Figure 1.

Phenotypic effects of slpr mutations. (A) Embryonic cuticle phenotype of a strong loss-of-function slpr allele, 921, shows a large anterior dorsal hole compared with wild type (WT). (B) In situ hybridization to reveal dpp transcripts in wild-type (slpr⁹²¹/+) or mutant (slpr⁹²¹/Y) embryos at stage 11, germ band extended, and stage 13, germ band retracted. Stages according to Campos-Ortega and Hartenstein (1997). dpp expression is observed in cells at the dorsal edge of the ectoderm (arrowhead) in wild-type but not in slpr mutant embryos at both stages. Other aspects of dpp expression are normal. (C) A collection of embryos from a slpr⁹²¹ mutant stock has been labeled with anti-Fasciclin III antibodies to reveal the shape of cells in the dorsal ectoderm. The bracket marks leading edge (LE) cells at the margin that have begun to stretch and elongate as dorsal closure proceeds in both wild-type (slpr⁹²¹/FM7,ftzLZ) and slpr⁹²¹ mutant embryos. However, late stage slpr⁹²¹/Y mutant embryos exhibit a terminal phenotype in which LE cells fail to remain elongated and have rounded up, concomitant with slackening of the dorsal ectodermal sheet.