The sensitivity of postfertilization mitotic delay arising from γ-radiation damage to sperm is (a) enhanced by reducing the cytoplasmic volume of diploid eggs and (b) reduced by removing the female pronucleus of half-sized eggs. These results can be explained if one assumes that these are repair processes which (a) exhibit a rate dependence on cytoplasmic volume and (b) act for a longer time in haploid eggs which have a longer postfertilization mitotic cycle than diploid ones. This recovery hypothesis is consistent with other data suggesting a role of protein synthesis in the repair of the damage by γ-radiation which leads to mitotic delay.

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