Recently, trans-acting HEases have been described in T4 and related phages that can promote the homing of either group I introns missing ORFs or group I introns that encode defunct HEases . Intron homing is initiated by the HEase that introduces a double-strand break , or nick, in an intronless allele . The homing process is accomplished by host DSB-restore or synthesis-dependent strand annealing pathway [78-81] that use the intron-containing allele as a donor to repair the break within the recipient intronless allele . The finish result is the nonreciprocal switch of the cellular intron element into the intronless allele .

The bacterial DUF199/WhiA protein is a transcription factor and its N-terminal area contains the identical protein fold as found in monomeric LAGLIDADG HEases encoded within group I introns . This similarity suggests that an invasive factor was co-opted to function a regulatory protein . The ability of group I intron RNAs to form complicated tertiary buildings has been harnessed in Clostridium difficile as a function of a two-element riboswitch that involves c-di-GMP as an allosteric activator .

Here, within the 5′ untranslated region of an mRNA, a c-di-GMP binding aptamer is located upstream of a group I intron; the binding of c-di-GMP to its aptamer modifies the group I intron fold and shifts the 5′ splice web site. In essence, the allosteric self-splicing intron has been domesticated as a metabolite sensor and genetic regulatory component.

The HEases have particular target websites, with some allowance for sequence variation in their homing websites . Recognition of variant homing websites ensures propagation in the face of substitutions that accumulate over time within the target web site.

It is generally thought that group I introns propagate by way of a population of intronless alleles with ‘tremendous-Mendelian’ inheritance, and that each one obtainable alleles for homing rapidly become occupied. At this level, the HEase can shortly accumulate deleterious mutations that inactivate the enzyme, or the HEase assumes one other function to avoid loss.

Alternatively, it's thought that group I introns can ‘escape’ to a new population of intronless alleles by transposition to new websites by reverse splicing. Reverse splicing is the reverse of the ahead splicing response, and theoretically allows a bunch I intron RNA to insert into a RNA molecule with four to 6 complementary bases to the P1 stem of the intron RNA . The finest circumstantial evidence for reverse splicing has been documented for rDNA introns the place associated introns are inserted in two completely different areas within rDNA genes .