In this proposal, we aim to understand two mechanisms of progenitor maintenance. The first mechanism is set up before neural induction and it inherently inhibits a population of apicobasally polarised progenitor cells from undergoing premature neurogenesis. The serine-threonine kinase aPKC is sufficient and necessary to maintain the progenitor state of these cells. In aim 1, we will identify phosphorylation targets of aPKC by a candidate and an unbiased proteomics approach and we will determine the transcriptome of these progenitors by microarray analysis. The second mechanism follows neural induction, and it operates within a second population of progenitors, which are apolar. This mechanism depends on the localised expression of transcription factors, such as Foxg1. Since FoxG1 is expressed in both progenitors and differentiated neurons in the forebrain, we reasoned that its activity may be distinguished by co-factors and post-translational modifications; these will be characteri sed in aim 2. To link the control of FoxG1 with its transcriptional output, we will identify the transcriptional targets of FoxG1 by ChIP-seq and microarray analysis. To link the two, in aim 3, we will undertake lineage-tracing experiments to understand whether different mechanisms of inhibiting differentiation early on, have a lasting impact on progenitor fate.