Abstract

It is generally believed that the presence of cytoplasmic sex ratio distorters in a population causes selective pressure on autosomal genes for a compensatory shift in the sex ratio. Investigations reveal that when within lineage transmission of a cytoplasmic distorter of the primary sex ratio is 100%, no compensatory autosomal sex ratio shift is favored. When transmission is less than 100%, a synergistic interaction occurs between autosomal and cytoplasmic sex ratio factors which results in a polymorphic population with individuals producing either 100% sons (autosomal) or 100% daughters (cytoplasmic). The outcome will only occur if there is sufficient autosomal sex ratio variability in the population for 100% son production. Some cytoplasmic factors cause male larval death, rather than a shift in the primary sex ratio. Such factors have no effect upon autosomal sex ratio selection, and therefore no compensatory sex ratio shift is expected. Even low levels of inbreeding can selectively favor male-killing cytoplasmic factors. Basic models of cytoplasmic sex ratio distortion suggest that cytoplasmic distorters (with high transmission) should increase to or near fixation, thus potentially driving a population to extinction. Models indicate that haplodiploid species are less vulnerable to this population level selection than are diplodiploid species. Among diplodiploid species, cytoplasmic distorters with incomplete transmission will achieve lower frequencies in species without autosomal sex ratio variability.

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