The dimensionality inequality (i.e. p ≥ m ) in the assumption is costless, since transposition captures its negation.
The length of detectable TSDs might therefore be a rough measure of the time elapsed since transposition.
Much of what is known about RTEs reflects their activity in the germline, since transposition events in somatic tissues would not be inherited from generation to generation [ 16].
Much of our accumulated knowledge of RTE biology reflects their activity in the germline, since transposition events in somatic tissues would not be inherited from generation to generation, and hence would not be captured in reference genome sequences.
Our working hypothesis was that newly transposed EhSINE1s would be identical in sequence to the parent copy and would have easily-recognisable TSDs, but that over time these similarities would decay, providing a rough measure of time since transposition.
Alternatively, it is possible that the binding is not specific across the entire TIR, or that some of the mutations that have accumulated since transposition actually inactivates the respective copies.
This alignment is found in multiple ORFs (likely due to in/dels occurring since transposition) which would transcribe in the 5′- to 3′-direction relative to all SDR scaffolds.
