Table 1. Aphidicolin-induced fragility and deletion prevalence.
| Region | Class | Aphidicolin-induced breaks |
Deletion prevalence (%) |
||
|---|---|---|---|---|---|
| Breaks | Metaphases | Percentage | |||
| FRA2F | Fragile site | 6 | 184 | 3.3 | 11 |
| FRA3B | Fragile site | 27 | 184 | 14.7 | 23 |
| FRA4F | Fragile site | 10 | 184 | 5.4 | 8 |
| FRA16D | Fragile site | 49 | 184 | 26.6 | 21 |
| Chr 3 (118 Mb) | Unexplained | 1 | 184 | 0.5 | 7 |
| Chr 4 (181 Mb) | Unexplained | 3 | 184 | 1.6 | 10 |
| Chr 9 (12 Mb) | Unexplained | 1 | 80 | 1.3 | 13 |
| Chr 16 (6Mb) | Unexplained | 0 | 184 | 0.0 | 9 |
| Chr 20 (15 Mb) | Unexplained | 1 | 184 | 0.5 | 14 |
| Control_7 | Negative control | 2 | 80 | 2.5 | 2 |
| Control_8 | Negative control | 0 | 184 | 0.0 | 1 |
Aphidicolin-induced breakage rates for genomic regions with unexplained HD clusters, fragile sites, and two control regions, control_7 (chr 7, 21 Mb) and control_8 (chr 8, 56 Mb). The rate of breakage induced under aphidicolin stress was determined as described in the Methods. For all but two regions (FRA2F and FRA4F) mapping of breaks was confirmed by fluorescence in situ hybridization (FISH). The deletion prevalence within the series of cancer cell lines was calculated as the sum of the homozygous and small hemizygous deletions across the region.