Prematurely increasing CDK1 activity leads to lagging chromosomes at anaphase I. (A and B) Oocytes microinjected with H2B-mCherry cRNA, with or without cyclin B–GFP cRNA, were cultured for 6.5 h after GVBD, incubated with 10 µM cycloheximide to allow normal anaphase I progression, and imaged live from MI through telophase I (TI). Images in A are maximal intensity projections of a confocal z series showing all the chromosomes (time stamps relative to anaphase onset). The inset shows lagging chromosomes at anaphase (brightness increased for clarity); bar, 2 µm. The percentage of anaphases with lagging chromosomes was averaged over three independent experiments (n ≥ 5 cells per experiment; *, P < 0.001). (C) Model schematic depicts the timing of K-MT stabilization when CDK1 activity rises normally (left) vs. prematurely (right) during MI. Normally, kinetochores interact with MTs laterally to achieve chromosome congression, and attachments are stabilized ∼7 h after GVBD when CDK1 activity is maximal (left). If K-MT attachments are stabilized too early, in the presence of multipolar spindle intermediates and multiple MTOCs close to the chromosomes, incorrect attachments can lead to lagging chromosomes at anaphase I (right).