The major mobility event of group II introns is homing (or retrohoming), in which the intron inserts site-specifically into intronless sites. For organellar introns, this occurs during crosses between two strains, where one strain contains the intron and the other does not. For bacterial introns, homing occurs when homing site DNA is introduced into a cell expressing the intron.

          The mechanism of homing is termed target-primed reverse transcription, and is carried out by catalytic activities of both intron RNA and RT protein, with both subunits required for each reaction step.

          The reaction begins by reverse splicing of the intron into the exon junction in double-stranded DNA. The reaction is RNA-catalyzed but facilitated by the RT protein, and is essentially the reverse of maturase-assisted splicing but occurs into DNA exons. Next, the En domain of the RT cleaves the antisense strand 9 or 10 bp downstream, and the RT reverse transcribes the intron using the cleaved DNA as a primer. Recombination and repair activities presumably complete intron insertion.

          There is also an endonuclease-independent pathway, in which bottom strand cleavage occurs at the replication fork during DNA replication. 

          At much lower frequencies, group II introns can insert into “unrelated”, or ectopic, sites (retrotransposition). The mechanism of retrotransposition is believed to involve reverse splicing of intron into cryptic homing sites. Because intron insertion at illegitimate sites is through reverse splicing, the intron will be able to splice out of its new site.