In the Drosophila CNS, neuroblasts undergo self-renewing asymmetric divisions, 
whereas their progeny, ganglion mother cells (GMCs), divide asymmetrically to 
generate terminal postmitotic neurons. It is not known whether GMCs have the 
potential to undergo self-renewing asymmetric divisions. It is also not known 
how precursor cells undergo self-renewing asymmetric divisions. Here, we report 
that maintaining high levels of Mitimere or Nubbin, two POU proteins, in a GMC 
causes it to undergo self-renewing asymmetric divisions. These asymmetric 
divisions are due to upregulation of Cyclin E in late GMC and its unequal 
distribution between two daughter cells. GMCs in an embryo overexpressing Cyclin 
E, or in an embryo mutant for archipelago, also undergo self-renewing asymmetric 
divisions. Although the GMC self-renewal is independent of inscuteable and numb, 
the fate of the differentiating daughter is inscuteable and numb-dependent. Our 
results reveal that regulation of Cyclin E levels, and asymmetric distribution 
of Cyclin E and other determinants, confer self-renewing asymmetric division 
potential to precursor cells, and thus define a pathway that regulates such 
divisions. These results add to our understanding of maintenance and loss of 
pluripotential stem cell identity.