(a) Genes encoding proteins localized to synapses are downregulated early upon entry into the neurogenic program, suggesting that some normal astrocyte functions are immediately compromised as neurogenesis is initiated. Interestingly, these same synapse-associated genes are upregulated again as cells differentiate into neuroblasts, suggesting that they are important for synapse maintenance in both astrocytes and neurons. (b) Common astrocyte marker genes such as Aqp4, S100b and Slc1a2, are maintained in astrocytes approximately until they enter transit-amplifying divisions. (c) Neurogenic astrocytes maintain normal astrocyte morphology even as they have upregulated Ascl1 and initiated DNA synthesis in preparation for transit-amplifying divisions (one-cell stage. Note that EdU, which was administered for the last 2 weeks prior to sacrifice, has been incorporated into the DNA of this single astrocyte. This indicates that astrocytes initiate S phase while still retaining astrocyte features.). As transit-amplifying divisions occur, astrocytic processes are gradually lost by the dividing cells (‘2–10 cells’. See also Video 1). (d, e) The astrocyte marker S100β is not expressed by neurogenic-lineage cells in the SVZ, neither in single Ascl1+ cells or clustered transit-amplifying cells ([red arrowheads]; each data point in (d) is one cell). In contrast, many striatal astrocytes express high levels of S100β (d, f [blue arrowheads]). Consequently, many (but not all) striatal transit-amplifying cells retain low amounts of residual S100β protein (d, g [blue arrowheads]) as remnants of their origin as parenchymal astrocytes. Thus, lingering S100β protein can be used as a short-term lineage-tracing marker for transit-amplifying cells derived from striatal astrocytes. (LV, lateral ventricle). Scale bar (c): 10 μm.