Monastrol

Mailhes JB, Mastromatteo C, Fuseler JW (2004) Transient exposure to the Eg5 kinesin inhibitor monastrol leads to syntelic orientation of chromosomes and aneuploidy in mouse oocytes. ❋ Vincent Gache Et Al. (2010)

To test if Aurora B activity was compromised by condensin depletion, we initially used the Eg5 inhibitor monastrol ❋ Alexander Samoshkin Et Al. (2009)

Alternatively, cells were treated with 20 µM monastrol (Tocris) for ❋ Alexander Samoshkin Et Al. (2009)

Moreover, recovery from mitosis-inhibition by monastrol revealed a high incidence of merotelic attachment that was nearly identical with condensin depletion, Aurora B inactivation, or both, indicating that the Aurora B dysfunction is the key defect leading to chromosome missegregation in condensin-depleted cells. ❋ Alexander Samoshkin Et Al. (2009)

For the cell population analysis, both condensin depletion and Aurora B inhibition showed a similar (90%) proportion of abnormal (unrecovered) metaphases with ample signs of syntelic and merotelic attachments still persisting as late as 40 min after the release from monastrol. ❋ Alexander Samoshkin Et Al. (2009)

Analysis of cells released from monastrol arrest in the presence of condensins depletion, ❋ Alexander Samoshkin Et Al. (2009)

Assaying S95 MCAK phosphorylation by quantitative immunoblotting after monastrol release showed that SMC2-depleted cells released for 30 min had a > ❋ Alexander Samoshkin Et Al. (2009)

Around 200 kinetochores (in cells stained for HEC1 and α-tubulin) were counted for each experiment 40 min after release from monastrol. ❋ Alexander Samoshkin Et Al. (2009)

During recovery of either control or condensin-depleted cells from treatment with monastrol ( ❋ Alexander Samoshkin Et Al. (2009)