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. 2021 Jul 12;17(7):e1009663. doi: 10.1371/journal.pgen.1009663

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.