Tail Wags Dog’s SINE: Retropositional Mechanisms of Can SINE Depend on Its A-Tail Structure

SIMPLE SUMMARY: The genomes of higher organisms including humans are invaded by millions of repetitive elements (transposons), which can sometimes be deleterious or beneficial for hosts. Many aspects of the mechanisms underlying the expansion of transposons in the genomes remain unclear. Short retrotransposons (SINEs) are one of the most abundant classes of genomic repeats. Their amplification relies on two major processes: transcription and reverse transcription. Here, short retrotransposons of dogs and other canids called Can SINE were analyzed. Their amplification was extraordinarily active in the wolf and, particularly, dog breeds relative to other canids. We also studied a variation of their transcription mechanism involving the polyadenylation of transcripts. An analysis of specific signals involved in this process allowed us to conclude that Can SINEs could alternate amplification with and without polyadenylation in their evolution. Understanding the mechanisms of transposon replication can shed light on the mechanisms of genome function. ABSTRACT: SINEs, non-autonomous short retrotransposons, are widespread in mammalian genomes. Their transcripts are generated by RNA polymerase III (pol III). Transcripts of certain SINEs can be polyadenylated, which requires polyadenylation and pol III termination signals in their sequences. Our sequence analysis divided Can SINEs in canids into four subfamilies, older a1 and a2 and younger b1 and b2. Can_b2 and to a lesser extent Can_b1 remained retrotranspositionally active, while the amplification of Can_a1 and Can_a2 ceased long ago. An extraordinarily high Can amplification was revealed in different dog breeds. Functional polyadenylation signals were analyzed in Can subfamilies, particularly in fractions of recently amplified, i.e., active copies. The transcription of various Can constructs transfected into HeLa cells proposed AATAAA and (TC)(n) as functional polyadenylation signals. Our analysis indicates that older Can subfamilies (a1, a2, and b1) with an active transcription terminator were amplified by the T(+) mechanism (with polyadenylation of pol III transcripts). In the currently active Can_b2 subfamily, the amplification mechanisms with (T(+)) and without the polyadenylation of pol III transcripts (T(−)) irregularly alternate. The active transcription terminator tends to shorten, which renders it nonfunctional and favors a switch to the T(−) retrotransposition. The activity of a truncated terminator is occasionally restored by its elongation, which rehabilitates the T(+) retrotransposition for a particular SINE copy.