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Abstract

The decapentaplegic (dpp) gene product, a TGF-beta related ligand, acts as an extracellular morphogen to establish at least two cellular response thresholds within the dorsal half of the Drosophila embryo. Null mutations in the screw (scw) gene are phenotypically similar to moderate dpp mutants and cause dorsal cells to adopt ventral fates. We show that scw encodes a novel TGF-beta protein and is an integral part of the signal that specifies dorsal pattern. Although scw is expressed uniformly during blastoderm stages, its effect on development appears graded and is restricted to the dorsal side of the embryo. Our results indicate that DPP activity alone is insufficient to specify different dorsal cell fates. We propose that SCW and DPP act together to establish distinct response boundaries within the dorsal half of the embryo, perhaps by forming heterodimers that have higher activity than homodimers of either molecule alone.

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Protein extracts derived from bone can initiate the process that begins with cartilage formation and ends in de novo bone formation. The critical components of this extract, termed bone morphogenetic protein (BMP), that direct cartilage and bone formation as well as the constitutive elements supplied by the animal during this process have long remained unclear. Amino acid sequence has been derived from a highly purified preparation of BMP from bovine bone. Now, human complementary DNA clones corresponding to three polypeptides present in this BMP preparation have been isolated, and expression of the recombinant human proteins have been obtained. Each of the three (BMP-1, BMP-2A, and BMP-3) appears to be independently capable of inducing the formation of cartilage in vivo. Two of the encoded proteins (BMP-2A and BMP-3) are new members of the TGF-beta supergene family, while the third, BMP-1, appears to be a novel regulatory molecule.

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G Rubin, Allan Spradling (1982)

Exogenous DNA sequences were introduced into the Drosophila germ line. A rosy transposon (ry1), constructed by inserting a chromosomal DNA fragment containing the wild-type rosy gene into a P transposable element, transformed germ line cells in 20 to 50 percent of the injected rosy mutant embryos. Transformants contained one or two copies of chromosomally integrated, intact ry1 that were stably inherited in subsequent generations. These transformed flies had wild-type eye color indicating that the visible genetic defect in the host strain could be fully and permanently corrected by the transferred gene. To demonstrate the generality of this approach, a DNA segment that does not confer a recognizable phenotype on recipients was also transferred into germ line chromosomes.