Like most nerdy kids, my first introduction to sex was in a library. We're not talking bodies writhing among the books: this was all part of my master plan to acquire All Knowledge before I was thirteen, by reading every book in the local lending library. Amidst all the texts and illustrations, of egg cells, spermatozoa, wombs, pre-natal development, colourful pictures of codpieces throughout the ages and articles on sex-segregated communal living in the South Seas, one question gradually surfaced in my mind: why do we start off microscopic?
Years passed and I didn't acquire All Knowledge, but that question kept coming back to me, and I was reminded earlier today of the answer that I gradually arrived at, when I read an article on declining fertility in clone trees, as reported by the BBC. Trees can't live forever without sex, study shows, they say. The research they're quoting was published in the free, online jounal PLoS Biology: Aging in a Long-Lived Clonal Tree. (Just to make things clear, these trees don't only reproduce clonally. Each tree may be either male or female, and if you put them near each other and supply some bees, they'll reproduce sexually. BUT they can also reproduce by sending out lateral root suckers, and sometimes a single tree can take over an entire location in that way.)
The two things may not immediately seem to be related but they are, and the key is that it's to do with "getting around" the second law of thermodynamics (the one about entropy always increasing with time).
The idea is, the second law says that in a macroscopic object such as a tree or a person, order should always be breaking down. Now animals and plants have repair mechanisms to deal with some of the ways that their bodies break down, and even the cells of which we are made have, themselves, extremely complex and efficient ways of repairing their genetic material when it is damaged. But our bodies consist of billions of cells, and in some of them, inevitably, the repair process fails and they accumulate damage: mutations.
What do we know about mutations? Mostly, they stop things working. Often the things that stop working are critical to the survival of the cell, and the cells die. Sometimes the things that stop working are critical to the body's control over the cell in the environment of the body, and the cell doesn't die when it should, and that can cause cancer. So despite the fact that we owe all the variety of life in the world to mutations, the fact is that most mutations are harmful, and, from the individual's point of view (be it the multicellular being or the cell itself), we don't want them.
Let's put some numbers on this. Each human being inherits about 3 x 10^9 base pairs of DNA from each parent, that's 6 x 10^9 base pairs altogether. Now one estimated is that in humans and other mammals, uncorrected errors occur at the rate of about 1 in every 50 million (5 x 10^7) nucleotides. And note that that's uncorrected errors, true mutations that have survived the repair processes. That mean that each new cell gets about 120 new mutations! The numbers for the Trembling Aspen (the variety of tree that the researchers examined) will be slightly different given its different genome, but from our point of view, essentially similar: the basic point is that every cell is a mutant, no two cells are the same.
Now consider what happens when plants reproduce (if that's quite the right word) clonally. Cells forming a portion of a root produce a bud that starts growing upwards and becomes a new stem or trunk; or, depending on the species, cells forming a portion of a branch produce a bud that starts growing downwards and becomes a new root. In either case, those cells are from the general population and may have been replicated many times since the original seed, accumulating mutations with each fission. It seems to follow from that, that the new individual (trunk, let's say) may already have accumulated significant genetic damage by the time it's "born".
Things aren't looking good for the Aspen. Stands of populus tremuloides can spread asexually for hundreds of thousands of years however, without noticeably degenerating. To some degree this is because of selection at the level of individual trunks or treelets ("ramets", in the parlance), there's also the phenomenon of rejuvenation familiar from coppicing in non-clonal trees, which doubtless applies here too. However the researchers cleverly argued that while surviving ramets in an old clone might maintain genetic fitness due to selection pressure for things like, oh, producing bark, making chlorophyl and so on, there wouldn't be any selection pressure against mutations in sites to do with sexual reproduction. (They are basically saying that if every other tree for a mile around is another male, a clone of yourself, then it doesn't matter if your flowers or pollen work properly or not, there ain't going to be any babies.)
So they looked for evidence of declining fertility amongst male aspen that had been reproducing clonally for a long time, and used that as a proxy for senescence generally. Unsurprisingly, they found it. It seems that, though an individual aspen and its clones may hang around for as long as a million years, they must still find a member of the opposite sex and produce seed before they eventually die.
So what's the connection with microscopic babies? It's just this: that whereas in a macroscopic-sized clone some of its many cells will be viable whereas others won't, in a human baby at the stage of a fertilised ovum either that one cell will be viable or it won't. If the cell isn't viable, then the embryo will not come to term, but if the cell is viable then you have a guarantee that you've started a new cell line without significant accumulated damage. In effect, you've managed to filter out your damaged DNA.
Nothing comes for free though, and it's never really possible to defeat the second law of thermodynamics. In this context it's relevant to consider what might otherwise be a surprising fact: just how frequent miscarriages are even in the developed world. Hunting around the internet I read that one pregnancy in seven miscarries, and it's estimated that the true figure may be as high as one in four: the difference being due to miscarriages that happen before the mother is even aware that she is pregnant.
I understand that the number of fertilised ova that do not implant is much higher than the number of miscarriages. Probably the great majority of fertilised ova are lost in that way.
ReplyDeleteI wonder how many of those are just bad luck, and how many are unable to implant because of genetic damage? There might also conceivably be some mechanism on the wall of the uterus that can reject ova that it doesn't "like". However it is, it's clearly the case that a LOT of genetic damage is being filtered out at this stage of the reproductive cycle.
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