Figure 6. The possible pathways of the NER-generated genetic instability of long transcribed CTG/CAG tracts in orientation II.

Figure 6

The possible pathways of the NER-generated genetic instability of long transcribed CTG/CAG tracts in orientation II. The CTG hairpin formed on the lagging-strand template during TRS replication (shaded circle) may be removed by the UvrA dimer (left panel), and once the correct template for the repair synthesis is restored, the TRS is replicated with no length changes. Bypass synthesis in NER-deficient strains will result in large deletions (middle panel). In the absence of the functional UvrA protein the UvrBC complex may specifically recognize and excise the CTG hairpin, which would also lead to large deletions.

From: Molecular Mechanisms of TRS Instability

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