Telomere fusions and translocations: a bridge too far?

Susanna Stroik, Eric A. Hendrickson

Research output: Contribution to journalReview articlepeer-review

2 Scopus citations

Abstract

Telomere fusions inevitably arise as a cell's last-ditch effort to protect exposed chromosomal ends when telomeres are lost due to aging-associated erosion, breakage, failed replication, or a plethora of other cellular mistakes. Fusion of an exposed chromosomal end to another telomere presumably presents a superficially attractive option to the cell as opposed to the alternative of the impending degradation of the unprotected chromosomal terminus. However, when allowed to progress to mitosis these fusion events subsequently foster non-disjunction or bridge:breakage events — both of which drive highly pathogenic genomic instability and additional chromosomal translocations. Thus, the question becomes how and when telomere fusion events arise and, most importantly, is there a mechanism available to resolve these telomere bridges such that proper repair, and not genomic instability, results? Recent evidence suggests that the formation, and then the resolution of, ultrafine bridges may facilitate this process.

Original languageEnglish (US)
Pages (from-to)85-91
Number of pages7
JournalCurrent Opinion in Genetics and Development
Volume60
DOIs
StatePublished - Feb 2020

Bibliographical note

Funding Information:
Work in the Hendrickson laboratory was supported in part by grants from the N.I.H. ( GM088351 ) and the NCI ( CA190492 ).

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