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Figure 1


Fig. 1. DV and AP patterning defects in spn-F mutants. (A,B) Eggshells from spn-F mutant females. (A) Wild-type eggshell; (B) strongly ventralized egg shell. (C,D) Wild type embryo (C); bicaudal embryo in egg of spn-F mutant (D). Only a few percent of spn-F eggs (1-3%, depending on background) gave rise to bicaudal embryos. (E,F) Oskar protein localization at the posterior pole of stage 10 wild-type (E) and spn-F (F) egg chambers (Oskar, red; cortical Actin, green). The Oskar protein is not tightly localized to the posterior pole in the mutant. (G,H) grk RNA in situ localization in stage 9 wild-type (G) and spn-F (H) egg chambers. In most mutant egg chambers at stages 9-10, grk RNA forms a broad, fuzzy band around the anterior. (I,J) Grk protein expression in stage 9 wild-type (I) and spn-F (J) egg chambers, with Grk in red, cortical actin detected with Phalloidin in green and DNA in blue. Grk protein is strongly reduced in the mutant egg chambers. (K,L) Defects in oocyte nuclear morphology in spn-F (DNA, blue). In wild-type egg chambers (K), the DNA in the oocyte is condensed into a tight sphere. In spn-F egg chambers (L), the DNA appears fragmented.





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