Hey guys, today in class I asked why we have introns if they are spliced out during RNA processing and I think I found the beginnings of an answer, here's the introduction to the article at http://www.pnas.org/content/96/18/10267.full:
"The evolutionary origin of spliceosomal introns has been the subject of much controversy. Introns are proposed to have been both lost and gained during evolution. If the gain or loss of introns are unique events in evolution, they can serve as markers for phylogenetic analysis. We have made an extensive survey of the phylogenetic distribution of seven spliceosomal introns that are present in Fugu genes, but not in their mammalian homologues; we show that these introns were acquired by actinopterygian (ray-finned) fishes at various stages of evolution. We have also investigated the intron pattern of the rhodopsin gene in fishes, and show that the four introns found in the ancestral chordate rhodopsin gene were simultaneously lost in a common ancestor of ray-finned fishes. These changes in introns serve as excellent markers for phylogenetic analysis because they reliably define clades. Our intron-based cladogram establishes the difficult-to-ascertain phylogenetic relationships of some ray-finned fishes. For example, it shows that bichirs (Polypterus) are the sister group of all other extant ray-finned fishes.
Two competing theories have been proposed to explain the origin of spliceosomal introns, which are widespread in eukaryote genomes but absent from prokaryotes. The “introns early theory” states that the introns are ancient and have been lost in different lineages (1, 2). On the other hand, the “introns late theory” maintains that the spliceosomal introns were inserted into the eukaryote genes later in evolution (3–6). Although the distribution of intron phases and the correlation between intron positions and protein module boundaries have been proposed as evidence for the ancient origin of introns (2), the restricted phylogenetic distribution of some introns suggests that they arose late in evolution (7–10).
We and others have identified extra spliceosomal introns in the pufferfish (Fugu) and some other teleosts that are absent from mammals (refs. 11–18; B. Peixoto and S.B., unpublished work). Likewise, extra introns were also found in some mammalian genes (16, 19, 20). These discordant introns could be the result of either loss of ancestral introns or gain of novel introns in different lineages. Because the spliceosomal introns are not self-splicing and are not known to be mobile, the loss or the gain of spliceosomal introns in a lineage is likely to be a unique event, occurring at a specific point in its evolution; hence it might serve as a decisive marker for evolutionary studies. To evaluate and confirm whether the extra vertebrate introns are the result of a loss or gain of introns, we made an extensive survey of the phylogenetic distribution of seven of these introns, including one each from the growth hormone gene (15), the major histocompatibility class II B-chain (MhcII) gene (13) and the mixed lineage leukemia-like (Mll) gene (16), and two each from the dystrophin gene (14) and the RAG1 gene (21). We also analyzed the distribution of introns in the rhodopsin gene, which has been shown to contain introns in mammals (22) and in primitive chordates such as lampreys (23) and skates (24), but not in some teleosts (25). "