Endosymbiosis: Bread Crumb Superhighway
As life ambles along evolutionarily, it leaves behind bread crumbs of evidence that we can use to retrace its route. As bread crumb trails go, the one left by the process of endosymbiosis is a veritable multilane superhighway. Endosymbiosis (from “endo”, meaning “inside”, and “symbiosis”, meaning “living in close association”) refers to the weird condition of one creature taking up residence inside another. The signature of evolution is scrawled layer upon layer, not only in gene sequences but also in cellular structures. We can even catch transitional compound organisms — chimaeric Frankensteinian constructs of surprising beauty — in the act of formation. As a biologist, this is one of my favourite topics of study. It’s one of those classic areas of science that is rife with fascinating and intricate stories of cooperation and collaboration that leave one’s jaw agape in wonder, whether one is a biologist or not.
Endosymbiosis helps us to understand who we are at the most basic level. Over the last few posts, I’ve been tracing the unexpectedly tangled branches of the tree of life up which we’ve climbed to our current perch. But as we’ve seen, the tree of life does more than just branch out with time (e.g. causing us to wave a genetic goodbye to our chimpanzee cousins about 6 or 7 million years ago). Some of its branches also meet and fuse, causing genetic material from different species to blend by various means. This blending makes a web perhaps a better analogy than a tree for the geneology of life on earth.
A quick recap of some of the methods of genetic blending: In the first post of this series (Cavemen in Your Genes), we saw how recent research yielded genetic evidence that we hybridized with another species of human called Neaderthals about 60,000 years ago. I then delved into the process of horizontal gene transfer in the next post (Evolution’s Usual Suspects: 1. Plagiarizing Wizards), describing how bacteria swap their genes and sometimes stick them in plant or animal (including our own) genomes. In the third post (Evolution’s Usual Suspects: 2. Hijackers in Rehab) we saw how entire ‘life’ forms (viruses) have uploaded themselves into our chromosomes millions of years ago and now reside permanently among our genes as lengths of DNA called endogenous retroviruses.
And now we come to (in my opinion) the most spectacular story of the set: endosymbiosis, in which organisms fuse at the level of their bodies, not just their genetic material. The roots of this process are billions of years in the past, but it still continues today. Endosymbiosis fundamentally altered our ancestors’ cellular structures. Endosymbiosis can therefore generate macroevolution at the grand scale that proponents of creationism erroneously claim is absent.
All of the previous cases of genetic fusion that I’ve discussed play out entirely on the stage of our chromosomes. Foreign genetic material is pasted between our genes and therefore alters our identity a little. But our cells still look the same after the alteration. The story of endosymbiosis, by contrast, takes some of the action outside the cell’s nucleus, into the cytoplasm. The resulting changes to the cell can be seen not only through the microscope, but often by the naked eye as well. The associated changes in physiology are even more profound.
Mitochondria: The Coppertop League
Think back on how satisfying it is to drink in a lungful of brisk spring air and to go jogging. Do you know why you can do this? The answer lies in a population of infinitesimally small particles swarming in our cells. Called mitochondria, these roughly bratwurst-shaped intracellular organelles (integrated structures within our cells that perform dedicated tasks) are the power plants of our cells. Small as they are (only about a micrometer in size, or a millionth of a meter — the size of bacteria), mitochondria contain the means to run the chemistry by which our food is struck with oxygen to liberate the energy stored within the organic food molecules (such as glucose). This process is called aerobic respiration. The extensive energy that it can wring from glucose using oxygen is what makes it possible for us to go to cafes, write blogs, work out, and generally be as active as we are. This is because it takes an enormous amount of energy to maintain the level of activity in our cells. We are very much attached to our precious mitochondria for survival.
Amazingly, although mitochondria are now an integral part of our cells, recent research indicates that they originally descended from bacteria that took up residence in our cells in the hazy past before our unicellular ancestors decided that bunching up into groups of cells was a good idea .
How can this be?
Mitochondria not only look like bacteria, but they also reproduce on their own in our cells — not under the direction of the nucleus, just like an independent life form. To facilitate this, they have their own protein manufacturing systems (ribosomes) and their own DNA. Both their ribosomes and their DNA are of a distinctly bacterial type, which is substantially different from that found inside our cells but outside of the mitochondria. (The difference has to do with the size of ribosomes, the shape of the chromosome, and a number of other things.) Now, molecular biologists have the ability to isolate and read the genetic code sequence of this mitochondrial DNA (commonly abbreviated mtDNA). When they compare this mtDNA sequence to all catalogued DNA sequences from other life forms on earth (a lot have been catalogued), do you know which organisms they are most similar to?
Not humans, not by a long shot.
Rather, the mtDNA sequence is most similar to a group of bacteria that includes Rickettsia, better known as the disease agents that cause epidemic typhus and Rocky Mountain spotted fever . This result may sound absurd at first, but it’s astoundingly sensible from an evolutionary perspective. Why?
Consider this: of all the organisms to which mtDNA could be similar, isn’t it curious that it most closely resembles a parasitic group of bacteria that can only survive inside the cells of their hosts? Rickettsia is a nasty pathogen that is difficult for the immune system to detect and destroy because it enters and dwells within our cells when we are infected by it. This parasite is so well adapted to surviving within host cells that it has lost some of its genes, relying on its host cells to make up for its short comings.
But this gene trimming prevents it from growing and reproducing outside of the host cells. In fact, microbiologists can only grow cultures of Rickettsia inside living cultures of host cells, such as chicken embryos. To infect cells, it enters them by biochemically inducing or forcing the cells to swallow them, by a process called phagocytosis (literally, “cell eating”). It’s very similar to how an amoeba engulfs its food, by forming a dent in the cell surface that expands inward around the Rickettsia and pinches off inside the cell to form a bubble or vesicle that encloses the Rickettsia cell. However, once inside, the Rickettsia evades digestion and instead purloins a meal at the host cell’s own table.
So we now have the elements for a hypothesis on how mitochondria evolved. A parasitic ancestral bacterium similar to Rickettsia could force its way into the cells of another species, most likely an archaean organism similar to Thermoplasma [2, 3]. The parasite was already predisposed to reside only within these host cells, freeloading on the predictable supply of nutrients that the host cell accumulated for itself.
Now, recall from my previous post (Evolution’s Usual Suspects: 2. Hijackers in Rehab) the discussion about the evolution of avirulence, where we explored how a particularly nasty or virulent disease agent can evolve by natural selection to become less virulent over many generations. This occurs because the less harm that the parasite does to its host, the less resistance it experiences from the host, and the more easily it can maintain the infection, thereby increasing its chance to reproduce itself and spread through the host population. This sort of evolution is especially likely to occur when there is a strong bond between the host and parasite: what befalls the host also befalls its guest.
The increasing dependence of the parasite on the host led to the loss of some genes from the parasite’s already depauperate genome (Rickettsia has the smallest genome of any bacterium — only about 1.1 milllion units or base pairs, compared to over 3 billion in humans). In fact, this loss of genes included those genes needed for a basic type of metabolism that we accomplish in our cells, called glycolysis. But this meant that the parasite was no longer able to survive outside of our cells.
Why would this kind of deleterious gene loss occur? Basically, the parasite became ‘lazy’ in a sense: since it could rely on the host for food procurement and pretreatment, there was no need to expend energy to maintain its own genes against damage, because they were redundant as far as the host’s metabolic capabilities were concerned. Traits that are not highly beneficial for survival and reproductive success tend to be lost from the gene pool over time. But because this loss of DNA prevented the parasite from ever leaving the host to infect another cell, the parasitic bacterium was now permanently stuck within its host. At this point, it had better behave nicely toward its host if it was to survive.
In such a strongly dependent situation, natural selection often favours the survival of organisms that mutually benefit each other (a condition known as mutualism, which can arise in several different ways that I won’t go into now). Again, this is because their fates are so intertwined that survival and successful competition is best guaranteed by working together. If you were tied to your enemy by a steel wire, you wouldn’t try to push them off a cliff, would you?
This kind of evolutionary pressure resulted in parasites that rewarded the parasite-host duo with enhancement of an activity that the aerobic (oxygen-‘breathing’) bacterial parasite was already good at: energy production by ‘burning’ food with oxygen. The most successful of their descendants made more and more energy and exported it to the host, which used it to compete more successfully by hunting down food with greater efficiency, escaping enemies more successfully, and becoming overall more supercharged and awesome. Hence, mitochondria evolved into the energy producing centers of our cells. But their close genetic relatedness to Rickettsia is evidence that they shared a common ancestor with a parasitic bacterium.
This idea was popularized by evolutionary biologist Lynn Margulis in the Serial Endosymbiosis Theory to explain the origin of organelles in cells. Over time, the close association of one creature living within the other’s cells (the condition called endosymbiosis) selected for ever-diminished virulence of the parasite and increasing interdependence of each organism on the other.
The evolution of mitochondria is a funky example of evolution moulding the descendents of a disease organism into an essential partner for survival. It also produced a brand new type of cell (a eukaryote, which contains internal organelles and a nucleus surrounded by membranes) that was qualitatively different from its predecessors (prokaryotes, such as bacteria, which are more homogeneous internally). So, in essence, we are composed partly of huge populations of bacterial batteries, to which we owe our lives and energy levels. Kind of humbling, no?
1. J. Cameron Thrash, Alex Boyd, Megan J. Huggett, Jana Grote, Paul Carini, Ryan J. Yoder, Barbara Robbertse, Joseph W. Spatafora, Michael S. Rappé, Stephen J. Giovannoni. Phylogenomic evidence for a common ancestor of mitochondria and the SAR11 clade. Scientific Reports, 2011; 1 DOI: 10.1038/srep00013
3. Poole AM, Neumann N (2011) Reconciling an archaeal origin of eukaryotes with engulfment: a biologically plausible update of the Eocyte hypothesis.Research in Microbiology. 162: 71-76 (FREE DOWNLOAD)