Joined: May 2002
This one appears to be somewhat speculative (and I don't have the full text) but it's highly relevant nonetheless.
Mol Neurobiol 2002 Oct-Dec;26(2-3):235-50
Structure of the sodium channel gene SCN11A: evidence for intron-to-exon conversion model and implications for gene evolution.
Dib-Hajj SD, Tyrrell L, Waxman SG.
|Exon/intron boundaries in the regions encoding the trans-membrane segments of voltage-gated Na channel genes are conserved, supporting their proposed evolution from a single domain channel, while the exons encoding the cytoplasmic loops are less conserved with their evolutionary heritage being less defined. SCN11A encodes the tetrodotoxin-resistant (TTX-R) sodium channel Nav1.9a/NaN, which is preferentially expressed in nociceptive primary sensory neurons of dorsal root ganglia (DRG) and trigeminal ganglia. SCN11A is localized to human chromosome 3 (3p21-24) close to the other TTX-R sodium channel genes SCN5A and SCN10A. An alternative transcript, Nav1.9b, has been detected in rat DRG and trigeminal ganglion. Nav1.9b is predicted to produce a truncated protein due to a frame-shift, which is introduced by the new sequence of exon 23c (E23c). In human and mouse SCN11A, divergent splicing signals prevent utilization of E23c. Unlike exons 5A/N in genes encoding TTX-sensitive sodium channels, which appear to have resulted from exon duplication, E23c might have evolved from the conversion of an intronic sequence. Although a functional role for Nav1.9b has yet to be established, intron-to-exon conversion may represent a mechanism for ion channels to acquire novel features.|
Given that intronic sequences, with the exception of some 5' and 3' conserved bases, are sequence non-specific, this would be the equivalent of a more or less random sequence being converted into a biological function.
edited to add this diddy:
Evolution of voltage-gated Na(+) channels.
Edited by theyeti on Dec. 10 2002,21:08