Fig 7. Model for exaptation of a TE into TER2 and the emergence of a telomerase regulatory lncRNA.

Duplication of the single copy ancestral TER gene was followed soon thereafter by exaptation of DRE into the A. thaliana TER2 locus. The majority of A. thaliana accessions retain DRE (e.g. Col-0), but a small subset lost it (e.g. Ler-0). TER2Δ is produced by accessions lacking DRE. DRE acts as a post-transcriptional sensor that modulates TER2 abundance in response to DNA damage. Under normal physiological conditions, TER2 is an unstable RNA. However, in the presence of DSBs, TER2 is rapidly induced. Whether this is due to direct RNA stabilization or inhibition of TER2 processing (to yield TER2s) is unknown. TER2 has a higher affinity for TERT than TER1 or TER2Δ and following induction by DNA damage accumulates in TERT containing complexes in vivo. TER2-mediated telomerase inhibition may reflect competitive inhibition of TER1 for TERT. The transient decrease in telomerase activity may promote DSB repair rather than de novo telomere formation, thereby stabilizing the genome.