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Figure 7 | Genome Biology

Figure 7

From: Expansion of a novel endogenous retrovirus throughout the pericentromeres of modern humans

Figure 7

Detection of K222 and recombinant K222/K111 sequences in individuals lacking the K111 5′ end. (A) Amplification of K222/K111 recombinant sequences. K222/K111 sequences were amplified with the primer 7972F and the primer P2, which binds to the K111 3′ flanking sequence (see Figure 2) in the DNA from individuals who lack the K111 5′ end (68, 90, and 95) and the cell line HUT78, which also lacks the K111 integration. As a positive control we used the DNA of individual 96, who is positive for K111 5′ end. (B) Amplification of K222 3′ integration. K222 was amplified with the primer 7972F and K222LTR-pCER:D22Z8R, the latter primer binding to the LTR-pCER:D22Z8 junction sequence present in K222, but not in K111. K111 3′ integration instead has a 5 bp sequence from the LTR and the target site duplication GAATTC not present in K222. Amplification of K222 3′ integration was seen in individuals having (96) or lacking (68, 90, and HUT78) the K111 5′ end. (C) Evolution of K222 and K222/K111 recombinant sequences in humans. A Bayesian inference tree of K222 and K222/K111 LTR sequences obtained by PCR in individuals lacking the K111 5′ end. The K222 sequences amplified are indicated with a K222 label. The tree reveals two different K222 LTR clades; K222 sequences similar to the K222 provirus (blue) and sequences that cluster to the K111 provirus (red). K222 sequences in individuals lacking the K111 5′ end clustering to K111 indicate the likely existence of K111 in the ancestral human lineage of those individuals. The K222/K111 recombinant clade (red) also suggests that K222 and K111 likely recombined by recombination/gene conversion during human evolution before K111 was lost from the lineage. Posterior probability values >85 are shown for the best tree.

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