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. 2018 Apr 1;32(7-8):537–554. doi: 10.1101/gad.311712.118

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© 2018 Begnis et al.; Published by Cold Spring Harbor Laboratory Press

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

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Figure 7. — Potential routes to rDNA jumping. (A) Telomere erosion triggers the RNAi-dependent translocation of subtelomeric rDNA to STE chromosome ends. (B) Two possibilities for the mechanism of RNAi-dependent translocation are diagrammed. In both scenarios, local instability is engendered by telomere erosion, which leads to increased local transcription and DDR activation. (Left) RNA Pol II (gray circle) switches template from the subterminal region of chromosome III to that of chromosome I (or II), perhaps due to nicks, DSBs, or stalled forks at eroding chromosome ends. (Insets) A variant branched structure (the bottom inset represents an isomer of the top inset) harboring a hybrid (STE- and rDNA-containing) RNA strand forms and prompts illegitimate translocation. Arrowheads represent potential cleavage sites for an enzyme that resolves branched DNA structures. (Right) The replisome (purple circle) undergoes template switching, with DNA replication proceeding from a difficult-to-replicate STE region to the similarly compromised rDNA intergenic spacer region.