Extended Data Fig. 1: slow-1 has a parent-of-origin effect and grow-1.1 and grow-1.2 are redundant antidotes.
From: Selfish conflict underlies RNA-mediated parent-of-origin effects
a, Corrected NIC203 genome assembly showing segmental duplication of the grow-1 antidote (top). Selfing of grow-1.1(+/−); grow-1.2(−/−) strain. All grow-1.1(−/−); grow-1.2(−/−) individuals were developmentally arrested during larval development and did not produce any viable offspring. Thus, grow-1.1 and grow-1.2 are genetically redundant (bottom). Data are presented as mean values +/−95% CI. b, Model illustrating the mechanism of action of the slow-1/grow-1 TA. In crosses between the carrier strain (slow-1/grow-1 Chr. III NIL) and non-carrier strain (EG6180), 25% of the F2 progeny is developmentally delayed because EG/EG homozygotes did not inherit the TA and cannot express the antidote to counteract the maternally deposited toxin. c, Quantification of slow-1 mRNA expression by smFISH (N = 3, n = 16–30 per repeat, two-sided unpaired t-test, p = 0.0006, mean +/−SEM) and RNA-seq in both NIL and EG6180 parental strains (two-sided unpaired t-test, p < 0.0001, mean +/−SEM). d, Previously, we showed that sup-35/pha-1 is active when maternally inherited (Ben-David, et al. Science 2017). To test whether sup-35/pha-1 is active when paternally inherited, we crossed DL238 hermaphrodites and N2 males. N2 carries two TAs, peel-1/zeel-1 and sup-35/pha-1. We observed 46.7% embryonic lethality among their F2 progeny (n = 340, mean +/−95% CI is shown), as expected from the activity of two TAs segregating independently. To confirm the activity of both TAs, we genotyped wild-type F2 progeny for both peel-1/zeel-1 (Chr. I) and sup-35/pha-1 (Chr. III) and found that the vast majority of WT progeny were either homozygous or heterozygous carriers, indicating that both peel-1/zeel-1 and sup-35/pha-1 non-carrier individuals died as embryos. e, Activity of the C. briggsae HK104 Chr. III msft-1 TA in reciprocal crosses. Penetrance of the toxin, the percentage of F2 non-carrier individuals that are phenotypically affected, is used as a proxy for TA activity (HK Chr. III TA: nM = 13, nP = 35, p = 0.42; two-sided Fisher’s exact test; mean +/−95% CI is shown). f, Illumina short-reads from NIC203, EG6180, and Chr. III NIL DNA libraries were aligned against the NIC203 mitochondrial genome. Each dot represents a SNP. As expected from our cross scheme, the Chr. III NIL has the EG6180 mitochondrial genotype. Those SNPs shared by all strains likely reflect an error in the original NIC203 assembly. g, The slow-1 parent-of-origin effect is also present in a reciprocal cross between NIC203 and EG6180 parental lines. The abundance of slow-1 transcripts is higher when the slow-1 locus is maternally inherited (two-way ANOVA, interaction p = 0.0005, Holm-Sidak post hoc test, pslow-1 < 0.0001, mean +/−SEM is shown). h, Expression pattern of mScarlet::SLOW-1 during embryonic development. In early embryos, SLOW-1 appeared to be associated with the nuclear envelope and was quickly degraded during embryogenesis. SLOW-1 was not detectable in the soma by the time embryos reached the comma-stage (N = 2, number of embryos imaged = 20). i, Expression pattern of mScarlet::SLOW-1 in the hermaphroditic gonad. Quantification of signal intensity in gonads of NIL and mScarlet::SLOW-1 strains (two-sided unpaired t-test, p < 0.0001, mean +/−SEM is shown).
