I previously offered a puzzle to think about:
You are given two flasks, A and B, each filled with a 10 mls of a solution that contains all the nutrients needed for Tetrahymena to survive and grow.
On Friday, you are given a tube that is filled with thriving Tetrahymena and transfer 10,000 of these cells to flask A. Drawing from the same tube, you then add 1,000 cells to flask B. You go home and celebrate Easter, returning to the lab on Monday. You find the cells in flask A to be thriving, having spawned millions of new cells. But when you look at flask B, the cells have not grown and divided. On the contrary, they all died!
Why did the cells in flask B all die in a sea of food?
The only difference between the two flasks if the density of cells. Flask A starts with 10,000 cells in 10 mls, thus it has a density of 1000 cells/ml. Flask B has a density of 100 cells per ml. Why is this significant?
If we think in terms of front-loading, perhaps we should look to complex, metazoan features to explain this protozoan phenomenon. And sure enough, this density-dependent survival is also well known among scientists who culture mammalian cells. In other words, if you take a few human cells and put them into a Petri dish with lots of nutrients, those cells will also die instead of developing into a massive population of cells. So why is this?
I have not forgotten the Tetrahymena quiz, but I wanted to throw out one more juicy tidbt about introns first. As I have suggested, introns may have facilitated the evolution of metazoan-like complexity and one possible mechanism is by making alternative splicing possible. Recall that alternative splicing enables a single genome to spawn immensely diverse set of gene products, something that would come in very handy when it comes to spawning multiple cell types. But we might get even more radical, as introns, along with alternative splicing may very well have facilitated the emergence of the brain. In fact, we could even make a reasonable case that without introns, there would be no brains to discover introns. Consider just three examples:
Posted in introns
We have seen that that last common ancestor of all eukaryotes had a genome that contained as many, if not more, introns as complex, metazoan life forms. So how did these ancient organisms process all these introns? Did they have a simple mechanism for doing so or did they rely on something like a modern-day spliceosome?
Recently, a study was published that addressed just this issue . It began by listing three possible hypotheses:
Investigating the distribution of splicing mechanisms and spliceosome components among eukaryotic lineages can reveal how splicing and the spliceosome evolved within eukaryotes. In this study, we investigate three hypotheses of spliceosome evolution.
The first is that the spliceosome appeared in eukaryotes shortly after the eukaryotic ancestor, possibly by invasion by self-splicing introns. It is possible under this hypothesis that some eukaryotic lineages do not contain introns or spliceosomal components.
The second hypothesis is that the eukaryotic ancestor had a basic spliceosome that increased in complexity in multicellular eukaryotes. This complexity increase through time would be similar to intron length which appears to have increased in multicellular eukaryotes. Under this scenario, we could expect to find some, but not many, highly conserved splicing proteins present throughout extant eukaryotes.
These first two hypotheses are not mutually exclusive in that an invading self-splicing intron could lead to a spliceosome that increased in complexity over time.
The third hypothesis is that the eukaryotic ancestor contained a spliceosome that is similar in complexity to the spliceosome present in today’s eukaryotes, with the expectation that we could find many spliceosomal proteins throughout eukaryotic lineages.
So which hypothesis is best supported by the evidence?