A complete account of the whole developmental process of neurogenesis involves 
understanding a number of complex underlying molecular processes. Among them, 
those that govern the crucial transition from proliferative (self-replicating) 
to neurogenic neural progenitor (NP) cells remain largely unknown. Due to its 
sequential rostro-caudal gradients of proliferation and neurogenesis, the 
prospective spinal cord of the chick embryo is a good experimental system to 
study this issue. We report that the NOTCH ligand DELTA-1 is expressed in 
scattered cycling NP cells in the prospective chick spinal cord preceding the 
onset of neurogenesis. These Delta-1-expressing progenitors are placed in 
between the proliferating caudal neural plate (stem zone) and the rostral 
neurogenic zone (NZ) where neurons are born. Thus, these Delta-1-expressing 
progenitors define a proliferation to neurogenesis transition zone (PNTZ). Gain 
and loss of function experiments carried by electroporation demonstrate that the 
expression of Delta-1 in individual progenitors of the PNTZ is necessary and 
sufficient to induce neuronal generation. The activation of NOTCH signalling by 
DELTA-1 in the adjacent progenitors inhibits neurogenesis and is required to 
maintain proliferation. However, rather than inducing cell cycle exit and 
neuronal differentiation by a typical lateral inhibition mechanism as in the NZ, 
DELTA-1/NOTCH signalling functions in a distinct manner in the PNTZ. Thus, the 
inhibition of NOTCH signalling arrests proliferation but it is not sufficient to 
elicit neuronal differentiation. Moreover, after the expression of Delta-1 PNTZ 
NP continue cycling and induce the expression of Tis21, a gene that is 
upregulated in neurogenic progenitors, before generating neurons. Together, 
these experiments unravel a novel function of DELTA-NOTCH signalling that 
regulates the transition from proliferation to neurogenesis in NP cells. We 
hypothesize that this novel function is evolutionary conserved.