Implication of the Drosophila beta-amyloid peptide binding-like protein AMX in Notch signaling during early neurogenesis

Lateral inhibition provides a mechanism to regulate neuroblast specification during early neurogenesis in Drososphila melanogaster embryos. This mechanism is mediated by the highly conserved Notch pathway. Defective lateral inhibition results in CNS hyperplasia at the expense of ectoderm development, hence genes causing this defect are called neurogenic. D. melanogaster almondex (amx) is a maternal neurogenic gene, crucially required for embryonic lateral inhibition. Genetic interaction studies previously revealed amx as a positive Notch pathway partner in several processes, acting potentially upstream of Notch. We show here that embryonic overexpression of Notch intracellular domain partially rescues maternal lack of amx, suggesting a role for AMX at the level of Notch processing. Our molecular data reveal that amx is ubiquitously expressed and encodes a conserved putative transmembrane protein, composed of several domains that are differently required for amx function in the fly. Sequence comparisons identify AMX as a Drosophila Beta-amyloid peptide Binding Protein (BBP) family member, a BBP-like protein or dBLP. Based on these data, we discuss the potential molecular function of AMX in early neurogenesis.