's no guarantee that the mutation will be passed on). Alleles can also become fixed in a population, i.e. all individuals possess the same type allele. Drift behaves according to probabilities, and there is an entire set of mathematics accorded to it.

4. Gene Flow: Transfer of genetic material between populations by means of reproduction between members of both populations. While genetic drift causes similarity within a population and differentiation between populations, gene flow does the opposite, causing similarity between populations and introducing new variations within a population.

There is also sexual selection: selection of mates based on sexual preferences (tall? short? smart? dumb? etc...). The ways these mechanisms work together is pretty much agreed upon; the large question is the method in which speciation occurs. The idea of a "species" is not a biological reality, merely a classification created by biologists, so when we consider speciation, we're considering how a population moves from one arbitrary classification to another, but it's still an important question in observations of paleobiology.

To answer your questions, in order, more directly:
1. See the mechanisms above.

2. No, there is no "intelligence." There was no "design" of an eye; it's merely the result of an accumulation of changes over time in a species (see the Dawkins book recommended above for a more thorough explanation). For example: all mammals have five digits per limb as a result of the common mammalian ancestor having five digits per limb, though some mammals today don't show it. Horses and whales, for example, are both mammals; horses seem to have one digit, while whales just have flippers, but inside, they both have bone structures with five digits per limb, simply because the ancestor did and evolution changed the species as was necessary. As for mutations: for a new allele, a mutation must occur, and that introduces new variation into a population's genetic frequencies, but that doesn't mean that a population isn't changing in the meantime via the other three mechanisms of evolution.

3. A "bacteria" becomes resistant because there are certain individuals in the population that are resistant (either possessing the resistance trait ancestrally or as a result of mutation), while most are not. When the bacteria start dying because of, say, antibiotics, those that are not resistant die out, while the resistant individuals stay alive. There is a niche created for more bacteria, so the still-living bacteria (the resistant ones) can have more and more children, who are also resistant, and thus the population gains the quality of being resistant. Then another drug could be introduced, and the population changes again in the same way. That, in a nutshell, is natural selection. In other species, instead of drugs vs resistance, think of predators and environmental pressures vs ways of dealing with predators and environmental pressures (of course, there are myriad more things on which selection works, but just as an example).

4. As mentioned above, there are different theories on how speciation (macroevolution) works (can it occur by drift alone? Or must selection create the changes?). There are also questions of exactitudes of the above mechanisms and considerations (what frequency is necessary for an allele to be given the title of "allele", for example). There are millions of hours of thought, computer simulation, and experiment being done to address questions like these, but in essence, the four mechanisms above are the agreed-upon means of evolution.
posted by The Michael The at 7:14 AM on February 26, 2004 [1 favorite]

IANAevolutionarybiologist, but I'd like to point out that in order to have "intelligence" to help with adaptation, an organism would have to have an "idea" of what a given mutation would change. "Hmm, well it's getting hotter in the environment, maybe if I shift this T to a C and this G to a T, I'll grow a bigger membrane to give off heat." It's hard to imagine how the system could know before mutating what phenotype changes the mutation would cause. (Computationally speaking, it's a very complicated question.)

The only mechanism I've heard of that might be able to accomplish this sort of thing (and again, IANAEB) is in the science fiction book Darwin's Radio, in which the genome somehow stores, unexpressed, previous failed mutations and every now and then pops out a kid with a whole cluster of them, allowing for much more sudden speciation. It strained my credulity even as science fiction.
posted by callmejay at 8:35 AM on February 26, 2004

It's well worth noting that natural selection is also found in non-living situations. Pebbles on a beach, for instance, sort themselves by size due to the effects of wave action.

Did a stone "plan" to arrive in the same strata as all the other similarly-sized stones? Did it require some sort of "intelligence" to do so? Did it "evolve" to that position?

Of course not. It all boils down to the same sort of statistical odds that govern life. Plants and animals don't "evolve" TO some destined form: evolution is the outcome of the selection process.

Natural selection is the mechanism, evolution is the consequence.
posted by five fresh fish at 9:30 AM on February 26, 2004

You all have covered the virus's adapation to antibiotics, but I still have a question: How exactly is it that STOPPING to take antibiotics can create virii that are immune to the antibiotic. I understand that when taking normal anitbiotics, a few may survive because of immunity...but if the anitbiotics wouldn't be able to kill that virii in the first place, why would stopping your anitbiotic treatment cause the proliferation of super-virii? I understand that they can cross genes, but wouldn't that super-virii live from the treatment anyways? Hope I'm asking this question properly...
posted by jmd82 at 11:45 AM on February 26, 2004

Antibiotics aren't used to treat viral infections; they're used to treat bacterial infections. Two entirely different classes of organisms.

The evolution of antibiotic resistance is a complex topic: books have been written about it. I think I might be able to give one capsule-view answer to your question, though. Antibiotic resistance is typically dose-dependant. In other words, resistant bacteria may be able to survive low concentrations of antibiotics, but at higher concentrations, their metabolisms can't keep up and they're poisoned by the antibiotic. If you stop a course of antibiotics early, the concentration at an infection site might never reach the threshold necessary to kill even slightly resistant bacteria. You've managed to select entirely against non-resistant bacteria, though. The slightly resistant bacteria can serve as the progenitors of future generations in which more robust forms of resistance now have the opportunity to evolve.
posted by mr_roboto at 12:00 PM on February 26, 2004

Ah, that makes sense, mr roboto (and thanks for the correction).
posted by jmd82 at 12:07 PM on February 26, 2004

Thanks everyone. So, mutation isn't the only way for genetic change to occur. Gotcha. And I like how five fresh fish put it -- evolution is the outcome, not the process. I always thought the following was kind of weird: "Hey, fellow plants, the climate's getting hot! Quick, try to evolve!"

And I'm glad jmd82 brought up the issue of insufficient antibiotic dosage creating resistant bacteria, because I was wondering about that.

Thanks again.
posted by Tin Man at 12:34 PM on February 26, 2004

mr roboto: I've been thinking about your response, but I've got a follow up idea if you know as much as you appear.

Say I'm disease X or Y...Both are the same bacteria, only X had a slight immunity to a given antibiotic while Y doesn't. Say I treat X but stop the treatment early so some of the slightly immune bacteria lives. Chances are that even though X is still alive, Y will still exist somewhere in the world. Now, I would think that X and Y have the same probability to evolve complete immunity to the antibiotic. However, the way you describe how immunity evolved makes it sound like X is more likely to develop a complete immunity than Y, almost like the slight-immunity genes X contains is a stepping stone to complete immunity.
This little part of evolution-in-action has always intrigued me...
posted by jmd82 at 12:50 PM on February 26, 2004

This could get messy....

Let me begin by saying that this is not my field of expertise. Though I know a lot about evolution, I came to my knowledge via biochemistry and molecular biology, rather than microbiology or evolutionary biology. A microbiologist could probably provide a very precise and accurate answer to this question.

You also need to realize that when I used the term "slightly resistant" in my earlier comment, well, that term needs to be connected to a more concrete scientific meaning in order to make sense in this explanation. This is going to require a little bit of molecular biology.

The fundamental unit of biological evolution is the gene: genes are encoded in DNA. Let's keep things simple, and say that a single gene functions by providing a cell with the instructions necessary to make a single protein. Proteins, in turn, are the active agents in biology on the molecular level. They provide structure, serve as a part of the cellular control system, facilitate the cell's chemical metabolism, and many, many other things. When a gene is mutated, the mutation affects the function of the corresponding protein; it might serve to hopelessly deform the protein (as the defective sickle cell anemia gene does to hemoglobin), or it might slightly improve the efficiency with which the protein metabolically processes a certain chemical, or it might give the protein a wholly novel function.

Antibiotic resistance, as I understand it, is typically facilitated by proteins called enzymes: "enzyme" is a general term for a protein that can make chemistry happen. In the case of antibiotic resistance, the chemistry that the enzyme facilitates is the degradation of the antibiotic molecule. Bacterial cells are filled with all sorts of enzymes that work on all kinds of chemicals--biology is, at a certain level, simply applied chemistry. And keep in mind that since mutations are always popping up, any population of bacteria will have slight differences in the libraries of enzymes available to each individual, since mutations will have occurred in certain individuals to alter the functionality of certain enzymes.

Upon encountering a novel antibiotic, it might turn out that one of the enzymes in one strain of bacteria (strain X, in your example) in a population has the capacity to slowly, feebly chemically degrade the antibiotic. This capacity might be enough to save strain X from an abbreviated course of treatment, however, and to allow the strain to form a colony in which every individual contains the anti-antibiotic enzyme. Remember, though, mutagenesis keeps happening, so some individuals might have, in addition to the original mutation, another mutation to the enzyme which improves its action on the antibiotic, thereby making these individuals even more resistant to treatment.

This is one important characteristic of evolution: new traits develop not as often through single, radical mutations as they do through the gradual accumulation of mutations over many generations. Each mutation is selected for a slight positive contribution to fitness (we're dealing with large-number statistics, remember), but when mutations are allowed to accumulate, the effect can be much larger than the sum of the parts.

When you don't finish a course of antibiotics, you allow the initial mutations to survive and be accumulated upon by future generations.

This whole discourse is a pretty radical simplification; mutations can affect DNA-level control mechanisms, too, potentially providing bacteria with higher levels of an antibiotic-degrading enzyme. And evolutionary paths need not be as simple as I've laid out here--a lineage need not always go up, up, up in fitness; evolution is robust to local minima, and it can work its way through valleys in fitness space.
posted by mr_roboto at 6:29 PM on February 26, 2004

Gotcha. That does pretty well answer my question, thanks.
Actually, I'm a 3rd year biochemistry and molecular biology major at UGA so I understand a lot of what you're saying. Alas, though our classes (namely biology) use certain things as a context for evolution, none of them have delved too deeply into the topic. I kind of wish our science department had a major that tied more closely into evolution- closest thing they have is an Evolutionary Biology class I want to take next semester if my class schedule permits.
posted by jmd82 at 10:09 PM on February 26, 2004

ok, so i'm a microbiology person, everything roboto said about it right but you also have to remember our immune system, by no means do antibiotics kill all of the bacteria causing an infection, they merely lower down to a level that our own immune system can handle. It is also true though that antibiotics are dosage dependant. So what happens when you take an antibiotic is that it kills a good percentage of the susceptible organisisms, and your immune system takes out the rest whether they are resistant or not. If you stop taking the antibiotic though you've selected for the resistant organisms for some time then stopped and left your immune system to handle more than it would have otherwise. Your immune system has no preference for resistant or non-resistant in what it kills so overall more resistant organisms will survive longer and possibly be spread.

Also, enzymes are a key aspect of resistance, but there are others, since you're a molecular major i will mention. You can have transmembrane proteins that pump out the antibiotic, or differentially permeable membrane which stop it from being allowed into the cell. Also the target itself can be altered, erythromycin for example targets the ribosome, so some bacteria have an altered, functional ribosome that erythromycin can't act upon. Lots of different ways, they're tricky :)
posted by rhyax at 11:23 AM on February 27, 2004