A NOVEL GROUP OF FAMILIES OF SHORT INTERSPERSED REPETITIVE ELEMENTS (SINES) IN XENOPUS - EVIDENCE OF A SPECIFIC TARGET SITE FOR DNA-MEDIATED TRANSPOSITION OF INVERTED-REPEAT SINES
K. Unsal et Gt. Morgan, A NOVEL GROUP OF FAMILIES OF SHORT INTERSPERSED REPETITIVE ELEMENTS (SINES) IN XENOPUS - EVIDENCE OF A SPECIFIC TARGET SITE FOR DNA-MEDIATED TRANSPOSITION OF INVERTED-REPEAT SINES, Journal of Molecular Biology, 248(4), 1995, pp. 812-823
We have isolated from Xenopus borealis members of a family of short in
terspersed repetitive elements (SINEs) that we have termed Xbr. Xbr el
ements are also present in other Xenopus genomes and are typically fra
med by 46 bp terminal inverted repeats (TIRs). These TIRs and those of
two previously described families of inverted-repeat SINEs from X. la
evis begin with the sequence TTAAAGGRR. Knowledge of this consensus, t
ermed the T2 motif, allowed us to define four previously uncharacteris
ed families of inverted-repeat SINEs from Xenopus database sequences.
We estimate that the group of seven SINE families that possess the T2
motif accounts for about 10% of all X. laevis SINEs. Novel evidence fo
r the transposition of inverted-repeat SINEs is provided: (1) by examp
les of the presence/absence of T2 elements at corresponding locations
in either duplicated genes or pseudotetraploid gene homeologues; and (
2) by the existence of contiguous elements from different T2 families
that are joined precisely by their TIRs. These examples provide novel
evidence for a DNA-mediated mechanism of T2 element transposition. The
y also show that the tetranucleotide, TTAA, which flanks integrated el
ements on both sides and is present once at unoccupied sites, is the o
bligate target site for T2 insertion. The use of a specific sequence a
s a target site for SINE insertion is unexpected, although such specif
icity is exhibited by a limited number of larger transposable elements
that encode their own transposase. The clear evidence for DNA-mediate
d transposition provided by T2 elements demonstrates that the evolutio
n and maintenance of SINE families in vertebrate genomes results from
two distinctive mechanisms.