Armadillo levels are reduced during mitosis in Drosophila

The Armadillo protein of Drosophila melanogaster is both a structural component of adherens junctions at apical cell membranes and also a key cytoplasmic transducer of the Wingless signalling pathway. We have used the Gal4-UAS system to over-express Armadillo in the Drosophila wing: this hyperactivates the Wingless pathway and leads to the formation of ectopic, supernumerary wing bristles. Here, we report that this adult phenotype is dominantly enhanced by mutations in cdc25(string) and, conversely, is suppressed by co-expression of Cdc25(String). Furthermore, we show that the steady state levels of Armadillo protein produced from the UAS transgene are also sensitive to cdc25(string) dosage in the cells of the larval imaginal wing disc. Consistent with the role of Cdc25(String) in promoting mitosis and with our genetic interaction data, we find a strong correlation between progression through mitosis and a reduction in Armadillo levels. Significantly, this is true whether Armadillo is over-expressed or not, and both cytoplasmic (signalling) and membrane-associated (junctional) Armadillo appears to be affected. We conclude that this phenomenon may reduce the efficacy of Wingless signalling and/or intercellular adhesion during cell division.     

Differential requirements for the neurogenic gene almondex during Drosophila melanogaster development

During early development, the neurogenic genes of Drosophila melanogaster are involved in the control of cell fates in the neurectoderm; almondex (amx) belongs to this category of genes. We have identified the amx locus and rescued the amx embryonic neurogenic phenotype with a 1.5 kb DNA fragment. Using a small deficiency, we generated a new amx mutant background called amx(m), which is a null allele. Besides the characteristic neurogenic maternal effect caused by loss of amx, amx(m) flies display a new imaginal phenotype resembling loss of function of Notch. We describe amx-induced misregulation of the Notch pathway target E(spl) m7 in embryos and genetic interactions between amx and Notch pathway mutants in adult flies. These data show that wildtype amx acts as a novel positive regulator of the Notch pathway and is required at different levels during development.     

Wnt1 regulates neurogenesis and mediates lateral inhibition of boundary cell specification in the zebrafish hindbrain

The formation of localised signalling centres is essential for patterning of a number of tissues during development. Previous work has revealed that a distinct population of boundary cells forms at the interface of segments in the vertebrate hindbrain, but the role of these cells is not known. We have investigated the function of the Wnt1 signalling molecule that is expressed by boundary and roof plate cells in the zebrafish hindbrain. Knockdown of wnt1 or of tcf3b, a mediator of Wnt signalling, leads to ectopic expression of boundary cell markers, rfng and foxb1.2, in non-boundary regions of the hindbrain. Ectopic boundary marker expression also occurs following knockdown of rfng, a modulator of Notch signalling required for wnt1 expression at hindbrain boundaries. We show that the boundary and roof plate expression of wnt1 each contribute to upregulation of proneural and delta gene expression and neurogenesis in non-boundary regions, which in turn blocks ectopic boundary marker expression. Boundary cells therefore play a key role in the regulation of cell differentiation in the zebrafish hindbrain. The network of genes underlying the regulation of neurogenesis and lateral inhibition of boundary cell formation by Wnt1 has a striking similarity to mechanisms at the dorsoventral boundary in the Drosophila wing imaginal disc.