Figure 1. A maternal-effect genetic incompatibility on Chr. III. (A) A marker on Chr. V was introgressed from the reference strain N2 into the DL238 wild isolate. Short-read sequencing of the introgression strain revealed homozygous N2 variants on Chr. III, indicating strong selection in favor of N2 variants during the generation of this strain. (B) DL238 males were crossed to hermaphrodites carrying a null allele of the peel-1/zeel-1 element (niDf9) in an otherwise N2 background (N2 peel-1-/-). F1 hermaphrodites were allowed to self-fertilize (top). Alternatively, F1 males (middle) or hermaphrodites (bottom) were backcrossed to the DL238 parental strain. Embryonic lethality was scored in the F2 progeny as percent of unhatched eggs. Dashed grey lines indicate expected embryonic lethality under the maternaleffect toxin and zygotic antidote model (see also Fig. S2). Sample sizes are shown in parentheses. Error bars indicate 95% binomial confidence intervals, calculated using the Agresti-Coull method (Agresti and Coull 1998) (C) Punnett square showing the expected lethality in the F2. An interaction between a maternal toxin (black rhombus) and a zygotic antidote (white circle) results in 25% embryonic lethality in the F2 and is compatible with the lethality observed in our crosses. (D) Embryonic lethality in the F2 progeny of a cross between wild-type N2 hermaphrodites and DL238 males. N2 carries an active copy of peel-1/zeel-1, while DL238 carries an inactive copy. Independent segregation of two fully penetrant parental-effect incompatibilities is expected to result in 43.75% embryonic lethality. Orange and blue bars denote N2 and DL238 haplotypes, respectively.
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