Evolution of Maturase Activity

What might be the driving force behind a mobile DNA endonuclease evolving a splicing activity? Colonization of self-splicing group I introns by homing endonucleases provides a safe haven for these elements, as intron splicing removes the otherwise disruptive ORF from RNA transcripts. In addition, as the endonuclease and intron coevolved into a "hybrid" mobile element, the intron was equipped with a mechanism to propagate itself in a population. Phylogenetic studies suggest that homing intron/ORFs follow a "life cycle" that includes three steps: (1) invasion of an intron-less allele, (2) degeneration of the endonuclease ORF, and (3) intron loss (Fig. 3; Cho et al. 1998; God-dard and Burt 1999). Intron/ORFs are normally maintained in a population only through promiscuous invasion. However, these elements could be fixed if they offer a selective advantage to the host. In one scenario, splicing regulation could be a means by which the host controls the invaded gene's expression (Fig. 3). As detailed above, the splicing of many group I introns is regulated by nuclear-encoded cofactors, suggesting that intron integration has presented its hosts with an opportunity to regulate mt gene expression. While establishing a vital role in the host's metabolism would preclude intron loss it would not ensure retention of the freeloading ORF, which is naturally subject

Fig. 3. Model for intron homing endonuclease ORF gain, loss and escape from the cycle by "permanent" fixation. The presence of the intron can confer an advantage if the host develops a means for controlling splicing. The endonuclease can maintain its presence if it develops an indispensable splicing cofactor function

Fig. 3. Model for intron homing endonuclease ORF gain, loss and escape from the cycle by "permanent" fixation. The presence of the intron can confer an advantage if the host develops a means for controlling splicing. The endonuclease can maintain its presence if it develops an indispensable splicing cofactor function to degeneration within the intron (Fig. 3). However, by establishing an essential role in intron splicing along with host cofactors, the intron-encoded protein may have assured its residency in the host. Therefore, selection for mat-urase function may be a means by which the selfish ORF protects itself from natural attrition. By gaining a functionally distinct site for RNA maturation, it can retain its native homing function, thus providing two powerful avenues to be sustained in a population.

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