Differential requirements for the neurogenic gene almondex during Drosophila melanogaster development

Abstract

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.

Maternal almondex, a neurogenic gene, is required for proper subcellular Notch distribution in early Drosophila embryogenesis

“…amx was characterized as a maternal‐effect gene because fertilized eggs obtained from amx 1 homozygous or hemizygous ( amx 1 /deficiency) females failed to hatch (Perrimon & Mahowald, ; Shannon, , ). These embryos showed a strong neurogenic phenotype described as neural hyperplasia at the expense of the epidermis in the neuroectoderm (Lehmann, Dietrich, Jimenez, & Campos‐Ortega, ; Lehmann, Jimenez, Dietrich, & Campos‐Ortega, ; Michellod, Forquignon, Santamaria, & Randsholt, ). This phenotype is characteristic of mutants with strong Notch signaling defects during early embryogenesis, when Notch signaling is required for lateral inhibition during neuroblast segregation (Poulson, , ).…”

“…This phenotype is characteristic of mutants with strong Notch signaling defects during early embryogenesis, when Notch signaling is required for lateral inhibition during neuroblast segregation (Poulson, , ). In amx m embryos, which were generated from a combination of deletion and duplication lines and are completely lacking in amx [actual genotype Df(1)FF8;P(Dsor1+) ], the Notch signaling target gene m7 in Enhancer of split complex is absent, demonstrating that amx is indeed required for proper activation of Notch signaling in this context (Michellod et al, ).…”

“…An epistasis analysis of amx 1 and the overexpression of various forms of Notch suggested that Amx acts at the level of Notch cleavage by γ‐secretase (Michellod & Randsholt, ). The same research group proposed that amx is required for Notch signaling during the development of the wing imaginal disc, since amx m flies with a maternal amx contribution have notched wings (Michellod et al, ). However, the notched‐wing phenotype does not occur in amx 1 homozygous flies with the maternal contribution, so it was proposed that the amx 1 allele, which carries a premature termination codon that removes 1/3 of the deduced amx C‐terminal fragment, is hypomorphic (Michellod & Randsholt, ).…”

Novel SyntheticMedeaSelfish Genetic Elements Drive Population Replacement inDrosophila; a Theoretical Exploration ofMedea-Dependent Population Suppression

“…For seven of these, pelle (22), tube (23), almondex (24), bloated tubules (25), concertina (26), anillin (27) and torso (28), we did not observe maternal effect killing, presumably due to inefficient gene silencing, possibly coupled with low levels of the maternal product being sufficient to provide sufficient activity for normal development. These elements were not characterized further.…”

A screen for gene paralogies delineating evolutionary branching order of early Metazoa

“…Almondex is a neurogenic TM2-domain containing protein characterized as a genetic modifier of Notch signaling in Drosophila (SHANNON 1972;SHANNON 1973;MICHELLOD et al 2003;MICHELLOD AND RANDSHOLT 2008). Thus, as a neurogenic locus this candidate gene family could have made biological sense if it linked Ctenophora as a sister-group to Eumetazoa in the proposed Neuralia clade (NIELSEN 2008).…”