non-L1 sequence to a new genomic location. This new location does not have to be in a homologous sequence or in close proximity to the donor DNA sequence. The donor DNA sequence remains unchanged throughout this process because it functions in a copy-paste manner via RNA intermediates; however, only those regions located in the 3' region of the L1 have been proven to be targeted for duplication. Nevertheless, there is reason to believe that this may not hold true every time as shown by the following example. The human ATM gene is responsible for the human autosomal-recessive disorder ataxia-telangiectasia and is located on chromosome 11. However, a partial ATM sequence is found in chromosome 7. Molecular features suggest that this duplication was mediated by L1 retrotransposition: the derived sequence was flanked by 15bp target side duplications (TSD), the sequence around the 5' end matched with the consensus sequence for L1 endonuclease cleavage site and a poly(A) tail preceded the 3' TSD. But since the L1 element was present in neither the retrotransposed segment nor the original sequence the mobilization of the segment cannot be explained by 3' transduction. Additional information has led to the belief that trans-mobilization of the DNA sequence is another mechanism of L1 to shuffle exons, but more research on the subject must be done. Helitron Another mechanism through which exon shuffling occurs is by the usage of helitrons. Helitron transposons were first discovered during studies of repetitive DNA segments of rice, worm and the thale crest genomes. Helitrons have been identified in all eukaryotic kingdoms, but the number of copies varies from species to species. Helitron encoded proteins are composed of a rolling-circle (RC) replication initiator (Rep) and a DNA helicase (Hel) domain. The Rep domain is involved in the catalytic reactions for endonucleolytic cleavage, DNA transfer and ligation. In addition this domain contains three motifs. The first motif is necessary for DNA binding. The second motif has two histidines and is involved in metal ion binding. Lastly the third motif has two tyrosines and catalyzes DNA cleavage and ligation. There are three models of gene capture by helitrons: the 'read-through" model 1 (RTM1), the 'read-through" model 2 (RTM2) and a filler DNA model (FDNA). According to the RTM1 model an accidental "malfunction" of the replication terminator at the 3' end of the Helitron leads to transposition of genomic DNA. It is composed of the read-through