... signalling from the niche. In the absence of BMP signalling, one GSC daughter differentiates into a cystoblast (CB) and this fate is stabilised by Brain tumour (Brat) and Pumilio (Pum)-mediated post-transcriptional repression of mRNAs, including that encoding the Dpp transducer, Mad. However, the identity...

... , and epistasis tests showed that baboon is epistatic to Smad2 for disc overgrowth. Rescue experiments indicate that Baboon binding, but not canonical transcription factor activity, of Smad2 is required for normal disc growth. Smad2 mutant discs generate a P-Mad stripe that is narrower and sharper than the normal...

... for Nemo in the inhibition of bone morphogenetic protein (BMP) signaling. Genetic interaction studies demonstrate that nemo can antagonize BMP signaling and can inhibit the expression of BMP target genes during wing development. Nemo can bind to and phosphorylate the BMP effector Mad. In cell culture...

...Ruslan Dorfman; Ben-Zion Shilo ABSTRACT The BMP pathway patterns the dorsal region of the Drosophila embryo. Using an antibody recognizing phosphorylated Mad (pMad), we followed signaling directly. In wild-type embryos, a biphasic activation pattern is observed. At the cellular blastoderm stage...

... this cell fate choice. * Author for correspondence (e-mail: [email protected] ) 20 06 2000 09 08 2000 © 2000 by Company of Biologists 2000 Limb Cell fate Cross-talk MAD MAP kinase Drosophila It has been shown that development of insect wings and legs...

... the anteroposterior (AP) and DV boundaries, respectively. MAD-dependent activation of the vestigial quadrant enhancer results in broad expression throughout the wing pouch but is excluded from cells near the DV boundary. This has previously been thought to be due to direct repression by a signal from the DV boundary...

... mutant for Mad 1-2 and smo 3 on photoreceptor development during stages following MF initiation. In contrast to single mutant Mad 1-2 or smo 3 clones, the doubly mutant clones block MF progression, suggesting that dpp and hh play redundant roles during this process. Interestingly...

... a genetic screen for dominant enhancer mutations of a hypomorphic allele of thick veins (tkv) , a type I receptor for dpp . We recovered new alleles of tkv, punt, Mothers against dpp (Mad) and Medea (Med) , all of which are known to mediate dpp signaling. We also recovered mutations in the 60A gene which...

... signaling pathway, we screened for mutations that act as dominant maternal enhancers of a weak allele of the dpp target gene zerknüllt . In this screen, we recovered new alleles of the Mothers against dpp ( Mad ) and Medea genes. Phenotypic analysis of the new Medea mutations indicates that Medea , like Mad...

... Smad, Medea , a close homolog of the human tumor-suppressor gene DPC4 . Embryos from germline clones of both Medea and Mad (a class I Smad) are ventralized, as are embryos null for the TGF-β-like ligand decapentaplegic ( dpp ). Loss of Medea also blocks dpp signaling during later development...

...Stuart J. Newfeld; Arun Mehra; Matthew A. Singer; Jeffrey L. Wrana; Liliana Attisano; William M. Gelbart ABSTRACT Mothers against dpp ( Mad ) is the prototype of a family of genes required for signaling by TGF-β related ligands. In Drosophila, Mad is specifically required in cells responding...

... of vertebrate BMP-2 and BMP-4, functions in dorsal-ventral axial patterning, and a genetic screen for components involved in signaling by dpp has identified a gene named mothers against decapentaplegic (Mad). Mad encodes a unique, predicted cytoplasmic, protein containing no readily identified functional motifs...

...Stuart J. Newfeld; Elena H. Chartoff; Jonathan M. Graff; Douglas A. Melton; William M. Gelbart ABSTRACT The proteins necessary for signal transduction in cells responding to ligands of the TGF-β family are largely unknown. We have previously identified Mad ( Mothers against dpp ), a gene...

... that the Mothers against dpp ( Mad ) gene is required for dpp signaling during eye development. Clonal analysis demonstrates a cell-autonomous function for Mad and genetic interactions indicate that Mad is an essential component of the signal transduction pathway downstream of the Dpp receptors in responding cells...