Wingless modulates the effects of dominant negative notch molecules in the developing wing of Drosophila.
The development and patterning of the wing in Drosophila relies on a sequence of cell interactions molecularly driven by a number of ligands and receptors. Genetic analysis indicates that a receptor encoded by the Notch gene and a signal encoded by the wingless gene play a number of interdependent roles in this process and display very strong functional interactions. At certain times and places, during wing development, the expression of wingless requires Notch activity and that of its ligands Delta and Serrate. This has led to the proposal that all the interactions between Notch and wingless can be understood in terms of this regulatory relationship. Here we have tested this proposal by analysing interactions between Delta- and Serrate-activated Notch signalling and Wingless signalling during wing development and patterning. We find that the cell death caused by expressing dominant negative Notch molecules during wing development cannot be rescued by coexpressing Nintra. This suggests that the dominant negative Notch molecules cannot only disrupt Delta and Serrate signalling but can also disrupt signalling through another pathway. One possibility is the Wingless signalling pathway as the cell death caused by expressing dominant negative Notch molecules can be rescued by activating Wingless signalling. Furthermore, we observe that the outcome of the interactions between Notch and Wingless signalling differs when we activate Wingless signalling by expressing either Wingless itself or an activated form of the Armadillo. For example, the effect of expressing the activated form of Armadillo with a dominant negative Notch on the patterning of sense organ precursors in the wing resembles the effects of expressing Wingless alone. This result suggests that signalling activated by Wingless leads to two effects, a reduction of Notch signalling and an activation of Armadillo.
Brennan
K
K
Department of Zoology, University of Cambridge, Cambridge, CB2 3EJ, United Kingdom.
Klein
T
T
Wilder
E
E
Arias
A M
AM
D000818:Animals; D051186:Armadillo Domain Proteins; D019521:Body Patterning; D002135:Calcium-Binding Proteins; D004268:DNA-Binding Proteins; D004330:Drosophila / Q000196:embryology* / Q000254:growth & development; D029721:Drosophila Proteins; D005656:Fungal Proteins / Q000235:genetics / Q000378:metabolism; D018507:Gene Expression Regulation, Developmental; D017930:Genes, Reporter; D006651:Histocytochemistry; D019476:Insect Proteins / Q000378:metabolism; D036341:Intercellular Signaling Peptides and Proteins; D047908:Intracellular Signaling Peptides and Proteins; D000072100:Jagged-1 Protein; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism*; D011518:Proto-Oncogene Proteins / Q000378:metabolism*; D051880:Receptors, Notch; D029701:Saccharomyces cerevisiae Proteins; D012679:Sense Organs / Q000254:growth & development; D000072099:Serrate-Jagged Proteins; D015398:Signal Transduction; D015534:Trans-Activators; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism; D014921:Wings, Animal / Q000196:embryology / Q000254:growth & development; D051155:Wnt1 Protein
C495305:ARM protein, Drosophila; D051186:Armadillo Domain Proteins; D002135:Calcium-Binding Proteins; D004268:DNA-Binding Proteins; D029721:Drosophila Proteins; D005656:Fungal Proteins; C052130:GAL4 protein, S cerevisiae; D019476:Insect Proteins; D036341:Intercellular Signaling Peptides and Proteins; D047908:Intracellular Signaling Peptides and Proteins; D000072100:Jagged-1 Protein; D008565:Membrane Proteins; C497759:N protein, Drosophila; D011518:Proto-Oncogene Proteins; D051880:Receptors, Notch; D029701:Saccharomyces cerevisiae Proteins; C000606278:Ser protein, Drosophila; D000072099:Serrate-Jagged Proteins; D015534:Trans-Activators; D014157:Transcription Factors; D051155:Wnt1 Protein; C064045:delta protein; C074622:wg protein, Drosophila