ArticleThe Journal of cell biology2019
SET binding to Sgo1 inhibits Sgo1-cohesin interactions and promotes chromosome segregation.
Article in The Journal of cell biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 9 citations in OpenAlex.
- Mechanisms of formic acid stress response in evolved yeast for microbial-electrocatalytic systems.Biodesign research · 2026Article
- α-Satellite RNA maintains centromeric cohesion through R-loops.Molecular cell · 2026Article
- The next decade of SET: from an oncoprotein to beyond.Journal of molecular cell biology · 2024Review
- Topoisomerase I is an evolutionarily conserved key regulator for satellite DNA transcription.Nature communications · 2024Article
- Topoisomerase I is an Evolutionarily Conserved Key Regulator for Satellite DNA Transcription.bioRxiv : the preprint server for biology · 2024Article
- Sgo1 interacts with CENP-A to guide accurate chromosome segregation in mitosis.Journal of molecular cell biology · 2024Article
- Centromeric transcription maintains centromeric cohesion in human cells.The Journal of cell biology · 2021Article
- SET levels contribute to cohesion fatigue.Molecular biology of the cell · 2021Article
- Functioning mechanisms of Shugoshin-1 in centromeric cohesion during mitosis.Essays in biochemistry · 2020Review
- Priming chromatin for segregation: functional roles of mitotic histone modifications.Cell cycle (Georgetown, Tex.) · 2020Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
At anaphase onset, Sgo1 function of cohesion protection must be disabled to allow timely chromosome segregation, but how this is achieved is not fully understood. Here, we show that SET, a known PP2A inhibitor, directly binds to a domain in Sgo1 in close proximity to the cohesin-binding motif. The Sgo1-cohesin binding can be disrupted by SET in a dose-dependent manner in vitro as well as by SET overexpression in cells, suggesting that SET is also an inhibitor to the Sgo1-cohesin binding. Furthermore, the SET binding-deficient Sgo1 mutant fully supports centromeric cohesion protection but delays chromosome segregation, suggesting that the SET-Sgo1 binding is required for timely chromosome segregation. Moreover, overexpression of SET WT, not the Sgo1 binding-deficient mutant, exacerbates the occurrence of cohesion fatigue in MG132-arrested cells. Conversely, SET depletion delays it. Thus, we propose that a major function of SET during mitosis is to disrupt the Sgo1-cohesin interaction, thereby promoting centromeric cohesion de-protection and timely chromosome segregation at anaphase onset.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.