Fig. 4.

The contribution of maternal 160 chromosomes to the repression of gonadal atrophy. (A) Wild-type testis (left) and atrophied testis (right). (B) Genetically identical progeny of crosses with or without an attached-X chromosome (XX̂) provide evidence that hybrid dysgenesis in males results from lack of maternally transmitted repression. Shown is the estimated probability of gonadal atrophy in genetically identical males that differ only in respect to the cytoplasm of the mother. Males that possess the X chromosome from strain 160 but whose mothers lack chromosomes from strain 160 show high levels of gonadal atrophy (n = 211). Males whose mothers possess 160 chromosomes do not (n = 228). (C) Maternal effects of individual strain 160 chromosomes on suppression of gonadal dysgenesis; the lower the bar, the greater the level of repression. The largest effects are due to the X chromosome and chromosome V.