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A KMD with a transmission ratio near 100% could be misunderstood as an essential gene (Fig 1A). To seek for potential KMDs lurking in the genome of S. pombe, we investigated the disagreement between homozygous and heterozygous deletion analysis from previous datasets (data S1). mug135 (meiotically upregulated gene) was previously annotated ‘essential’ since mug135Δ haploid offspring from mug135(+)/mug135Δ are inviable(16). However, no meiotic defect was reported for mug135Δ/mug135Δ(17,18), raising mug135 a potential selfish KMD. We independently deleted mug135 in the haploid lab strain and observed no overt defect. Diploids lacking both mug135 copies also exhibited normal spore viability (Fig. 1B). However, mug135(+)/mug135Δ heterozygotes mainly give rise to a 2:2 pattern and the viable colonies are almost always mug135(+) (Fig. 1B). These results confirm that mug135 is actually a KMD, dispensable when homozygous, while skewing transmission ratio in heterozygotes. According to this characteristic, we renamed mug135 as tdk1 (transmission-distorting killer). 

tdk1 locates on the left arm of chromosome III and contains a single 1074-nt-long open reading frame (ORF) (Fig. 1C and fig. S1). Through inspecting the Illunima sequencing data of 161 natural isolates, we found that tdk1 has fixed in all these natural strains(19). Since the repeat region in the middle is challenging to assemble and seems versatile, we constructed a haplotype tree of tdk1 from 56 typical haploid strain according to single-nucleotide polymorphisms (SNPs) in the non-repeat region. There are eight haplotypes in total, forming three main types—one including tdk1from lab strain, one containing six nonsynonymous mutations (S65A, R102K, E230D, I235M, R255K and D288E) and the other with three nonsynonymous mutations (K50R, D241Y and G319E) (hereafter referred to as tdk1(6SNP) and tdk1(3SNP)) (fig. S2A). We picked two strains of tdk1(6SNP) type and two of tdk1(3SNP), manipulated them into heterothallic, and found that neither tdk1(6SNP) in JB939 or JB953 is able to distort transmission ratio (fig. S2B). Nevertheless, both tdk1(3SNP) from JB1180 and JB1206 are still active killers (fig. S2C). We then introduced these six mutations into lab strain and found that tdk1(6SNP) is not an active killer in reference strain, but shows resistance to killing by tdk1 (Fig. 2A). In other words, the six nonsynonymous mutations of tdk1(6SNP) from natural populations has rendered tdk1 a resistant type.

To study the molecular mechanism of tdk1, we ectopically integrated plasmids containing tdk1 gene under its endogenous promoter into tdk1Δ strain. tdk1 inserted at ade6 locus on the right arm of chromosome III or leu1 locus on chromosome II both distort transmission ratio efficiently (Fig. 1, C and D). The observation that no specific target locus is required for killing action of tdk1 and the locus-independent manner point to the poison-antidote model. When the start-codon was mutated, tdk1 became incapable of killing siblings with no tdk1 insertion and fails to resist the toxicity from tdk1 (Fig. 1D). Additively, codon-scrambled tdk1 driven by the promoter of another meiotically upregulated gene and terminated by the terminator of a constitutive gene (mug24p-tdk1(SCR)-ADH1t) also distort transmission ratio efficiently (fig. S3A), and no in-frame isoform was detected by western blotting against Tdk1 (fig. S3, B and C), ruling out the participation of transcripts other than Tdk1 polypeptide. Taken together, these results demonstrate that tdk1 is a single-gene selfish killer, and the same Tdk1 polypeptide performs both as a poison and antidote. 

Interestingly, tdk1(+) and tdk1Δ spores from tdk1(+)/tdk1Δ are indistinguishable and germinate properly, differing from ‘spore killers’ which disable spores (Fig. 1, F and G, movies S1 and S2). A selective germination system was designed to examine the respective phenotype of tdk1(+) and tdk1Δ cells during spore germination (fig. S4A). Live-cell imaging revealed that although tdk1Δ spores germinate normally, 80.6% of them displayed severe defect during the first mitosis after germination. Chromosome segregation of tdk1Δ cells is largely hindered, leading to high level of nuclear displacement (61.2%) or "cut" phenotype (19.4%) (Fig. 1, F and G, movies S1 and S2). These results suggest that tdk1kills non-carrier siblings by preventing chromosome segregation during developmental growth rather than by disabling spores.
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