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. 2008 Aug;179(4):1785–1793. doi: 10.1534/genetics.108.087072

TABLE 1.

Gonadal dysgenesis in the offspring of control, TP, and H(hsp/P) stocks

Stocka Experimentb No. of vials No. of ♀♀ GD ± SEc (%)
y w 1 25 460 100.0 ± 0.0
2 14 176 99.6 ± 0.4
M5B#1 1 25 433 86.4 ± 3.2
2 18 200 90.9 ± 2.0
TP5-N 1 25 489 51.5 ± 5.4
2 23 399 60.1 ± 4.2
TP6-N 1 29 289 44.2 ± 6.8
2 16 161 58.1 ± 8.6
SP-A 2 20 266 100.0 ± 0.0
SP-B 1 25 420 100.0 ± 0.0
KP-3 1 25 462 99.4 ± 0.5
KP-7 2 20 268 96.1 ± 1.7
KP-14 2 18 209 99.7 ± 0.4
TP5-A 2 24 137 98.9 ± 0.8
TP5-B 2 16 241 99.7 ± 0,3
TP5-C 1 24 331 99.7 ± 0.4
TP5-D 2 23 331 99.3 ± 0.5
TP6-A 1 26 373 100.0 ± 0.0
TP6-B 1 25 490 100.0 ± 0.0
TP6-C 1 22 287 100.0 ± 0.0
a

y w is an M strain and M5B#1 is an M′ strain (Simmons et al. 2007a). TP5-N and TP6-N are strains with the native telomeric P elements on the X chromosome and are the same strains analyzed by Simmons et al. (2007a); other entries are strains with H(hsp/P) transgenes that contain the indicated P element.

b

The two experiments were carried out at different times.

c

Unweighted mean percentage of GD ± standard error.