Delaminated neuroblasts in Drosophila function as stem cells during embryonic central nervous system

The Snail protein family contains a key signature of four to six conserved zinc fingers. These proteins function as transcriptional regulators during embryonic development, cancer formation and apoptosis (Hemavathy et al., 2000; Manzanares et al., 2001). Drosophila Snail was the first member identified and shown to be a repressor essential for mesoderm development (Grau et al., 1984; Nusslein-Volhard et al., 1984; Boulay et al., 1987; Kosman et al., 1991; Leptin, 1991; Ip et al., 1992; Hemavathy et al., 1997). Expression pattern analyses revealed that Snail is also present in embryonic wing disc primodia and neuroblasts (Alberga et al., 1991; Kosman et al., 1991; Leptin, 1991; Ip et al., 1994). Snail acts redundantly with Escargot, another member of this zincfinger protein family, to control wing disc development (Whiteley et al., 1992; Hayashi et al., 1993; Fuse et al., 1996). However, single and double mutants of snail and escargot do not have a significant phenotype in the developing central nervous system (CNS) (Ashraf et al., 1999). The absence of a CNS phenotype in the null mutants of snail is due to the redundant function provided by escargot and worniu, the third member of the protein family. These three genes are clustered in 35D1 region of the second chromosome. In deletion mutants that uncover these three genes, the ventral nerve cord is severely underdeveloped, as revealed by analysis of multiple neuronal markers (Ashraf et al., 1999). Some of the early CNS markers affected include fushi tarazu (ftz) and evenskipped (eve). ftz is initially expressed in many ganglion mother cells (GMCs) and later in many neurons (Goodman and Doe, 1993). In the deletion mutants, ftz expression in GMCs is almost abolished, and such defect can be rescued efficiently by transgenic expression of snail, worniu or escargot (Ashraf et al., 1999). During CNS development, clusters of cells in the neuroectoderm receive instructions from proneural genes to become competent to form neuroblasts (Campos-Ortega, 1993). These proneural genes include the achaete-scute complex, ventral nervous system defective (vnd), intermediate neuroblast defective (ind) and muscle segment homeobox (msh) 4757 Development 128, 4757-4767 (2001) Printed in Great Britain © The Company of Biologists Limited 2001 DEV5927