Homeostatic balance between dorsal and cactus proteins in the Drosophila embryo.
The maternal-effect gene dorsal encodes the ventral morphogen that is essential for elaboration of ventral and ventrolateral fates in the Drosophila embryo. Dorsal belongs to the rel family of transcription factors and controls asymmetric expression of zygotic genes along the dorsoventral axis. The dorsal protein is cytoplasmic in early embryos, possibly because of a direct interaction with cactus. In response to a ventral signal, dorsal protein becomes partitioned into nuclei of cleavage-stage syncytial blastoderms such that the ventral nuclei have the maximum amount of dorsal protein, and the lateral and dorsal nuclei have progressively less protein. Here we show that transgenic flies containing the dorsal cDNA, which is driven by the constitutively active hsp83 promoter, exhibits rescue of the dorsal- phenotype. Transformed lines were used to increase the level of dorsal protein. Females with dorsal levels roughly twice that of wild-type produced normal embryos, while a higher level of dorsal protein resulted in phenotypes similar to those observed for loss-of-function cactus mutations. By manipulating the cactus gene dose, we found that in contrast to a dorsal/cactus ratio of 2.5 which resulted in fully penetrant weak ventralization, a cactus/dorsal ratio of 3.0 was acceptable by the system. By manipulating dorsal levels in different cactus and dorsal group mutant backgrounds, we found that the relative amounts of ventral signal to that of the dorsal-cactus complex is important for the elaboration of the normal dorsoventral pattern. We propose that in a wild-type embryo, the activities of dorsal and cactus are not independently regulated; excess cactus activity is deployed only if a higher level of dorsal protein is available. Based on these results we discuss how the ventral signal interacts with the dorsal-cactus complex, thus forming a gradient of nuclear dorsal protein.
Govind
S
S
Department of Molecular Biology, Princeton University, NJ 08544.
Brennan
L
L
Steward
R
R
D000727:Androgen-Binding Protein / Q000235:genetics*; D000818:Animals; D030801:Animals, Genetically Modified; D003593:Cytoplasm / Q000502:physiology; D004268:DNA-Binding Proteins / Q000235:genetics*; D004330:Drosophila / Q000196:embryology / Q000235:genetics*; D029721:Drosophila Proteins; D005260:Female; D006360:Heat-Shock Proteins / Q000235:genetics; D009024:Morphogenesis / Q000235:genetics; D010641:Phenotype; D010750:Phosphoproteins / Q000235:genetics*; D015398:Signal Transduction / Q000235:genetics*
D000727:Androgen-Binding Protein; D004268:DNA-Binding Proteins; D029721:Drosophila Proteins; D006360:Heat-Shock Proteins; D010750:Phosphoproteins; C027519:probasin; C077938:cact protein, Drosophila