Table 2. Offspring analysis including embryonic lethality, brood size and segregation of male progeny in the genotypes used in this study.
Genotype | Embryonic lethality (%, mean ± SD) | Brood size (mean ± SD) | Males (%, mean ± SD) |
---|---|---|---|
WT | 1 ± 1 | 217 ± 35 | 0 |
rmif-2(jf113) | 40 ± 4 | 129 ± 50 | 10 ± 3.8 |
rmh-1(jf54) | 68 ± 9 | 130 ± 26 | 14 ± 5.6 |
rmif-2(jf113); rmh-1(jf54) | 56 ± 37 | 72 ± 83 | 5 ± 3 |
rmif-2::ha | 0.4 ± 0.5 | 210 ± 25 | 0 |
rmif-2::3xflag | 0.3 ± 0.2 | 266 ± 26 | 0 |
him-6(ok412) | 41 ± 5.6 | 202 ± 22 | 6 ± 2.6 |
rmif-2(jf113) him-6(ok412) | 99.2 ± 1.6 | 15 ± 14 | 0 |
top-3::ollas | 0.5 ± 0.4 | 269 ± 50 | 0 |
ha::degron::rmh-1 | 0.5 ± 0.5 | 210 ± 49 | 0 |
The CRISPR-Cas9 rmif-2 deletion allele revealed a role in meiotic segregation. Embryonic lethality, reduced brood size, and a high incidence of males in the progeny suggest a defect in meiotic chromosome segregation. Counts are derived from the following numbers of hermaphrodites: WT, 10; rmif-2, 10; rmh-1, 10; rmif-2;rmh-1, 10; rmif-2::ha, 10; rmif-2::3xflag, 9; him-6, 10; rmif-2 him-6, 10; top-3::ollas, 14; and ha::degron::rmh-1, 6. A Mann-Whitney test for statistical differences in lethality was performed: WT vs rmif-2 **** (p<0.0001); WT vs rmh-1 *** (p<0.001); WT vs rmif-2;rmh-1 * (p = 0.0134); WT vs rmif-2::ha (ns) (p = 0.3695); WT vs rmif-2::3xflag * (p = 0.0155); WT vs him-6 **** (p<0.0001); WT vs rmif-2 him-6 **** (p<0.0001); WT vs top-3::ollas ns (p = 0.5135); WT vs ha::degron::rmh-1 ns (p = 0.6762); rmif-2 vs rmh-1 * (p = 0.0115); rmif-2 vs rmh-1;rmif-2 * (p = 0.0338); rmh-1 vs rmh-1;rmif-2 ns (p = 0.1014); him-6 vs him-6 rmif-2 **** (p<0.0001); rmif-2 vs him-6 rmif-2 **** (p<0.0001). WT–wild type.