(A) The metaphase extension observed in Cyclin B3 RNAi-treated embryos was SAC
independent, as a similar delay in metaphase was observed in SAC-deficient
mad2p embryos (unpaired t test,
control versus Cyclin B3 RNAi in
mad2p embryos, p <
0.0001). Error bars represent the SD.
(B and C) Colchicine treatment in
mad2p embryos with or without
Cyclin B3 knockdown. Chromosomes were visualized by an H2AvD-GFP transgene.
Mitotic exit was delayed in Cyclin B3 RNAi-treated embryos (chromosome
decondensation at 07:44 in control versus 12:46 in Cyclin B3 RNAi-treated
embryos). Scale bar, 5 mμ.
(D) Duration of mitotic phase in the Cyclin B3 knockdown embryos was
significantly longer than that in either control or the other cyclin
RNAi-treated embryos (unpaired t test, p < 0.0001). Error bars represent
the SD.
See also Figure S3 and
Movie S3.