Identification of Chromosomal Regions Involved in decapentaplegic Function in Drosophila

Corresponding author: William M. Gelbart, Department of Molecular and Cellular Biology, Harvard University, 16 Divinity Ave., Cambridge, MA 02138, gelbart{at}morgan.harvard.edu (E-mail).

Communicating editor: J. A. BIRCHLER

Signaling molecules of the transforming growth factor ß (TGF-ß) family contribute to numerous developmental processes in a variety of organisms. However, our understanding of the mechanisms which regulate the activity of and mediate the response to TGF-ß family members remains incomplete. The product of the Drosophila decapentaplegic (dpp) locus is a well-characterized member of this family. We have taken a genetic approach to identify factors required for TGF-ß function in Drosophila by testing for genetic interactions between mutant alleles of dpp and a collection of chromosomal deficiencies. Our survey identified two deficiencies that act as maternal enhancers of recessive embryonic lethal alleles of dpp. The enhanced individuals die with weakly ventralized phenotypes. These phenotypes are consistent with a mechanism whereby the deficiencies deplete two maternally provided factors required for dpp's role in embryonic dorsal-ventral pattern formation. One of these deficiencies also appears to delete a factor required for dpp function in wing vein formation. These deficiencies remove material from the 54F-55A and 66B-66C polytene chromosomal regions, respectively. As neither of these regions has been previously implicated in dpp function, we propose that each of the deficiencies removes a novel factor or factors required for dpp function.

This article has been cited by other articles:

				N. T. Takaesu, C. Hyman-Walsh, Y. Ye, R. G. Wisotzkey, M. J. Stinchfield, M. B. O'Connor, D. Wotton, and S. J. Newfeld dSno Facilitates Baboon Signaling in the Drosophila Brain by Switching the Affinity of Medea Away From Mad and Toward dSmad2 Genetics, November 1, 2006; 174(3): 1299 - 1313. [Abstract] [Full Text] [PDF]

				N. T. Takaesu, E. Herbig, D. Zhitomersky, M. B. O'Connor, and S. J. Newfeld DNA-binding domain mutations in SMAD genes yield dominant-negative proteins or a neomorphic protein that can activate WG target genes in Drosophila Development, November 1, 2005; 132(21): 4883 - 4894. [Abstract] [Full Text] [PDF]

				J.-Y. Ji, M. Haghnia, C. Trusty, L. S. B. Goldstein, and G. Schubiger A Genetic Screen for Suppressors and Enhancers of the Drosophila Cdk1-Cyclin B Identifies Maternal Factors That Regulate Microtubule and Microfilament Stability Genetics, November 1, 2002; 162(3): 1179 - 1195. [Abstract] [Full Text] [PDF]

				P Vilmos, K Gaudenz, Z Hegedus, and J L Marsh The Twisted gastrulation family of proteins, together with the IGFBP and CCN families, comprise the TIC superfamily of cysteine rich secreted factors Mol. Pathol., October 1, 2001; 54(5): 317 - 323. [Abstract] [Full Text] [PDF]

				W. Li, E. Noll, and N. Perrimon Identification of Autosomal Regions Involved in Drosophila Raf Function Genetics, October 1, 2000; 156(2): 763 - 774. [Abstract] [Full Text]