Distinct mechanisms govern the localisation of Drosophila CLIP-190 to unattached kinetochores and microtubule plus-ends
J Cell Sci Dzhindzhev et al.
118: 3781
Supplemental Figure 2 (Adobe PDF) -
Fig.
S2. Genes depleted
by RNAi. Listed are the genes depleted by RNAi and the effects of the
RNAi as an evidence for efficient depletion.
Supplemental Figure 3 (Adobe PDF) -
Fig.
S3. Checkpoint-defect
induced by Mad1 RNAi. (A) Low mitotic index in Mad1 RNAi. The mitotic index of
asynchronously growing S2 cells after control (red bar) or Mad1 RNAi (green
bar; n=1000 for
both). (B) Failure to arrest in overnight colchicine treatment after Mad1 RNAi.
The mitotic index of S2 cells, treated overnight with colchicine, after control
(red bar) or Mad1 RNAi (green bar; n=1000 for both). (C) Segregation defects in
Mad1 RNAi. The percentage of S2 cells in late anaphase or telophase displaying
chromosome bridges or lagging chromosomes after control (red bar) or Mad1 RNAi
(green bar; n=100
for both).
Supplemental Figure 4 (Adobe PDF) -
Fig.
S4. Checkpoint-defect
induced by BubR1 RNAi. (A) Low mitotic index in BubR1 RNAi. The mitotic
index of asynchronously growing S2 cells after control (red bar) or BubR1 RNAi
(green bar; n=1000 for both). (B)
Failure to arrest in overnight colchicine treatment after BubR1 RNAi. The
mitotic index of S2 cells, treated overnight with colchicine, after control
(red bar) or BubR1 RNAi (green bar; n=1000 for both).
