Fig. 9. Dorsal closure defects are seen following expression of Drac1 and crb transgenes with the GAL4^c381 driver. (A-C) Dorsal views of UAS-lacZ^1-71;GAL4^c381 embryos stained with anti-ß-galactosidase antibodies to show expression of the driver in the amnioserosa but not the epidermis during (A,B) and after dorsal closure (C). (D) Lateral view of cuticle of UAS-Drac1V12;GAL4^c381 embryo showing germband retraction failure and puckers extending out from the dorsal surface. (E) Dorsolateral view of the cuticle of the UAS-Drac1N17;GAL4^c381 embryo showing the large dorsal hole. (F) Dorsolateral view of cuticle of UAS-crb^wt;GAL4^c381 embryo showing large dorsal hole. (G) Dorsal view of stage 14 UAS-Drac1V12;GAL4^c381 embryo stained with anti-phosphotyrosine antibodies to show contraction of the amnioserosa, germband retraction failure and bunching of the epidermis. (H,I) Lateral views of the leading edge in embryos stained with anti-phosphotyrosine antibodies. (H) Stage 14 UAS-Drac1V12;GAL4^c381 embryo showing robust accumulation of phosphotyrosine at the leading edge and extensive epidermal cell elongation. (I) A stage 14 UAS-crb^wt;GAL4^c381 embryo showing loss of leading edge phosphotyrosine nodes and lack of epidermal cell elongation. The arrowhead marks a portion of the leading edge where phosphotyrosine nodes are intact.

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