Neurons and glia originate from a common precursor, the neural stem cell (NSC). These multipotent precursors display a high degree of plasticity in vitro, but the basis of this plasticity and the mechanisms underlying the neuron-glial switch in vivo are unclear. Now, Angela Giangrande and colleagues (see ) show that the transcription factor Glial cells missing (Gcm, also called Glial cell deficient; Glide) triggers a conserved chromatin signature that converts Drosophila NSCs to a glial fate. The researchers show that overexpression of Gcm in fly NSCs produces glia at the expense of neurons. This gliogenic potential of Gcm decreases with time and does not affect quiescent NSCs, suggesting that it is dependent on temporal cues rather than on the mitotic potential of NSCs. Finally, the investigators demonstrate that the glial fate switch is associated with a chromatin signature, which includes low levels of histone H3 lysine 9 acetylation and is similar to that observed in vertebrate glia, suggesting that this epigenetic mechanism for specifying glia has been conserved throughout evolution.
