amx and the Notch pathway. M.Agnes Michellod , N. Remillieux-Leschelles , F. Forquignon , P. Santamaria , N.B. Randsholt , Génétique du Développement de la Drosophile. Centre de Genetique Moleculaire, Gif/Yvette, France.

   The Notch signaling pathway is one of the mechanisms involved in choices between different cell fates, in many tissues and at multiple steps during development. Loss of N signaling has striking effects on early neurogenesis. Genes belonging to this pathway are called neurogenic because of their predominant embryonic phenotype: neural hyperplasia of the CNS at the expense of the epidermis. almondex(amx) is also a neurogenic gene. amx is located on the X chromosome (8D5-6) and is a maternal effect lethal gene. Embryos issued of homozygous amx¹ mothers never hatch and exhibit a strong neurogenic phenotype. Genetic studies have placed amx upstream of the other neurogenic genes. We have identified the amx genomic region and rescued the sterility of homozygous amx¹ females with a genomic fragment containing a single transcription unit.amx is 1.4 Kb long with a single 1.1 Kb transcript that is expressed in the ovary follicular cells, in a dynamic pattern in the embryo, and ubiquously in imaginal structures. The amx gene potentially encodes a 284 amino acid transmembrane protein with a C type lectin signature. Interestingly, lectins play important roles in cell-cell and cell-ECM adhesion, in good agreement with the notion that amx is required for N signaling. We have generated new amorphic amx alleles (amx⁰) which have stronger phenotypes than the hypomorphic amx¹.amx⁰ adults exhibit new zygotic phenotypes such as notches of the wing margin, supernumerary thoracic machrochaetes, wing vein defects and small eyes. Furthermore, double mutant Namx⁰/amx⁰ females show a strong enhancement of all N phenotypes, suggesting again functional interactions between amx and Notch. Altogether, our data suggest that amx function has two components: an almost dispensable zygotic one and an indispensable maternal one. Our working hypothesis is that AMX is required to maintain cell-cell adhesion during the establishment of lateral signaling, especially during early neurogenesis.