Mobile DNA, or transposable elements, constitutes much
of the genome in all organisms. Some elements, retrotransposons, copy themselves
in a two-stage process, first from DNA to RNA by transcription, then from RNA
back to DNA by reverse transcription. By contrast, DNA transposons move via a
simple ‘cut-and-paste’ mechanism, without involving an RNA intermediate.
A major question within the field of mobile DNA is when
does most transposition take place? Contrary to the long-standing assumption
that all transposition occurs during germ-cell development as opposed to
somatic-cell development, a growing body of evidence is emerging for the
insertion of mobile elements in somatic cells.
In a recent article published in Mobile DNA, Eickbush and Eickbush report the somatic retrotransposition
of R2 elements in the early development of Drosophila. They highlight that transposition events early in
development can give rise to both somatic and germline mosaicism, often misinterpreted as germline events in the next generation. This adds to previous
findings of the L1 insertions transposition, which has been shown to occur in
human and mouse somatic cells.
From an evolutionary perspective, somatic insertion events
are ‘dead ends’, in that they are not inherited from one generation to the
next, providing no apparent benefit to the re-arrangement of genetic material
in this way.
Haig Kazazian, in a commentary published in BMC Biology, discusses this recent evidence
for somatic retrotransposition, and the important questions it raises:
mobile DNA can be destructive to gene function and host organisms possess
mechanisms for suppressing transposition, especially in the germline. So why
does somatic retrotransposition occur? Why don’t host controls on retrotransposition
block it in early embryogenesis?”
<w:LsdException Locked="false" Prio
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