Louis J. Sheehan, Esquire Introns 2004471

Some introns, such as Group I and Group II introns, are actually ribozymes that are capable of catalyzing their own splicing out of a primary RNA transcript. This self splicing activity was discovered by Thomas Cech, who shared the 1989 Nobel Prize in Chemistry with Sidney Altman for the discovery of the catalytic properties of RNA.

Sometimes group III introns are also identified as group II introns, because of their similarity in structure and function.

Nuclear or spliceosomal introns are spliced by the spliceosome and a series of snRNAs (small nuclear RNAs). There are certain splice signals (or consensus sequences) which abet the splicing (or identification) of these introns by the spliceosome.

Group I, II and III introns are self splicing introns and are relatively rare compared to spliceosomal introns. Group II and III introns are similar and have a conserved secondary structure. The lariat pathway is used in their splicing. They perform functions similar to the spliceosome and may be evolutionarily related to it. Group I introns are the only class of introns whose splicing requires a free guanine nucleoside. They possess a secondary structure different from that of group II and III introns. Many self-splicing introns code for maturases that help with the splicing process, generally only the splicing of the intron that encodes it.[4]

There are two competing theories that offer alternative scenarios for the origin and early evolution of spliceosomal introns (Other classes of introns such as self-splicing and tRNA introns are not subject to much debate, but see [5] for the former). These are popularly called as the Introns-Early (IE) or the Introns-Late (IL) views.[6]

The IE model, championed by Walter Gilbert,[7] proposes that introns are extremely old and numerously present in the earliest ancestors of prokaryotes and eukaryotes (the progenote). In this model introns were subsequently lost from prokaryotic organisms, allowing them to attain growth efficiency. A central prediction of this theory is that the early introns were mediators that facilitated the recombination of exons that represented the protein domains.[8] Such a model would directly lead to the evolution of new genes. Unfortunately, the model cannot account for the variations in the positions of shared introns between different species.[9]

The IL model proposes that introns were more recently inserted into original intron-less contiguous genes after the divergence of eukaryotes and prokaryotes. In this model, introns probably had their origin in parasitic transposable elements. This model is based on the observation that the spliceosomal introns are restricted to eukaryotes alone. However, there is considerable debate on the presence of introns in the early prokaryote-eukaryote ancestors and the subsequent intron loss-gain during eukaryotic evolution.[10] It is also suggested that the evolution of introns and more generally the intron-exon structure is largely independent of the coding-sequence evolution.[11]

Nearly all eukaryotic nuclear introns begin with the nucleotide sequence GU, and end with AG (the GU-AG rule). These, along with a larger consensus sequence, help direct the splicing machinery to the proper intronic donor and acceptor sites. This mainly occurs in eukaryotic primary mRNA transcripts.

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