AbstractFour female‐sterile mutants, fs(l)K451, fs(1)K1214, fs(1)K575TS, and fs(1)384, were studied in terms of chorion structure and chorion protein composition. The first three of these mutants cause morphological defects, ie, substantial underproduction and disruption of the endochorion, correlated with underproduction of the six major chorion proteins, s15–s38; the phenotypes are consistent with the observation that these mutants interfere with amplification of the major chorion genes that encode the s15–s38 proteins [Orr et al.: Proc Natl Acad Sci USA 81:3773–3777, 1984; Komitopoulou et al.: Dev Genet 7:75–80, 1986]. The fourth mutant, fs(1)384, and its alleles do not interfere with production of the major chorion proteins and the morphologically detectable bulk of the endochorion but lead to failure of endochorionic organization. Apparently this complementation group is responsible for a minor chorion product, which is evidently important morphogenetically and which is processed posttranslationally in a complex manner [Bauer and Waring: Dev Biol 121:349–358, 1987].