scat+ is a selfish gene analogous to Medea of Tribolium castaneum.

Peters and Barker (1993) elegantly demonstrate a curious means of inheritance of murine severe combined anemia and thrombocytopenia (Scat). Originally classified as a recessive autosomal disease with alleles scat (recessive) and scat+ (dominant), it was found that if both mother and offspring are scat homozygous, then the progeny are unaffected. Only when the mother is heterozygous and the offspring scat homozygous are the disease symptoms witnessed. An interesting precedent for such a condition results from the action of a selfish gene, Medea, in populations of flour beetles (Tribolium castaneum). Medea of T. castaneum is a maternal effect lethal (Beeman et al., 1992) that produces a disease that in its genetics is directly analogous to Scat. Medea is a nuclear gene with alleles M and m. As with Scat, the mm offspring of A4m mothers die while the heterozygous offspring survive and the offspring of mm mothers never show high early mortality. Similarly, the M gene in the offspring need not be maternally derived to permit survival of embryos in mothers containing M. The spread of both M and scat+ becomes transparent when they are considered as selfish genes (cf. Bull et al., 1992). Originally, all mice would have been scat homozygous. scat may well be an amorph. That is, it is not necessarily a gene that produces a required product. The same is true for them allele of Medea. This amorphy is consistent with the viability of scat homozygotes developing in mothers that are also scat homozygotes. Consider now a mutant gene that when in a mother injects “toxin” into the f’etus. Let us assume that in linkage disequilibrium with this gene is another mutant gene that when in the fetus can neutralize the toxin. This toxin-anti-toxin gene complex is scat+. A mother that is heterozygous for the mutant gene complex will, at the point of invasion of the gene into the population, produce equal proportions of heterozygotes and scat homozygotes. Owing to the action of the scar+ toxin, the scat/scat embryos die. However, owing to the possession of thescat+ anti-toxin, thescat+/scatembryos survive. This differential mortality has the effect of increasing the frequency of the scat+ gene. This could be due to the reduction in the frequency of scar genes due to their differential removal (this effect is most significant in small populations) and/or because +/scat offspring receive more resources and/or less competitive interference than they would otherwise. scat+, IikeMedea, may spread until it isat fixation. When every individual is homozygous scar, no disease will be witnessed as every embryo will have the anti-toxin. Mothers may, however, be producing something (scat+ toxin) that will be imported into the embryo but once there will be neutralized (by scat+ anti-toxin). Redundancy of this variety is one of the fingerprints of selfish genes. Letter to the Editor