Let me now provide a couple of clues to support the hypothesis that introns facilitated the evolution of multicellular life.
First, as a general rule, introns are far more common in multicellular genomes than single-celled genomes. Consider the human genome. It has 21, 746 genes and only 1,760 are without introns. Compare this to the genome of baker’s yeast. It has about 6200 genes and only about 250 have introns. In other words, while 92% of human genes have introns, only about 4% of the single-celled yeast genes have introns. What’s more, only about dozen yeast genes have more than one intron, while the typical human gene has around ten introns.
And this pattern is reflected in many other genomes. For example, Plasmodium falciparum, the protozoan that causes malaria, has about 5300 genes and only 121 have introns (about 2%). And trypansomes, the protozoa that cause African Sleeping Sickness, do not appear to have any introns.
Our second clue was already provided in the previous posting. Bacteria, which lack introns (remember, we’re talking about protein-coding genes) also have not been successful in spawning an organism as complex as a mammal. There are probably several reasons for this, and the lack of introns may be one of them.
So not only is high intron density correlated with complex, metazoan life, but cells that lack introns have never succeeded in generating something analogous to complex, metazoan life.
One way to explain this difference is that single-celled life forms come in large populations and would thus experience stronger purifying selection that would remove introns – stream-lining such genomes over time. Yet even if true, this would not negate the putative role of introns, but would only help to explain part of the process by which they would exert their influence. But as it stands, the purifying selection explanation is probably incomplete.
Anyway, in the next entry, let’s deepen the first clue a bit.