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

Autor: Kosushkin SA; Laboratory of Eukaryotic Genome Evolution, Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, 119991 Moscow, Russia., Ustyantsev IG; Laboratory of Eukaryotic Genome Evolution, Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, 119991 Moscow, Russia., Borodulina OR; Laboratory of Eukaryotic Genome Evolution, Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, 119991 Moscow, Russia., Vassetzky NS; Laboratory of Eukaryotic Genome Evolution, Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, 119991 Moscow, Russia., Kramerov DA; Laboratory of Eukaryotic Genome Evolution, Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, 119991 Moscow, Russia.
Jazyk: angličtina
Zdroj: Biology [Biology (Basel)] 2022 Sep 26; Vol. 11 (10). Date of Electronic Publication: 2022 Sep 26.
DOI: 10.3390/biology11101403
Abstrakt: 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.
Competing Interests: The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.
Databáze: MEDLINE
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