Identification of novel maternal neurogenic genes that are potential components of Notch signaling in Drosophila. Takuma Gushiken1,2, Kenjiroo Matsumoto1,2, Takahiro Seto2, Ryo Hatori1,2, Shunsuke Shimaoka1,2, Tomoko Yamakawa1, Takeshi Sasamura1, Kenji Matsuno1. 1) Department of Biological Science, Osaka university, Japan; 2) Department of Biological Science and Technology, Tokyo University of Science, Japan.
Notch signaling regulates many cell-fate specifications through local cell-cell interaction in Drosophila development. Notch signaling is involved in lateral inhibition that prevents proneural cells that neighbor a neuroblast from choosing the neuroblast-fate during neuroblast segregation. Thus, in the absence of Notch signaling, proneural cells differentiate into neuroblast at the expense of epidermoblasts. Therefore, the disruption of Notch signaling leads proneural cells to differentiate into neuroblast at the expense of epidermoblasts and results in the hyperplasia of neuronal cells in Drosophila embryos, which is referred to as the neurogenic phenotype.
Although mutants that show neurogenic phenotype in their homozygotes have been studied extensively in Drosophila, we probably failed to identify many mutants that potentially lead to neurogenic phenotype, because maternal supply of their gene functions can suppress this phenotype. To overcome this problem, we screened mutants that showed neurogenic phenotype in embryos homozygous for them and lacking their maternal contribution. This phenotype is designated as maternal neurogenic phenotype, and genes whose mutants show maternal neurogenic phenotype are called maternal neurogenic genes.
To identify novel maternal neurogenic genes, we screened mutants on the left arm of the second chromosome, which covers about 20% of the Drosophila genome. From this screen, we identified 2 mutants that showed maternal neurogenic phenotype. The summary of this screen and molecular genetics analyses of these maternal neurogenic genes will be presented. These studies will contribute to the understanding of the molecular mechanisms of Notch signaling.