| 2007 |
hSgo2 (Tripin) localizes to the inner centromere and its localization depends on BUB1 and Aurora B kinases. hSgo2 is essential for MCAK to localize to the centromere; depletion of hSgo2 causes MCAK delocalization, leading to uncorrected kinetochore attachment defects and lagging chromosomes. hSgo2 associates with PP2A and is proposed to spatially regulate MCAK activity at the inner centromere/kinetochore. |
siRNA depletion, immunofluorescence localization, co-immunoprecipitation, live-cell imaging |
The Journal of cell biology |
High |
17485487
|
| 2007 |
During mammalian meiosis I, SGO2 accumulates at centromeres during diplotene and co-localizes differentially with cohesin subunits RAD21 and REC8 at metaphase I centromeres. During meiosis II and mitosis, SGO2 shows a tension-dependent redistribution within centromeres during chromosome congression. |
Immunofluorescence, co-localization with cohesin subunits during male mouse meiosis |
EMBO reports |
Medium |
17205076
|
| 2010 |
Aurora B phosphorylates hSgo2 at its N-terminal coiled-coil region and middle region. These phosphorylations separately promote binding of hSgo2 to PP2A and MCAK, respectively, and are essential for localizing PP2A and MCAK to centromeres. hSgo2 plays a dual role in chromosome congression and centromeric protection of cohesin in HeLa cells. |
In vitro kinase assay, phosphosite mutagenesis, co-immunoprecipitation, siRNA depletion, immunofluorescence |
Genes & development |
High |
20889715
|
| 2010 |
In aged mouse oocytes, depletion of Sgo2 accompanies loss of centromeric cohesin, consistent with Sgo2's role in protecting centromeric cohesin during meiosis I. Reduced cohesin is not due to age-related failure of the spindle checkpoint to delay separase-mediated cleavage. |
Immunofluorescence of chromosome spreads from aged vs. young oocytes, cohesin and Sgo2 quantification |
Current biology : CB |
Medium |
20817533
|
| 2013 |
In mammalian oocytes, Sgol2 protects centromeric cohesin via its interaction with PP2A; it silences the spindle assembly checkpoint (SAC) via direct binding to Mad2; it promotes chromosome congression, bi-orientation, and K-fiber formation; and it limits bivalent stretching. The K-fiber/bivalent-stretching effects are PP2A-independent and mediated by MCAK recruitment and inhibition of Aurora C kinase activity, respectively. |
Oocyte knockout/depletion, co-immunoprecipitation (PP2A, Mad2, MCAK), dominant-negative Aurora C, live-cell imaging, rescue experiments |
eLife |
High |
24192037
|
| 2017 |
In mouse oocyte meiosis I, Mps1 kinase activity is required for Sgo2 localization to the centromere region and for centromeric cohesin protection. Bub1 kinase activity also contributes to Sgo2 localization (preferentially to the pericentromere via H2A-T121 phosphorylation) but is dispensable for cohesin protection when Mps1 is functional. Sgo2 at the centromere (not pericentromere) is the critical pool for protection. |
Small-molecule kinase inhibition (Mps1 inhibitor), oocyte-specific Bub1 kinase-dead knock-in mice, immunofluorescence, functional cohesin protection assay |
Nature communications |
High |
28947820
|
| 2017 |
In fission yeast, Sgo2 controls a Mad2-independent, APC/C-inhibitory pathway that delays anaphase onset. This pathway requires Sgo2 and SAC components Bub1, Mph1/Mps1, and Mad3 (first KEN box), but not Mad1 or Mad2. The pathway is terminated when the chromosome passenger complex (CPC) interacts with Klp9/MKLP2. |
Fission yeast genetic epistasis, double-mutant analysis, spindle checkpoint component deletions, anaphase timing assays |
Cell reports |
Medium |
28178520
|
| 2019 |
SET/TAF1 localizes to the inner centromere by directly interacting with Sgo2. This interaction maintains Aurora B kinase activity by inhibiting PP2A at the inner centromere, thereby correcting erroneous kinetochore-microtubule attachments. SET levels at centromeres decline with increasing inter-kinetochore distance (tension), contributing to chromosome bi-orientation. |
Co-immunoprecipitation, immunofluorescence, SET overexpression and depletion, kinetochore tension assay |
The Journal of cell biology |
Medium |
31527146
|
| 2022 |
SGOL2 physically interacts with RAB1A (validated by mass spectrometry and Co-IP) and inhibits RAB1A ubiquitination, thereby stabilizing RAB1A protein levels and promoting prostate cancer cell proliferation and migration. |
Co-immunoprecipitation, mass spectrometry, ubiquitination assay, siRNA knockdown, rescue experiments |
Aging |
Medium |
36566018
|
| 2025 |
SGO2 does not play an essential role as a separase inhibitor during meiosis I in mouse oocytes. Using a separase biosensor, securin and cyclin B1-CDK1 each independently and sufficiently suppress separase activity; SGO2 inhibition of separase is not required. SGO2 is destroyed during meiosis I but this is not linked to essential separase regulation. |
Separase biosensor, mouse oocyte knockout/perturbation, live imaging of separase activity |
PLoS biology |
High |
40267054
|
| 2025 |
In mouse hybrid oocytes (M. m. domesticus × M. spicilegus), SGO2 mislocalizes to chromosome arms instead of centromeres due to abnormally elevated BUB1 kinase activity, causing cohesin over-protection and failure of homologous chromosome separation. This establishes that BUB1 activity determines SGO2's centromeric vs. arm targeting in oocytes. |
Hybrid mouse cross, immunofluorescence of SGO2 localization, BUB1 kinase activity assay, aneuploidy/segregation assays |
bioRxivpreprint |
Medium |
|
| 2025 |
In mouse oocytes, cohesin is not protected at metaphase II arrest; centromeric cohesin protection by Sgo2-PP2A is operative in meiosis I but not present at metaphase II. Prior kinetochore individualization in meiosis I is required for separase to cleave centromeric cohesin in meiosis II. |
Knockout mouse models (separase inhibitor elimination via securin/cyclin B1 KO), structure-function assays, separase activity monitoring |
bioRxivpreprint |
Medium |
|