Principles of Evolution, Ecology and Behavior

E&EB 122 - Lecture 17 - Key Events in Evolution

Chapter 1. Introduction [00:00:00]

Professor Stephen Stearns: Okay, we’re in the middle of the section on macroevolution. We’ve had three lectures about macroevolutionary principles: speciation; how to build a tree; and then what kinds of uses you can put a phylogenetic tree to. Now we’re going to do three lectures on different ways to look at the history of life. And the first cut, the first lecture, the one today, is an abstract conceptual view of the history of life, and it looks at it as a series of major transitions in the organization of life and how information is transmitted.

And this is the structure of the lecture. We’ll talk about what life is, how we think it originated, the origin of cells and eukaryotes, some other key events; and then we’ll summarize with the principles that are involved in key events, in major transitions in evolution.

Well, life is basically anything that has the properties of multiplication, variation in heredity, plus metabolism. So it’s not necessarily carbon-based or silicon-based or based on anything else; it has these abstract properties. And what we really mean by metabolism is something about thermodynamics.

A living thing that has metabolism is using free energy that it’s getting from the environment, and it’s using that to maintain a partially isolated system–it’s a local system; your body is a partially isolated local system–and it’s doing so to keep it in an ordered state–it’s preserving the information that evolution and development have given it–and it’s doing so against an entropy gradient. So basically we eat energy and we excrete entropy, and the next time you’re looking at the toilet flushing down, think about all that entropy that you’re putting down into the system. Okay? So this is what metabolism does.

Now if you try to do experiments in the laboratory in which you’re watching the evolution of RNA molecules, or if you try to do in silico experiments in the computer in which you are looking at the origin of structures–and that can get to be pretty sophisticated stuff–you’re not dealing with a living system. That’s artificial. Because with RNA, we’re providing the metabolism, we’re putting the ATP and the enzymes into the test tubes, and in programs for artificial life, the things that are evolving in the computer are actually getting their energy basically from the electrical cable that we’ve got plugged into the wall, feeding the computer.

So if you can get, independent of any human intervention, any system that’s got multiplication, variation and heredity–so the basics to make natural selection work–and you can arrange metabolism, then it’s going to start to evolve, and it will be alive.

So our problem is to figure out how did this all get going? The first major transition was the transition from an abiotic world to a living world; the origin of life. And to do that we had to get multiplication, variation, heredity and metabolism. And the answer is increasingly that it is likely that metabolism came first, and that heredity and multiplication came second; variation was probably there from the start.

So I’m going to actually dwell on some things that are now chemically fairly trivial, and some things that are logically non-trivial and involve paradoxes. Because this is an area that we know it did happen; and we can now break down the steps in increasing detail, but important things are not understood.

Chapter 2. The Transition from Non-Life to Life [00:04:15]

So the environment at the origin. Gosh, I went through this thing yesterday and I got all the words on it, and then I start talking and they’re not there. So the environment at the origin. The Big Bang is now dated at about 13.5 billion years. It was just a few years ago it was dated at 20 billion years. So the universe, as we know it, is a big younger than I had thought a decade ago. And in stars, the nuclei of all of the elements were synthesized out of hydrogen, basically, and some of the novae and supernovae created things that are heavier than iron; and a lot of that is important cofactors for enzymes in your body. You could not actually function biochemically as you do if you did not have things that had been cooked up in the explosions of giant stars.

Now the solar system is formed basically from recycled star stuff, about 5 to 4.5 billion years ago, and there’s intense planetoid bombardment of the inner planets going on at that time. Nothing living could have existed on the face of the earth, because temperatures were simply too high; the surface of the planet was really a toxic wasteland of boiling lava and very, very extreme temperatures and pHs. The initial atmosphere got blown off. The moon was formed, possibly because of the impact of a large planetoid that hit the forming earth and actually blew a chunk of it off.

And at that point the earth had short days; it was spinning very rapidly. It had condensed from a cloud of stuff, and as it fell in, it brought angular momentum into the system. And so the earth started off with a higher rotation speed than it currently has.

Then about a billion years after the planet forms, the atmosphere is reducing, the temperature has fallen to where liquid water can exist on the surface of the planet. And life probably originates on a positively charged mineral surface, and it seems now likely that it was probably at a deep hydrothermal vent.

So there was a hot high-pressure acid around a positively charged mineral surface. There was a lot of chemical energy at that interface. We don’t know that for sure, but this does seem to be the kind of a context in which you can get certain chemical reactions to work, that won’t work elsewhere.

So you need the building blocks of life. You need linear lipids; they can make membranes and they can make compartments. You need amino acids to make proteins. You need purines and pyrimidines to make nucleotides. You need sugars and phosphates to link things together. And so there’s a branch of Origin of Life research that specializes in the chemical conditions under which you’ll get this building blocks.

And then after you get the building blocks, and get them to work together, you need things that will make copies of themselves. So if you can get reproduction, variation in reproductive success, some kind of inheritance, then natural selection will take over. If you can get some kind of primitive genetic molecule, it can get honed into an RNA or a DNA structure. If you can get some kind of primitive cell, with a very simple membrane, then natural selection can hone it into a selective filter, where there are pores in the cell that let certain things in and out, and so forth.

So you have to have–you can start with fairly simple things, and natural selection will refine them fairly rapidly, but you have to start with at least these simple things. So that’s kind of a bootstrap operation. You’ve got to get those first replicators up and running before natural selection will take over and create complexity and precision and make it into a sophisticated system.

So how do you get the building blocks? Well there were some very interesting experiments, done by a grad student at the University of Chicago, Stanley Miller, working with Harold Urey, and what basically he did was he would put methane, nitrogen, ammonia, ammonia chloride; he would put in carbon monoxide, nitrogen, hydrogen, different kinds of mixtures, into a vessel, and then he would pass an electric spark through it. And he found that it was fairly easy to get these amino acids to fall out.

And, by the way, most of this guy’s Ph.D. thesis consisted not of performing that experiment, but of doing the analytical chemistry afterwards to convince everybody that this was actually what he had gotten. Okay? In 1953, that was not so easy; we didn’t have all these beautiful gas chromatographs and whatnot to do the identifications.

Okay, so the basic structure of this is that you make something out of fairly small, simple molecules, likely to be in the atmosphere or in the water, on the surface of the earth, 3.5 to 4 billion years ago. And you give it some energy in the form of an electric charge, or you heat it, or whatever, and you see what comes out. So amino acids are pretty easy.

When I was 15-years-old, I was fascinated by this experiment in high school, and I tried to repeat it, and I blew up the chemistry lab, and I produced a toxic cloud of cyanide gas–which you can get out of these guys–and that caused the evacuation of the entire building, with 200 students sitting outside on the lawn, in the middle of morning classes; it was deeply satisfactory. [Laughter]

Okay, so we have a bit of ambivalence on this issue of abiotic synthesis. Some things we get real easy. Okay? We get amino acids, fatty acids, sugars and purines pretty easily. Some things are hard. So pyrimadine nucleotides; ribose is not so easy. A linear, long-chain, fatty acid, that you might find really useful for making a membrane, that’s not so easy. And it’s not easy to get these things all in the same synthetic environment. So you have to imagine that well perhaps we’re getting different chemical reactions going on in different micro environments, and they’re mixing somehow.

But then once we’ve got the building blocks, you run into what is not a chemical synthesis problem, you run into an abstract logical problem. Okay? That’s the error threshold. So the amount of information that you can maintain by selection is limited by copying fidelity. Basically what that says is that if you have a very high mutation rate, you are destroying all of the information that you’ve accumulated, and you’re not transmitting enough of it to the next generation to be able to usefully accumulate information on how to do something better. So that’s the error threshold. If you don’t really have high copying fidelity, then mutations will kill you.

And if you have a small genome–basically if you have a small genome that’s big enough to do something–it can actually have a higher mutation rate than a large genome. A small genome is small enough so that the probability of a mutation at any one place in it is fairly small. A big genome is extremely likely to have a bunch of mutations. So there’s a relationship between the size of the genome and the amount of mutation that can be tolerated.

Chapter 3. Eigen’s Hypercycles [00:12:23]

So Manfred Eigen–he’s a German guy who got a Nobel Prize for his work in biochemistry–was thinking about the origin of life, and he said, “Well, the relevant mutation rate is non-enzymatic replication. We’re going to be making copies of molecules, and at the origin there aren’t any enzymes anymore.” Okay? Enzymes are things that are produced by living systems; we don’t have them. We have to imagine ourselves back into the situation where we don’t have enzymes but we want replication.

And for that, it turns out–he did the calculations–the maximum genome size is about 100 nucleotides. So if we’re dealing with replication of a DNA-like or an RNA-like molecule, you can only get up to a genome of about 30 amino acids with the kinds of mutation rates you get with non-enzymatic replication.

Well that’s much, much too small for an enzyme. You’re not going to get an enzyme out of that. Anything bigger than that, you need to make the replication more accurate, and in order to make it more accurate you need an enzyme. You need translating machinery to take the genome and make it into that enzyme; you need the enzyme then to be working on making the genome replicate accurately.

And that takes a lot more than 100 nucleotides; it takes more like 1000 to 10,000 nucleotides to construct any of the things that we know of now that can do that. And so you can’t get enzymes without a big genome, and you can’t get a big genome without enzymes. It’s a catch-22. Where are you going to go?

So Eigen tried to cook up a way out of this, and he called it hypercycles. And the word hyper immediately makes you think of something that’s almost quasi-metaphysical. It’s nothing complicated. Okay? Here’s what a hypercycle is. Each one of these little things here is a chemical reaction, and this little loop that I’m pointing at, where B is making something that’s making more B, indicates that B is actually capable of making more of itself; it’s a chemical reaction that can make more of itself.

And there are a lot of such chemical reactions. Often, in a chemical reaction, you’ll get product out of one side, plus some other stuff that’s like what you started with. And this big dark arrow here indicates that some of what B makes is actually a precursor for C. So C needs something that B is making, and it takes it and makes more of itself, and then it ships something on that D needs to make more of itself; and D takes that and makes more of itself and ships something on that makes A; etcetera. Okay?

So if you can set up–it’s called a hypercycle because it’s a cycle with cycles inside of it; it’s a cycle of cycles. The rate at which any one of these can replicate increases with the amount of product that’s being given to it by any of the others. And that means that B can make more B if it’s getting more from A; C can make more C if it’s getting more from B.

That means that in order to function, the elements have to cooperate for substrate. They can’t compete for substrate. They have to take what they need and pass some on. And if this is then going to get refined and become more sophisticated, and perhaps get to the point where it acquires an information molecule like DNA, then it has to competitively exclude other such systems.

You could imagine a surface at a hot thermal vent, 3.5 billion years ago, with many different such things; a high degree of variation in just tiny little micro, local chemical reaction systems. And if this is ever going to bootstrap life and get underway, then it has to be isolated in a compartment and start competing with other such systems, because only then will natural selection kick in.

There is a problem with this kind of thing. It’s just sitting there in its happy, hot thermal vent, taking its chemical energy out of the environment. And it’s open, it’s an open system. A selfish mutant could invade and destroy it. Somebody could come in, who was say an alternate version of C, and take stuff from B and make a lot more C, but not ship anything on to D; it could make a lot more C. That would essentially be a selfish act. Okay? That means taking but not giving back.

And in this system here, an altruistic mutant won’t spread; and altruistic means taking some and passing enough along. So if this thing is open, and it’s not isolated from the environment, any one of these steps in the hypercycle could be invaded by a chemical alternative that would destroy the hypercycle.

So these things are a model. Okay? We’re not saying that this is what actually happened, but it is a model of how a small group of cooperating molecules might have evolved, before there was a genetic code. If we could get them to be sufficiently complex, then they would start competing with each other, and then, at a certain point in the complexity, they might invent genes and have a competitive upper hand by then being able to transmit the information on what was working. So that would certainly give them an upper hand in competition.

And they would solve Eigen’s paradox, because each one has a small genome, but in sum they would add up to the information in a big genome. So if you could somehow stabilize these small competitive systems so that they had internal cooperation but they were competing between themselves, you could get life going.

So one way out of this problem of the invasion of mutants is to actually put them into compartments. Okay? So you actually have to get the chemical reaction system isolated inside something like a membrane; and that means it’s a local group.

Will, are you finding certain things here resonating? Will’s a political scientist, and he’s interested in the interaction between cooperation within groups and competition between groups. Those basic ideas, that actually resonate in economics and political science, are there in evolutionary biology, right at the origin of life.

In order to get this going, in order to get the whole process going, basically what you need to do is isolate one of those hypercycles, let it grow, have some kind of division going on, with some inheritance, and then have a mutation that’s going to improve one of the descendents, so that this one, that has a better hypercycle, can out-compete that one.

Once you get that process going, then you’re going to retain cooperation within compartments, you’re going to increase competition between compartments, and natural selection can take off and start to produce the very early primitive cells. That’s not so easy. You got to get the compartments, and there’s some issues about the compartments.

You need them so that you can keep the cooperators on the inside and you can put the parasites and the defectors on the outside; so you can keep the guys that you like and you want to work with in there with you, and you can tell the other guys to go away.

What this does, it’s associating cause with effect strongly, in the sense that if you’re cooperating and you are shipping your product on to the next member of the hypercycle, that actually is an effect that’s retained within the system and then comes back to help you. If it’s open, you have no guarantee it’s going to come back to help you. So there’s no guarantee of reciprocity. But if you can contain the cycle, then reciprocity is going to occur because the cycle is shielded from the outside.

And it means that all of the elements in the cycle have a common stake in the success of the compartment. They are all in the same boat; they’re all in it together. If they get better at what they do, together, by cooperation, they will improve their competition with the other similar things on the outside.

Now, we don’t know where the long-chain fatty acids came from. So I’m just going to pull them out of the air; we’re back in Greek comedy, deus ex machina–a machine lowers a god onto the stage and he gives us long-chain fatty acids. So we have our long-chain fatty acids; and, in fact, we have a special kind. They’ve got a hydrophilic end and a hydrophobic end. There’s a b-o missing there; that’s hydrophobic. So one end likes water and one end hates water. And if you do that, if you make those things and you throw them into water–so you have an aqueous solution–this is what you’ll get.

Chapter 4. The First Cells [00:21:36]

These are things which are either micelles or primitive little spheroids or sometimes linear things, that actually start looking pretty much like a biological membrane. The fatty tails are sticking in and associating with each other, and the hydrophilic parts are sticking out and associating with all of those nice charged water molecules.

Well, make a mixture of those things, and then put in a surface–so you have either the water surface or you have a mineral surface–and this is what naturally happens. This is called abstriction; you will get a little bump forming.

We’re talking about stuff that’s there for free, in the sense that you don’t have to have any natural selection going on to give this to you, in the chemical structures. These things, once you get them, will do this spontaneously. Okay? So you can get something like this happening–this is a nice little sphere that’s starting to bulge up off the surface–and if you make them big enough, they will divide.

So they will grow and they’ll actually kind of start pulsing around a little bit, just from Brownian motion. And if you get these little spheroids, that are lipid bilayers, up to a certain size they will actually divide. So you can see that it might not actually have been necessary for natural selection to arrange the first replication events for cellular compartments. That might have been something that was just happening physically and chemically, so that part of the bootstrapping was there for free.

Making it efficient, making it good, making it precise, making it complicated, that’s a whole ‘nother story; that took a lot of evolution. But just that very simple initial step of having a sphere of a bilipid membrane that had a hypercycle in it–maybe one in each compartment that would then divide–that was probably there for free.

Now, if you want to make it grow, then one of the things you want to put inside it is a hypercycle that will make more membrane building blocks, because that will just make the thing grow. So perhaps that was actually the kind of chemical reaction that was going on in some of the early semi-cells or proto-cells; they were making the building blocks of lipid bilayers.

However, then you’ve got a problem of how to get the different substrates that you need in through the membrane; that’s the problem of membrane transport. You’ve got to have the membrane. You’ve got to isolate your reactions so that they can be cooperative and not de-stabilized by parasites. But once you’ve isolated them, then you have the problem of moving things in and out through the membrane. So there’s got to be a period, back at the origin of life, during which membrane properties can evolve, and that in a replicating entity that’s not yet fully cut off from its environment.

And the solution to that, one possible solution is a semi-cell. That would be you make a cup on the surface of water, or on the surface of a mineral, and you don’t completely close the perimeter. So the thing’s kind of leaky; stuff can go in and out of the edges of the cup. And that will solve the problem. Okay? It allows a partial openness, it gives you a certain degree of control over who comes in and out, and that might’ve helped to adjust these early semi-cells.

If you want to have a look at a fairly recent article–this is now five years old–Rasmussen was talking about transitions from non-living to living matter in Science. And then this would be a good way, in Web of Science, to go and trace the more recent literature. They will all–all the more recent articles will almost certainly cite this one; and then it also cites you back all the way to the Miller-Urey experiments in 1953.

So there’s really growing interest in how a simple life form could be synthesized in the lab, and there is a desire to see whether or not we can understand the origin of life well enough so that we can make alternate forms of life, so that we can make self-replicating and self-repairing nanomachines.

And Drew Endy, up at MIT, runs an international competition every year where bright young molecular geneticists and microbiologists get together and they try to engineer biological machines. And the point of the competition is to try to make the most complex and sophisticated little biological machine that you can. And he’s got funding from MIT to bring these people from all over the world. So every year there’s an international competition and a team comes in from Beijing and a team comes in from Paris, and if Yale puts one together, a team goes up from Yale, and they all play with their biological machines, which are at the scale of viruses and bacteria.

So out of this kind of creative play, we may actually learn a lot, that then applies back to the real origin of life, rather than the geeky post-modern nanomachine, so I see some hope in that kind of playful research.

Chapter 5. The First Eukaryotic Cells [00:27:03]

Okay, now I will wave my hands and a miracle occurs and it’s later on in the evolution of life. We’re now going to discuss the prokaryotic/eukaryotic transition. And the prokaryotic/eukaryotic transition is thought to be a major transition because it contains a significant change in the transmission of information.

Every major transition in the evolution of life has consisted either of a difference in the way that genetic information was transmitted and/or in the unit of selection; a thing that was actually evolving. So both of those things are going on here.

What’s going on in the transition from the prokaryotes, up here, to the eukaryotes, down here, is–one thing that’s going on–is that you’re going from an organism, like a bacterium, that has a single circular chromosome anchored to a cell wall, to an organism that has a nucleus within which the chromosomes are–there are then often multiple chromosomes inside the nucleus, plus organelles that are out in the cytoplasm, plus a lot of cell structure that’s simply not present in the prokaryotes.

So one of the things that you have is an organizing center, out of which actin filaments will grow, and these are used in meiosis and mitosis. And associated with that organizing center is a little circular chromosome which is actually thought to indicate that this was originally an independent bacterium, and that these actin filaments are evolutionary homologous with a bacterial flagellum.

You have got vacuoles, you’ve got endoplasmic reticulum; all kinds of stuff. And all eukaryotes, if they have a cilium, they have a characteristic 9 + 2 structure, in the cilium, and this is thought to have been constructed from multiple bacterial precursors, and so forth. So you’ve got compartments forming, you’ve got organelles, and you’ve got a difference in the way that genetic information is compartmentalized and transmitted.

So the prokaryotes have a rigid outer cell wall, they have a circular chromosome attached to the cell wall; and importantly the transcribed mRNA is translated directly. You can see that here. You can see the mRNA coming off of the DNA helix, and you can see little ribosomes here chunking out protein, that are these little squiggly things; whereas down here, that process is being done at the endoplasmic reticulum, and it’s not direct, it’s indirect.

In the eukaryotes there’s an internal cytoskeleton. You’ve got lots of little micro environments that are giving you the opportunity to create local industry within the cytoplasm. There are several linear chromosomes, inside a nuclear envelope; transcription and translation are separated; and there are organelles. And, with eukaryotes, you get meiosis. So you get a precise and organized way of making genetically different offspring in each generation.

Now, in order to go from prokaryote to eukaryote, you got to lose your cell wall. And that’s a real issue, because the cell wall, in a bacterium, is protecting it from swelling up and bursting like a balloon, due to osmotic pressure. So the bacterium is using a rigid cell wall to protect itself from the influx of water. And in order to do that, in order to lose the cell wall, you need something to stabilize it on the inside, and that’s the cytoskeleton. So the cytoskeleton is really an extremely important morphological invention in this transition.

Student: Professor.

Professor Stephen Stearns: Yep?

Student: How does this view connect with the fact that cytoskeleton elements have been discovered in bacteria as well? Also cytoskeleton elements are present in bacteria.

Professor Stephen Stearns: Well you would need to have cytoskeleton elements in the precursor, wouldn’t you? You couldn’t make the transition unless they were already there. If you made the transition without them, you would blow up. So I’m not surprised that there are cytoskeletal elements in bacteria.

Okay, and remember, it’s 3 billion years later. So a lot of stuff could’ve gone on, in the bacteria. I think that what you’re on to actually is an interesting system to see whether or not you could actually do experimental evolution. What is the state of the cell wall in this bacteria? Do you know?

Student: [Inaudible]

Professor Stephen Stearns: They don’t have a cell wall.

Student: They have a normal cell wall.

Professor Stephen Stearns: They have a normal cell wall. If this idea is correct, then of course it should be possible–it might take a long time–to experimentally select them, to lose their cell walls. But in order to do so, they would probably have to organize their fibrils, their cytoskeleton, in a very precise way before they could do it. Just having them–they’re probably using it for some other reason.

Student: They actually–some of cytoskeleton is thought to re-mediate, or regulate, cell wall synthesis.

Professor Stephen Stearns: Is thought to re-mediate–

Student: Thought to regulate cell wall synthesis.

Professor Stephen Stearns: I can’t hear the last part of that.

Student: Is thought to regulate cell wall synthesis.

Professor Stephen Stearns: Cell wall synthesis. Some of the cytoskeleton is actually involved in cell wall synthesis. So that would suggest that it was there for a long time. That is actually how evolution works; it invents things for one purpose, and then takes advantage of them for another.

So what you’re telling me is actually that this scenario now has all kinds of supporting information, because the bacteria probably had evolved for a long time, using the cytoskeleton for another purpose. But then, having gotten it, they were in a position to use it to keep from blowing up, if they got rid of their cell wall. But they did have to get rid of their cell wall to become a eukaryote. Okay? By the way, I definitely accept the fact that I don’t know everything. So I appreciate that.

Now if you put your DNA into a nucleus, and you no longer have it as a single circular chromosome, then it is possible that without having to attach it to a cell wall, it might make it easier to make multiple chromosomes. And you get a big advantage from that in terms of how big a genome you can have, because you can then start replication in parallel, at multiple points, rather than going around a single circular chromosome to do it.

And that means that there really would be no upper limit on genome size. If you can make 100 small chromosomes and start them all off at the same time, in replication, you’ll get through the replication step very quickly. So there’s an issue about the origin of chromosomes. That’s actually a major transition in the sense of how is the genetic material organized

On the one hand there’s this replication advantage. Okay? So you can make copies a lot faster if you do it in parallel, in small pieces, than in sequence, in big pieces. And so that would be a cost of having a bigger chromosome. You might want to have a chromosome of intermediate size. And if it’s taking an interaction between two or more genes to produce either an organism or to produce a biochemical reaction system that has a certain ratio, that is well balanced in terms of product, then linking the genes that are involved in that ensures that they’ll both be found in all of the offspring, and that’s a benefit of making a bigger chromosome.

So there would be a tendency for the genome to agglutinate, if this were the only thing going on. But it’s balanced by this cost; this benefit is balanced by that cost. And I’m sure there are other things as well; I’m sure you can probably think of some.

Now once you make chromosomes and you synchronize their replication, then essentially what you’ve done is you have eliminated the competition of the genes. Because by putting the genes onto a chromosome, you’ve put them all into the same boat. You’re no longer getting a situation where one gene might be replicating at a higher rate than another gene, which would lead to unbalanced biochemistry and unbalanced development.

So you’ve given them a stake in the same process, and that process is the replication of the chromosome on which they are sitting. So particularly for the genes that were involved in replication, if they needed to cooperate to replicate, this would be an important consideration.

Now if you’ve got a primordial cell that has a lot of reactions going on in it, that are being controlled by genes that are all on separate chromosomes, and if those chromosomes are not being divided evenly at mitosis and meiosis, then it’s possible that all those reaction systems are going to get out of balance. Okay? And so if you’ve got unlinked genes with products that need a certain ratio, then getting them onto the same chromosome and regulating them all together, gives you a big advantage over your competitors, at that point. I’m sorry this is running off. I think it shows up on your printouts.

Chapter 6. Symbiotic Organelles [00:37:07]

Okay, now the other thing that’s going on in the eukaryotes is they’ve got these symbiotic organelles that were originally independent bacteria: the mitochondria, the chloroplasts, and possibly the spindle apparatus. So one thing that we notice when we look at the chloroplasts in the mitochondria is that the chloroplasts have a much bigger genome than do the mitochondria, and the mitochondrial genes have been transferred into the nucleus.

We can sequence the mitochondria–we know that they were independent purple bacteria–and we can estimate from the size of the genome of a purple bacterium how much has now been transferred into the eukaryotic nucleus; and we can see that a great deal has been transferred into the eukaryotic nucleus.

So one of the reasons to do that is essentially efficiency. If you put those genes into the nucleus, you’re just maintaining two copies of them, rather than thousands of copies out in the population of mitochondria that are living in the cell. Another is conflict resolution. Basically you’re cutting way down on the opportunity for different variants to exist in mitochondrial processes.

If you’re constructing all of the mitochondria out of essential elements that are in your nuclear genome, you’ve gotten control over them, in a way, and you are making them all look the same, rather than mutating and possibly having the option of creating a runaway mitochondrial cancer that would destroy your metabolism.

Now why not put all the genes into the nuclear genome? Well there are a couple of reasons. One is that the genetic code is actually different in the mitochondria and in eukaryotes and in the nuclear genome and in the chloroplast. So the tRNA and ribosomal RNA genes, the translation machinery had to be retained in the mitochondrion; at least that much.

Now that explains the mitochondrion, but it doesn’t explain the chloroplast. It looks like the chloroplast retains more genes because it has to move macro molecules through more layers of membrane. Remember, the world record on a chloroplast is that it has four membranes around it, and all chloroplasts have two membranes around them. So it’s harder to move big molecules through them, and so if you need them to make the chloroplast function, you have to make more of them locally. So that’s probably one reason for the retention of more genes in the chloroplast genome than in the mitochondrial genome.

Do we think that the organelles were originally slaves of the things that ate them? Was it a relationship that might have been like a farmer and livestock, the way that corals harvest dinoflagellates, that are helping them make their carbonate skeletons?

Well, there’s some evidence. We can look at where are the tapping proteins made that are inserted into the organelle membranes? And those are encoded in the nucleus. Okay? And it looks like they evolve from host proteins. So it looks like there have been manipulative steps where the host was actually tapping in to the symbiotic organelles; that’s one piece of evidence.

But there’s also thought that they may have been mutualists, and the excretory products of one of them, which was a eubacterium, it was making hydrogen and CO2. And the missing piece of this sentence basically is that that would then have been food for the archaean ancestor of the eukaryotic nucleus. So they could have actually been mutualists. So there is a slave hypothesis and there’s a mutualistic hypothesis, and that hasn’t been settled.

Why not just have one; why do plants need to have two? And if you look at their ancestors, you can see that purple non-sulfur bacteria and cyanobacteria–so those are the ancestors of mitochondria and chloroplasts–they can do both; they can both photosynthesize and they can respire.

However, the purple bacteria can’t photosynthesize when there’s oxygen, and the cyanobacteria use the same machinery for both functions, and so that means that the host cell would not be able to separately control photosynthesis and respiration; which one might want to uncouple. And so it appears that mitochondria lost photosynthesis and chloroplasts lost respiration, in coming into the cell.

So I won’t run through all of this; you can read through it if you want. Basically what’s going on here is the world record for membranes around a chloroplast is 4; it’s in a dinoflagellate. And what’s going on here is that one thing eats cyanobacterium, and that makes a chloroplast that has the outer membrane of a cyanobacterium and the outer membrane of the cell that ate it, wrapped around it; so that makes two. And then it happens two more times. And so the world record for this is in a dinoflagellate. Okay?

And it turns out that the things that got eaten to make dinoflagellates had separated, so that there were different kind of chloroplasts that got eaten by different things, that both ended up making dinoflagellates. And so it looks like, in that sense, dinoflagellates might be polyphyletic. It’s a complicated sequence here. And you will notice in here that you have got some interesting words: rhodophytes; photosynthetic stramenophiles; haptophytes; the dinoflagellates themselves.

It would be worth doing a Google Image search on those things, just to familiarize yourself with this bit of Protistan biodiversity. There are more things out there, in the world, than our fantasies can imagine. And these guys are specialists in all kinds of weird genetics. So I just want to cue you to that.

We’re not going to go–this isn’t a course in protistology, but there’s been an awful lot of interesting evolutionary biology that’s gone on in these single-celled creatures. So that’s a dinoflagellate. They’re cool things. They have a–it’s kind of a bit like a small algal cell sitting inside of a complicated glass case.

So there are some other key events: origin of the genetic code; origin of multicellularity; origin of germline and soma; origin of social groups; origin of language. It’s a big topic, and in each one of these steps there are several very important things going on, and there are certain similarities of the process in each one of those steps. So I’d like to summarize those, with a few principles that are involved.

Chapter 7. Summary [00:44:20]

So one of the things that’s happening here is that there is a new level of selection, there’s a new level of replication; the hierarchy is growing. So you go from the hypercycle into competing groups of protocells, and those eventually make a prokaryote.

And then there are symbiotic events, and you actually then have selection operating on a eukaryotic cell that’s got two or three genomes in it. And then in the process the genetic material, of course, is also going through its reorganization into chromosomes. And then after that, you get multicellularity; you get cells that are probably genetically almost identical, that are growing together; you get division of labor within that.

So one of the things that happens is that the babushka doll, the number of levels in the hierarchy grows. When that new upper level originates, then there’s an opportunity for functional specialization and division of labor. In the multicellular organism we call this division of labor the origin of cell layers and organ systems, so that some cells make brains and other cells make hearts; some do respiration, some do excretion. That would be a multicellular division of labor.

In a social insect colony, we would say that the queen has specialized on reproduction, and then we have the different castes that are doing things. Some of them are cleaning up the garbage in the colony; some of them are feeding the queen; some of them are foraging outside. And you can see the analogy to a human society as well. So there’s functional specialization with division of labor.

There is a change in the system of information transmission. So when you go from prokaryotes to eukaryotes, you have to arrange for information to be transmitted, not only in the nuclear genome, but also in the cytoplasmic genomes. And then you have the evolution of meiosis, and you have sexual reproduction; which is a huge change in the way information is transmitted.

Probably since the origin of sex, the biggest- highest impact change in information transmission has been the origin of language and culture, which gives a method of transmitting information from generation to generation, that is independent of the DNA, and allows the process to be going on in different directions at two levels.

Then often in the process of forming this higher level of replication, you have a bunch of lower level units that are coming together to make a higher level unit, and they need to cooperate to do that properly, but they could be invaded by selfish mutants, they could be de-stabilized, and so there’s a conflict issue. And this conflict is sometimes stabilized by selection for cooperation.

You’ve heard me use several times in this lecture a phrase like ‘they’re all in the same boat’ or ‘they are all sharing mutual interests’, as in the genes getting together on a chromosome, or the chemical reactions coming together in a single protocell.

Those are all principles of conflict resolution, because if you are in a tightly spatially organized system, where your own welfare depends directly upon cooperation with another thing in that system, and your system is in competition with some outside system, and the performance of your system is actually a direct function of how cooperative you are, then there is strong selection for integration, within that group. And it’s thought that this is the kind of thing that’s going on when you have a key event in the origin of a new higher level in the evolutionary hierarchy.

So those are some of the key events in evolution. They are a rather abstract way of looking at the history of life. And next time we’re going to look at major events in the geological theater, and so the lecture next time is more for people who like firecrackers on the 4th of July, and the clash of meteorites.

[end of transcript]

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