Sarah Schaack*, Eunjin Choi, Michael Lynch and Ellen J Pritham
Corresponding author: Sarah Schaack firstname.lastname@example.org
Genome Biology 2010, 11:R46 doi:10.1186/gb-2010-11-4-r46
(2011-02-28 14:07) Nottingham University
Quoting from the intro:
"Although, DNA transposons are generally not thought to exhibit replicative gains
when mobilized, for members of subclass 1, copy number can increase due to homologue-dependent
DNA repair after excision at homozygous loci, which can result in the reconstitution
of a TE in the donor location and, therefore, replicative gain."
My understanding is slightly different from this. Class 2 DNA transposons become
amplified by two mechanisms operating during S phase of the cell cycle. Following
excision, the empty donor site is restored to a filled donor site by homologous recombination
with the sister chromosome (ie. the product of replication). Furthermore, if the
transposon excises behind one replication fork and inserts in front of another fork,
it makes further copy number gains.
In some organisms the repair of double strand breaks by homologous recombination is
restricted to S phase. During the rest of the cell cycle non homologous end joining
predominates. There is therefore very little scope for replicative gains by homologous
repair from the homolog. I do not know if this is true in daphnia, but it probably
English and Jones 1995 did some nice work in this area with the Ac/Ds system in maize.
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