Table 2.
Distribution of prophase and early prometaphase microtubule motion for each experimental condition
| Prophase |
Prometaphase |
|||||
|---|---|---|---|---|---|---|
| Slow | Fast | Totals | Slow | Fast | Totals | |
| Control | ||||||
| P (%) | 54 | 7 | 61 | 84 | 15 | 99 |
| n = 55 | n = 7 | n = 62 | n = 57 | n = 10 | n = 67 | |
| AP (%) | 26 | 13 | 39 | 0 | 1 | 1 |
| n = 26 | n = 13 | n = 39 | n = 0 | n = 1 | n = 1 | |
| Totals (%) | 80 | 20 | 20 cells | 84 | 16 | 20 cells |
| n = 81 | n = 20 | n = 57 | n = 11 | |||
| p150-CC1a | ||||||
| P (%) | 55 | 1 | 56 | 91 | 0 | 91 |
| n = 30 (50) | n = 1 (2) | n = 31 (52) | n = 30 (67) | n = 0 (0) | n = 30 (67) | |
| AP (%) | 40 | 4 | 44 | 6 | 3 | 9 |
| n = 22 (37) | n = 2 (3) | n = 24 (40) | n = 2 (4) | n = 1 (2) | n = 3 (6) | |
| Totals (%) | 95 | 5 | 12 cells | 97 | 3 | 9 cells |
| n = 52 (87) | n = 3 (5) | n = 32 (71) | n = 1 (2) | |||
| Kif2a/MCAKb | ||||||
| P (%) | 50 | 13 | 63 | 100 | 0 | 100 |
| n = 15 (38) | n = 4 (10) | n = 19 (48) | n = 27 (60) | n = 0 (0) | n = 27 (60) | |
| AP (%) | 33 | 4 | 37 | 0 | 0 | 0 |
| n = 10 (25) | n = 1 (3) | n = 11 (28) | n = 0 (0) | n = 0 (0) | n = 0 (0) | |
| Totals (%) | 83 | 17 | 8 cells | 100 | 0 | 9 cells |
| n = 25 (63) | n = 5 (13) | n = 27 (60) | n = 0 (0) | |||
| Monastrolc | ||||||
| P (%) | 12 | 2 | 14 | 100 | 0 | 100 |
| n = 5 (10) | n = 1 (2) | n = 6 (12) | n = 31 (56) | n = 0 (0) | n = 31 (56) | |
| AP (%) | 55 | 31 | 86 | 0 | 0 | 0 |
| n = 23 (46) | n = 13 (26) | n = 36 (72) | n = 0 (0) | n = 0 (0) | n = 0 (0) | |
| Totals (%) | 67 | 33 | 10 cells | 100 | 0 | 11 cells |
| n = 28 (56) | n = 14 (28) | n = 31 (56) | n = 0 (0) | |||
To make the number of measured marks comparable between treatments involving a variable number of analyzed cells, the observable n for each experimental treatment has been supplemented with a value in parentheses that represents the number of marks expected in 20 cells (the number of cells analyzed for both prophase and early prometaphase controls).
a p150-CC1 does not alter the frequency of slow P motion. During prophase, 50 slow P marks would be expected in 20 injected cells (similar to the 55 slow P marks recorded in controls). During early prometaphase, 67 slow P marks would be expected in 20 injected cells (similar to the 57 slow P marks recorded in controls).
b Kif2a/MCAK injection does not alter the prophase distribution of rates but slightly alters the early prometaphase distribution. In control prophase cells, ∼60% of all motion is P (∼40% is AP) and ∼80% is slow (∼20% is fast). This is identical to the distribution after injection. In control early prometaphase cells, ∼100% of all motion is P and ∼85% is slow (∼15% is fast). After injection, 100% of all motion is slow P.
c Monastrol treatment causes a true decrease in prophase P motion, evidenced by the 12 marks expected to move poleward in 20 monastrol-treated cells (compared with the 62 marks recorded in controls), and a true increase in AP motion, evidenced by the 72 marks expected to move away from the pole in 20 monastrol-treated cells (compared with the 39 marks recorded in controls).