Neural progenitors of the Drosophila larval brain, called neuroblasts, can be 
divided into distinct populations based on patterns of proliferation and 
differentiation. Type I neuroblasts produce ganglion mother cells (GMCs) that 
divide once to produce differentiated progeny, while type II neuroblasts produce 
self-renewing intermediate neural progenitors (INPs) and thus generate lineages 
containing many more progeny. We identified Taranis (Tara) as an important 
determinant of type I lineage-specific neural progenitor proliferation patterns. 
Tara is an ortholog of mammalian SERTAD proteins that are known to regulate cell 
cycle progression. Tara is differentially-expressed in neural progenitors, with 
high levels of expression in proliferating type I neuroblasts but no detectable 
expression in type II lineage INPs. Tara is necessary for cell cycle 
reactivation in quiescent neuroblasts and for cell cycle progression in type I 
lineages. Cell cycle defects in tara mutant neuroblasts are due to decreased 
activation of the E2F1/Dp transcription factor complex and delayed progression 
through S-phase. Mis-expression of tara in type II lineages delays INP cell 
cycle progression and induces premature differentiation of INPs into GMCs. 
Premature INP differentiation can also be induced by loss of E2F1/Dp function 
and elevated E2F1/Dp expression suppresses Tara-induced INP differentiation. Our 
results show that lineage-specific Tara expression is necessary for proper brain 
development and suggest that distinct cell cycle regulatory mechanisms exist in 
type I versus type II neural progenitors.