del Campo EM, Casano LM, Gasulla F, Barreno E. Presence of multiple group I introns carefully associated to micro organism and fungi in plastid 23S rRNAs of lichen-forming Trebouxia. Stahley MR, Strobel SA. Structural evidence for a two-metallic-ion mechanism of group I intron splicing. Vicens Q, Cech TR. Atomic stage structure of group I introns revealed.

Cech TR, Damberger SH, Gutell ER. Representation of the secondary and tertiary structure of group I introns. Tocchini-Valentini GD, Fruscoloni P, Tocchini-Valentini GP. Evolution of introns within the archaeal world. Haugen P, Simon DM, Bhattacharya D. The pure historical past of group I introns.

That is, the goal website of the endonuclease corresponded to the intron-insertion website. One of probably the most intriguing questions about cellular group I introns concerns their evolutionary origin. The current consensus is that HEases and group I introns had distinct evolutionary origins, and that HEases have on a number of unbiased occasions invaded an endonuclease-free intron.

Koonin proposed that group I introns advanced as parasitic selfish-RNAs in abiotic compartments that housed early types of the ‘RNA world’. If indeed these parts are historical, it is surprising that now they've such a restricted distribution, being absent in the Archaea and only not often encountered among micro organism. An fascinating statement is that CRISPR/Cas methods are extraordinarily prevalent in Archaea, however much less so in bacteria, correlating with the absence of group I introns from Archaea. Recent research present a second mechanism, termed collaborative homing, for the origin of mobile introns. Work on two completely different phages revealed techniques where a free- standing HEase and an ORF-much less group I intron converged on the same conserved goal web site .

Two mechanisms that may lead to the formation of such a composite cell intron have been proposed. Loizos et al. noted that in the sunY gene of the T4 phage the intron sequences flanking the HEase ORF (I-TevII) had been similar to the exon junction sequences that comprise the I-TevII goal sequence.

This work was supported by a CIHR Operating Grant (MOP-97780) and a CIHR New Investigator Salary Award to DRE. GH’s research on mobile introns is supported by a Discovery Grant from the Natural Sciences and Engineering Research Council of Canada. MH wish to acknowledge assist by the Egyptian Ministry of Higher Education and Scientific Research. The mechanisms that promote and stop group I introns from proliferating amongst bacterial genomes are poorly understood, as is the long-term impact of introns on organismal viability.