Abstract
Accurate chromosome segregation requires the removal of all chromatin bridges, which link chromosomes before cell division. When chromatin bridges fail to be removed, cell cycle progression may halt, or cytokinesis failure and ensuing polyploidization may occur. Conversely, the inappropriate severing of chromatin bridges leads to chromosome fragmentation, excessive genome instability at breakpoints, micronucleus formation, and chromothripsis. In this mini-review, we first describe the origins of chromatin bridges, the toxic processing of chromatin bridges by mechanical force, and the TREX1 exonuclease. We then focus on the abscission checkpoint (NoCut) which can confer a transient delay in cytokinesis progression to facilitate bridge resolution. Finally, we describe a recently identified mechanism uncovered in C. elegans where the conserved midbody associated endonuclease LEM-3/ANKLE1 is able to resolve chromatin bridges generated by various perturbations of DNA metabolism at the final stage of cell division. We also discuss how LEM-3 dependent chromatin bridge resolution may be coordinated with abscission checkpoint (NoCut) to achieve an error-free cleavage, therefore acting as a “last chance saloon” to facilitate genome integrity and organismal survival.
Highlights
“A last chance saloon” refers to a bar that allows for the legal consumption of alcoholic beverages just before crossing into another jurisdiction where alcoholic beverages are not allowed
To ensure faithful genome maintenance during cell division, chromosomes have to be properly segregated into daughter cells, which requires the removal of all physical connections between sister chromatids
Mechanisms of Chromatin Bridge Resolution. In this mini-review, we discuss recent advances in how chromatin bridges arising from different perturbations of DNA metabolism are processed just before cells divide during cytokinesis, as well as pathological and non-pathological outcomes of chromatin bridge processing
Summary
Reviewed by: Eleni Petsalaki, University of Crete, Greece Juan Martin-Serrano, King’s College London, United Kingdom. When chromatin bridges fail to be removed, cell cycle progression may halt, or cytokinesis failure and ensuing polyploidization may occur. The inappropriate severing of chromatin bridges leads to chromosome fragmentation, excessive genome instability at breakpoints, micronucleus formation, and chromothripsis. In this mini-review, we first describe the origins of chromatin bridges, the toxic processing of chromatin bridges by mechanical force, and the TREX1 exonuclease. We focus on the abscission checkpoint (NoCut) which can confer a transient delay in cytokinesis progression to facilitate bridge resolution. We discuss how LEM-3 dependent chromatin bridge resolution may be coordinated with abscission checkpoint (NoCut) to achieve an errorfree cleavage, acting as a “last chance saloon” to facilitate genome integrity and organismal survival
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