Singling out of a unique neural precursor from a group of equivalent c
ells, during Drosophila neurogenesis, involves Notch-mediated lateral
signaling. During this process, activation of the Notch signaling path
way leads to repression of neural development. Disruption of this sign
aling pathway results in the development of an excess of neural cells.
The loss of activity of dynamin, which is encoded by the gene shibire
and is required for endocytosis, results in a similar phenotype. Here
we have investigated the requirement of shibire function for Notch si
gnaling during the segregation of sensory bristles on the notum of the
ny. Overexpression of different constitutively active forms of Notch
in shibire mutant flies indicates that shibire function is not necessa
ry for transduction of the signal downstream of Notch, even when the r
eceptor is integrated in the plasma membrane. However, when wild-type
Notch is activated by its ligand Delta, dynamin is required in both si
gnaling and receiving cells for normal singling out of precursors. Thi
s suggests an active role of the signaling cell for ligand-mediated re
ceptor endocytosis in the case of transmembrane ligands. We discuss th
e possible implications of these results for normal functioning of Not
ch-mediated lateral signaling. (C) 1997 Academic Press.