PICH promotes sister chromatid disjunction and co-operates with topoisomerase II in mitosis

Nielsen, Christian Friberg; Huttner, Diana; Bizard, Anna H.; Hirano, Satoshi; Li, Tian-Neng; Pálmai-Pallag, Timea; Bjerregaard, Victoria A.; Liu, Ying; Nigg, Erich A.; Wang, Lily; Hickson, Ian D.

doi:10.1038/ncomms9962

Cited by 100 publications

(174 citation statements)

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“…Therefore, PICH may act as a “tension sensor” to decorate UFBs as they are put under tension generated by the mitotic spindle. It has been shown that the timely resolution of C-UFBs depends on the ATPase activity of PICH as replacement of wild-type PICH with an ATPase-dead mutant of PICH prolongs C-UFB persistence [20]. Whether the ATPase activity of PICH is involved in resolving HR-UFBs remains to be determined.…”

Section: Proteins That Recognize and Process Hr-ufbsmentioning

confidence: 99%

“…PICH colocalizes with topoisomerase IIα on C-UFBs and stimulates topoisomerase IIα-mediated decatenation activity in vitro [20]. It also serves as the main recruitment factor for a variety of proteins to UFBs.…”

Section: Proteins That Recognize and Process Hr-ufbsmentioning

confidence: 99%

“…Conditions that increase the frequently of UFB formation, or interfere with UFB resolution by inhibiting the functions of UFB-binding proteins, can lead to DNA damage and cell division defects, such as cytokinesis failure and micronucleus formation [19,20]. Therefore, it is important to understand how UFBs originate and how they are resolved before cytokinesis.…”

Section: Introductionmentioning

confidence: 99%

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A new class of ultrafine anaphase bridges generated by homologous recombination

Chan

West

2018

Cell Cycle

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Ultrafine anaphase bridges (UFBs) are a potential source of genome instability that is a hallmark of cancer. UFBs can arise from DNA catenanes at centromeres/rDNA loci, late replication intermediates induced by replication stress, and DNA linkages at telomeres. Recently, it was reported that DNA intertwinements generated by homologous recombination give rise to a new class of UFBs, which have been termed homologous recombination ultrafine bridges (HR-UFBs). HR-UFBs are decorated with PICH and BLM in anaphase, and are subsequently converted to RPA-coated, single-stranded DNA bridges. Breakage of these sister chromatid entanglements leads to DNA damage that can be repaired by non-homologous end joining in the next cell cycle, but the potential consequences include DNA rearrangements, chromosome translocations and fusions. Visualisation of these HR-UFBs, and knowledge of how they arise, provides a molecular basis to explain how upregulation of homologous recombination or failure to resolve recombination intermediates leads to the development of chromosomal instability observed in certain cancers.

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Section: Proteins That Recognize and Process Hr-ufbsmentioning

confidence: 99%

Section: Proteins That Recognize and Process Hr-ufbsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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A new class of ultrafine anaphase bridges generated by homologous recombination

Chan

West

2018

Cell Cycle

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“…A number of studies have investigated the mechanisms by which UFBs are generated and resolved (Wang et al , 2010bNaim and Rosselli 2009;Nielsen et al 2015). It is known that UFBs can be induced by exposure to a range of stressors, and that they often arise from defined genomic loci (centromeres, common fragile sites [CFSs], telomeres, and ribosomal DNA [rDNA]).…”

mentioning

confidence: 99%

Knotty Problems during Mitosis: Mechanistic Insight into the Processing of Ultrafine DNA Bridges in Anaphase

Sarlós

Biebricher

Petermann

et al. 2017

Cold Spring Harb Symp Quant Biol

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To survive and proliferate, cells have to faithfully segregate their newly replicated genomic DNA to the two daughter cells. However, the sister chromatids of mitotic chromosomes are frequently interlinked by so-called ultrafine DNA bridges (UFBs) that are visible in the anaphase of mitosis. UFBs can only be detected by the proteins bound to them and not by staining with conventional DNA dyes. These DNA bridges are presumed to represent entangled sister chromatids and hence pose a threat to faithful segregation. A failure to accurately unlink UFB DNA results in chromosome segregation errors and binucleation. This, in turn, compromises genome integrity, which is a hallmark of cancer. UFBs are actively removed during anaphase, and most known UFB-associated proteins are enzymes involved in DNA repair in interphase. However, little is known about the mitotic activities of these enzymes or the exact DNA structures present on UFBs. We focus on the biology of UFBs, with special emphasis on their underlying DNA structure and the decatenation machineries that process UFBs.

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“…Loss of PICH or its ATPase activity results in the formation of anaphase bridges and micronuclei following cytokinesis. 2,3 How PICH is appropriately localized to centromeres and kinetochores, and its precise molecular role in preventing chromatin bridges, are not fully understood. A recent study from Sridharan and Azuma provides new insights by identifying small ubiquitin-related modifier (SUMO)-interacting motifs (SIMs) in PICH that are essential for both its localization and function in preventing chromatin bridges.…”

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confidence: 99%