Drosophila larval neurogenesis is an excellent system for studying the balance 
between self-renewal and differentiation of a somatic stem cell (neuroblast). 
Neuroblasts (NBs) give rise to differentiated neurons and glia via intermediate 
precursors called GMCs or INPs. We show that E(spl)mγ, E(spl)mβ, E(spl)m8 and 
Deadpan (Dpn), members of the basic helix-loop-helix-Orange protein family, are 
expressed in NBs but not in differentiated cells. Double mutation for the E(spl) 
complex and dpn severely affects the ability of NBs to self-renew, causing 
premature termination of proliferation. Single mutations produce only minor 
defects, which points to functional redundancy between E(spl) proteins and Dpn. 
Expression of E(spl)mγ and m8, but not of dpn, depends on Notch signalling from 
the GMC/INP daughter to the NB. When Notch is abnormally activated in NB progeny 
cells, overproliferation defects are seen. We show that this depends on the 
abnormal induction of E(spl) genes. In fact E(spl) overexpression can partly 
mimic Notch-induced overproliferation. Therefore, E(spl) and Dpn act together to 
maintain the NB in a self-renewing state, a process in which they are assisted 
by Notch, which sustains expression of the E(spl) subset.