Biology Reference
In-Depth Information
Helena
is a LINE-like element. The transposition mechanisms used by these ele-
ments are different and the mutants examined all showed evidence that trans-
position occurred in the appropriate manner. The four TEs appear to have
been mobilized due to “genomic stress” brought about by the dysgenic cross
(
Petrov et al. 1995
). The stress could have been caused by breakage of double-
stranded DNA, and can be caused by exposure to UV light and other agents.
This can increase transcription and/or mobilization of retroelements. Thus, the
production of ds breaks from the mobilization of a single TE might induce a cel-
lular response that releases other TEs from repression.
P
elements with defective
31-bp terminal repeats are unable to transpose because these repeats are the
site of action of the transposase. The location of
P
in the chromosome is impor-
tant in determining the frequency of transposition. Although transposition is
more-or-less “random” at the genome scale,
P
elements containing specific gene
sequences show some specificity by frequently inserting near the parent gene
(which is called “homing”) (
Taillebourg and Dura 1999
).
P
elements also tend to
insert into upstream promoter regions of genes (
Spradling et al. 1995
).
9.5 Transposition Method of
P
Elements
P
elements move from site to site in the genome (jump) by a “cut-and-paste”
method (
Engels et al. 1990, Gloor et al. 1991, Sentry and Kaiser 1992, Engels
1997
). When a
P
jumps, it leaves behind a ds gap in the DNA. A matching
sequence is then used as a template to repair the gap. This matching sequence
can occur on the sister chromatid or elsewhere in the genome. If the transpo-
sition occurs in an individual that is
heterozygous
for the
P
insertion, and the
matching site on the homologous chromosome is used as the template for DNA
replication and repair, there can be a precise
loss
of the
P
sequence in the origi-
nal site, although there is no
net loss
in the genome because the
P
element has
simply changed locations. However, if a
P
jumps after the chromosomes have
duplicated (when there are two chromatids per chromosome), but before the
cell divides, one of the sister chromatids will still have a
P
in its original position.
In this situation, the homologous
P
may serve as the template for filling in the
gap left when the
P
moved to a new position in the genome. Under these cir-
cumstances, the number of
P
elements in the genome is
increased
by one. The
P
element is
replaced
in its original site by gap repair
and
also is present in a new
site in the genome.
The cut-and-paste mechanism of transposition implies that
P
elements don't
have to confer an advantage on the organism to invade and persist in the
genome. In fact, a mathematical simulation model indicates that
P
elements
can become fixed in populations even when fitness is reduced by 50% (
Hickey
