Worm Breeder's Gazette 16(1): 30 (October 1, 1999)
These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.
Division of Molecular Biology, The Netherlands Cancer Institute, Center for Biomedical Genetics, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands
We have inspected the genome sequence of Bristol N2 for all Tc1 and Tc3 transposon sequences (we are currently investigating the other Tc elements). 31 Tc1 elements and the 20 Tc3 elements were aligned (see Figure 1). It turns out that virtually all Tc1 and Tc3 elements can be individually recognized by their pattern of single nucleotide polymorphisms.
One striking feature is that virtually all Tc1 and Tc3 elements are intact (this in contrast to other transposons in plants, flies and vertebrates, where the majority of copies are deleted or otherwise trans-defective). Most of the Tc1 elements have unique nucleotide changes, insertions and deletions in both coding and non-coding regions. Out of 46 SNPs found in the open reading frame, 34 lead to a change of amino acid or to the introduction of a stop codon. Six elements do not to encode full length transposase. There are only three types of Tc1 that share multiple SNPs or are identical (it is unclear if Tc1.13 and Tc1.15 are different elements*). Two of these (Tc1.4 & Tc1.5 and Tc1.8 & Tc1.9) occur twice, a third type of Tc1 (Tc1.10, Tc1.26 & Tc1.27) is found three times. Except for Tc1.10, these similar elements are in each case located within 0.7 map units from each other. This is most easily explained by a local reintegration of an excised Tc1 element (notice that the donor copy is thought to be restored by templated DSB repair, see Plasterk, 1992).
Most of the nucleotide changes in the Tc3 elements are not unique, although each Tc3 element has a unique combination of SNPs. Many changes are found in multiple elements; Surprisingly, changes in the inverted repeats are often found in both inverted repeats. This might indicate a constant SNP shuffling between the inverted repeats of one element.
The Bristol N2 strain is totally inactive for germ line transposition, so presumably the Tc1 and Tc3 transposons must have jumped before the strain became silenced for transposition. We are now sequencing new Tc1 alleles found in the mut-7 strain NL917 (Ketting et al., in press). Since each copy can be recognized individually, we can in principle trace the pattern of jumping by scoring their SNP pattern. We thus far analyzed 24 unc-22::Tc1 alleles, and found at least five of these to be derived from Tc1 donors located on chromosome IV (on which unc-22 is located), again suggesting a bias of Tc1 for local jumps, apparently not absolute.
A surprising result is that seven of these newly inserted Tc1 elements contain new SNPs or combinations of the SNPs found in the N2 set described above. We are now investigating if and how Tc1 excision or insertion could involve gene conversion or recombination between Tc1 elements.