The Effect on Embryogenesis of a Sex-linked Female-Sterility Factor inDrosophila melanogaster

Eggs from females homozygous for a sex-linked mutant factor, fsnasA, will not support the development of a viable embryo. Approximately half of the eggs produced by fsnasA females are abnormal, containing little or no yolk. Twenty per cent, of the embryos die during the first 2 hours of development. The remaining embryos develop into monster larvae which are not capable of hatching from the eggs. The major effect of the factor is on the synchrony of cleavage and blastoderm mitoses. Moreover, the regular pattern in which disturbances occur suggests stratification of the egg cytoplasm. Gastrulation and all subsequent developmental processes are abnormal. Germ-band formation and the development of mesodermal elements are strongly affected. The posterior mid-gut invaginates from the ventral surface of the embryo, and the proctodaeum and Malpighian tubules never form. The possible effects of the factor on the processes of chromosome duplication during cleavage are discussed in connexion with Painter’s theory. The developmental effects of fsnasA are compared with those of a sex-linked recessive lethal factor X2. The basic similarities of the two are probably the result of abnormal rates of mitotic division during blastoderm stages. Differences between the two suggest there may be a posterior to anterior gradient in regional differentiation of the embryo. Gonad formation in fsnasA embryos from pole cells which migrate through the blastoderm wall during the early stages of gastrulation supports Poulson’s theory of gonad formation. The broader implications of studies on female-sterility genes in Drosophila are briefly discussed.