| 2006 |
Human SGO1 directly binds to protein phosphatase 2A (PP2A), and this interaction is required for centromeric localization of SGO1. Bub1 targets PP2A to centromeres in a Bub1-dependent manner, and PP2A at centromeres counteracts Plk1-mediated removal of SGO1 from centromeres. |
Co-immunoprecipitation, RNAi knockdown, localization rescue experiments |
Developmental cell |
High |
16580887
|
| 2005 |
Budding yeast Sgo1 is required for sensing lack of tension at the kinetochore during mitosis (spindle checkpoint tension-sensing component), but not for responding to microtubule depolymerization; Sgo1 degradation upon sister chromatid separation prevents cell cycle arrest in anaphase. |
Genetic analysis, spindle checkpoint assays, chromosome segregation assays in budding yeast |
Science (New York, N.Y.) |
High |
15637284
|
| 2012 |
CDK-mediated, mitosis-specific phosphorylation of human SGO1 activates its cohesion-protection function and enables direct binding to cohesin. Phospho-SGO1-bound cohesin contains PP2A, PDS5, and hypophosphorylated sororin but lacks WAPL. SGO1-PP2A dephosphorylates PDS5-bound sororin, protecting centromeric cohesin from WAPL-mediated removal. |
In vitro binding assays, phosphorylation-deficient mutants, Co-IP, RNAi rescue experiments |
Nature cell biology |
High |
23242214
|
| 2008 |
A major splice variant of SGO1, sSgo1, localizes to centrosomes in interphase and spindle poles in mitosis (distinct from full-length Sgo1 at kinetochores). sSgo1 interacts with Plk1 and its spindle pole localization is Plk1-dependent. sSgo1 is required for centriole cohesion, preventing premature centriole separation. |
RNAi, GFP localization, Co-immunoprecipitation, dominant-negative expression |
Developmental cell |
High |
18331714
|
| 2009 |
In Xenopus egg extracts, Sgo1 plays a role in stabilizing cohesin along chromosome arms, which is antagonized by the mitotic kinases Plk1 and Aurora B; Wapl and Pds5 directly modulate cohesin conformational changes for dissociation during prophase. |
In vitro Xenopus egg extract system, immunodepletion, add-back experiments |
Genes & development |
High |
19696148
|
| 2005 |
In budding yeast meiosis, Sgo1 localizes to cohesin-associated regions at the centromere and the 50-kb surrounding region, establishing a cohesin-protected domain. This domain requires the 120-bp core centromere, Bub1, and the meiosis-specific factor Spo13. Cohesins and kinetochore proteins Iml3 and Chl4 are necessary for Sgo1 association with pericentric regions. |
ChIP, genetic epistasis, meiotic chromosome analysis in budding yeast |
Genes & development |
High |
16357219
|
| 2013 |
In human cells, cohesin and H2A-pT120 specify two distinct pools of Sgo1-PP2A: one at inner centromeres (cohesin-dependent) and one at kinetochores (H2A-pT120-dependent). Kinetochore tension triggers Sgo1 dephosphorylation and redistribution from inner centromeres to kinetochores; incomplete redistribution causes chromosome nondisjunction. |
Localization studies, phospho-specific antibodies, RNAi, tension manipulation |
Current biology : CB |
High |
24055156
|
| 2015 |
Human SGO1 is a direct reader of the Bub1-mediated H2A-pT120 mark at kinetochores. Bub1 also recruits RNA Polymerase II to unattached kinetochores, promoting active transcription that enables kinetochore-bound Sgo1 (recruited by H2A-pT120) to reach cohesin embedded in centromeric chromatin. Sgo1 interacts with Pol II in human cells and with RNA in vitro. |
In vitro binding assays, Co-IP, live imaging, Pol II inactivation in mitosis |
Molecular cell |
High |
26190260
|
| 2007 |
NEK2A directly binds human Sgo1 in vitro and co-localizes with Sgo1 at the kinetochore. NEK2A phosphorylates Sgo1 at Ser14 and Ser507, and expression of non-phosphorylatable Sgo1 mutants causes chromosome congression defects including syntelic and monotelic attachments. |
In vitro kinase assay, 32P incorporation, Co-IP, expression of phosphorylation-deficient mutants |
Cell research |
High |
17621308
|
| 2007 |
In budding yeast, Bub1 kinase domain is required for proper localization of Sgo1 to centromeres, and both Bub1 kinase activity and Sgo1 are required for accurate chromosome biorientation after nocodazole treatment. |
Genetic analysis, localization studies, chromosome segregation assays in budding yeast |
PLoS genetics |
High |
18081426
|
| 2008 |
Human Sgo1 is degraded during mitotic exit via the APC/C-Cdh1 pathway. Sgo1 contains two functional degradation motifs (KEN box and D box); deletion of both is required to stabilize the protein. Bub1 contributes to Sgo1 steady-state protein levels through an APC/C-independent mechanism. Non-degradable Sgo1 does not impair mitotic progression. |
In vitro ubiquitination assay, mutagenesis of degrons, overexpression of Cdh1, cell cycle analysis |
The Journal of biological chemistry |
High |
19015261
|
| 2011 |
In human cells, HP1α is recruited to mitotic centromeres by INCENP (CPC subunit), not by Sgo1. Both HP1-INCENP and HP1-Sgo1 interactions require the HP1 chromo shadow domain binding to PXVXL/I motifs. A Sgo1 mutant deficient in HP1 binding is functional in centromeric cohesion protection and localizes normally to centromeres in mitosis, demonstrating that HP1-Sgo1 interaction is dispensable for cohesion protection. |
Biochemical pull-down, structural analysis, functional complementation with HP1-binding deficient mutants |
Molecular biology of the cell |
High |
21346195
|
| 2010 |
Human Sgo1 is first recruited to centromeric heterochromatin in G2 in an HP1-dependent manner, then becomes diffusely localized in early prophase, before returning to centromeres in prophase via Bub1 kinase activity. Centromeric cohesion is maintained even when Bub1 kinase is absent and Sgo1 is absent from mitotic centromeres, because Sgo1 establishes protection in G2. |
Live-cell imaging, Bub1 kinase-dead complementation in Bub1-null MEFs, cell cycle-staged localization |
Journal of cell science |
High |
20124418
|
| 2014 |
In budding yeast, Sgo1 together with PP2A-Rts1 ensures localization of condensin to centromeric chromatin; failure to recruit condensin results in abnormal pericentric chromatin conformation. Sgo1 is also required for maintaining Aurora B/Ipl1 localization on kinetochores during metaphase, suggesting a dual role in promoting biorientation. |
Genetic epistasis, ChIP, localization studies in budding yeast |
PLoS genetics |
High |
24945276
|
| 2011 |
In budding yeast, Sgo1 overexpression partially rescues chromosome segregation defects of bub1Δ cells. Sgo1 is identified as a possible partner of Mps1; Mps1 is required for Sgo1 localization to kinetochores, and Sgo1 overexpression rescues metaphase Mps1 inactivation defects. Bub1, Sgo1, and Mps1 facilitate chromosome biorientation independently of the Aurora B pathway. |
High-copy suppressor screen, genetic epistasis, localization studies in budding yeast |
Molecular biology of the cell |
Medium |
21389114
|
| 2012 |
In budding yeast, Bub1 and Sgo1 regulate pericentric chromatin geometry and dynamics in response to altered microtubule dynamics; Bub1-mediated H2A phosphorylation and Sgo1 recruitment soften the chromatin spring, causing radial expansion of pericentric chromatin and cohesin ring. |
Live imaging, FRAP, genetic analysis in budding yeast |
Current biology : CB |
Medium |
22365852
|
| 2014 |
In budding yeast, Sgo1 recruits the Rts1 isoform of PP2A to pericentromeric chromatin, and artificial recruitment of Rts1 to a single chromosome is sufficient to perform Sgo1 function on that chromosome. Sgo1 removal from chromosomes before anaphase depends on tension between sister chromatids, not on APC/C-mediated degradation. Sgo1 is an APC/C substrate in budding yeast with an unusual D-box-related sequence motif. |
Genetic epistasis, artificial tethering experiments, APC/C degradation assays in budding yeast |
Journal of cell science |
High |
25236599
|
| 2016 |
In budding yeast, the Bub1-H2A-Sgo1-PP2A-Rts1 axis prevents premature spindle assembly checkpoint silencing prior to tension generation; Sgo1 mutants with abolished binding to H2A or PP2A-Rts1 show premature SAC silencing, establishing this pathway in tension-sensitive checkpoint maintenance. |
Genetic epistasis, checkpoint duration assays, separation-of-function Sgo1 mutants in budding yeast |
Genetics |
Medium |
28040741
|
| 2016 |
In Xenopus egg extract system, Bub1 targeting to centromeres (via CENP-C and CENP-T independently through the KMN network) is sufficient for Sgo1 recruitment in the absence of other kinetochore components. Mps1 is required for this Bub1-dependent Sgo1 recruitment pathway even in the absence of checkpoint signaling. |
Xenopus cell-free system, forced targeting experiments, immunodepletion |
Chromosoma |
High |
27116032
|
| 2018 |
In budding yeast, CENP-A (Cse4) interacts with Sgo1 in vivo and in vitro. The N-terminal coiled-coil domain of Sgo1 is sufficient for CENP-A interaction and for association with centromeric (but not pericentromeric) chromatin. Depletion of CENP-A results in loss of Sgo1 from centromeric chromatin. |
Co-IP in vivo, in vitro binding assay, domain mapping, ChIP, chromosome segregation assays |
Cell cycle (Georgetown, Tex.) |
High |
28980861
|
| 2020 |
In Xenopus egg extracts and biochemical reconstitution, Sgo1 directly interacts with the dimerization domain of Borealin (CPC subunit). Borealin and PP2A can bind simultaneously to the coiled-coil domain of Sgo1. A Borealin mutant disrupting the Sgo1-Borealin interaction causes defects in CPC chromosomal recruitment and Aurora B-dependent spindle assembly but not spindle assembly checkpoint signaling at unattached kinetochores. |
Biochemical reconstitution, in vitro binding assays, Xenopus egg extracts, separation-of-function mutants |
Molecular biology of the cell |
High |
32697622
|
| 2022 |
Using an integrative structure-function approach, the Sgo1 N-terminal 'histone H3-like' tail interacts with the Survivin BIR domain as a hotspot for CPC-Sgo1 assembly; downstream Sgo1 residues and Borealin contribute to high-affinity binding. Sgo1 and H3T3ph use the same surface on Survivin to bind CPC, suggesting spatiotemporally restricted interactions. Disrupting Sgo1-Survivin interaction perturbs CPC centromere localization and function. |
Structure-function analysis, mutagenesis, biochemical binding assays, functional validation |
The Journal of cell biology |
High |
35776132
|
| 2014 |
Aurora B kinase interacts with and phosphorylates Sgo1 in vitro and in vivo. Aurora B-mediated phosphorylation of Sgo1 regulates the distribution of Sgo1 between centromeres and chromosome arms; expression of Aurora B kinase-dead mutants of Sgo1 causes mislocalization from centromeres to chromosome arms. |
Co-IP, in vitro kinase assay, expression of kinase-dead mutants, localization analysis |
Biochemical and biophysical research communications |
Medium |
25451264
|
| 2019 |
SET, a known PP2A inhibitor, directly binds a domain in Sgo1 adjacent to the cohesin-binding motif and disrupts Sgo1-cohesin binding in a dose-dependent manner in vitro and in cells. SET-binding-deficient Sgo1 mutant fully supports centromeric cohesion protection but delays chromosome segregation, indicating SET promotes timely chromosome segregation by disrupting Sgo1-cohesin interaction. |
In vitro binding assay, Co-IP, dose-response experiments, separation-of-function Sgo1 mutants |
The Journal of cell biology |
High |
31227592
|
| 2024 |
Human CENP-A directly interacts with Sgo1 and determines Sgo1 localization to centromeres during mitosis. Lysine and arginine residues in the C-terminal domain of Sgo1 are critical for CENP-A binding. Mutation of these basic residues perturbs localization of both Sgo1 and Aurora B to centromeres, resulting in aberrant chromosome segregation and premature chromatid separation. |
Co-IP, biochemical domain mapping, mutational analysis, localization studies |
Journal of molecular cell biology |
Medium |
37777834
|
| 2014 |
Homozygous founder mutation in SGOL1 (K23E) causes CAID syndrome (Chronic Atrial and Intestinal Dysrhythmia). Patient fibroblasts show accelerated cell cycle progression, higher senescence rate, enhanced TGF-β signaling activation, and karyotypes displaying centromeric cohesion defects (railroad appearance). Morpholino knockdown of sgol1 in zebrafish recapitulates the human abnormalities. |
Human genetics, patient fibroblast analysis, zebrafish morpholino knockdown |
Nature genetics |
High |
25282101
|
| 2006 |
Two major isoforms of human Sgo1 have entirely different subcellular localization patterns: the long isoform localizes to kinetochores during G2 and mitosis, while the short isoform (sSgo1, lacking exon 6) localizes to mitotic spindles and does not associate with kinetochores at any stage. |
GFP fusion localization, cell cycle staging |
Cell cycle (Georgetown, Tex.) |
Medium |
16582621
|