A flurry of studies during the past decade has unraveled many functions of transcription factors and regulators in neuronal development in the mammalian brain. Prior to these studies, transcription factors were generally considered to govern
the transition from precursor cells to postmitotic neurons, and this transition was thought to unleash a differentiation program, resulting in the mature morphology of neurons. A major conclusion of studies of the past decade is that transcription factors continue to play key regulatory roles in postmitotic neurons to specify and regulate the development of distinct morphological compartments. Another related key conclusion is the concept that different transcription factors are dedicated to distinct phases of neuronal Screening Library mouse morphogenesis and connectivity. This, however, is an oversimplification. Although some transcription factors have a restricted expression pattern and orchestrate specific aspects of development, others operate in a pleiotropic manner to regulate several steps of development. In some cases, transcription factors operate as nodes to coordinate two different aspects of neuronal development, such as neuronal branching and migration or dendrite growth and synapse formation. In addition, the functions of different transcription factors
may overlap temporally to control a specific feature of neuronal morphology and connectivity. An important goal of future research LY2157299 in the study of transcriptional regulation of neuronal morphogenesis will be to define the relationship between different transcription factors regulating distinct phases of neuronal development. For example, Suplatast tosilate it will be interesting to determine whether and how the functions of FOXO6, NeuroD, Sp4, and sumoylated
MEF2A intersect in the course of orchestrating granule neuron dendrite arbor development in the cerebellar cortex. Do any of these transcriptional factors regulate the expression of another factor acting in a subsequent or preceding step of dendrite development? Do any of these factors interact with other transcription factors and thereby regulate their activity? Finally, do upstream signals impinging on a specific transcription factor, such as CaMKIIα or calcineurin that control NeuroD and MEF2A activity respectively, influence the activity of another transcription factor acting on a different stage of dendrite development? Another important goal of future studies will be to determine the extent of programs of gene expression regulated by different transcription factors acting at distinct stages of neuronal development. Advances in genomic technologies will facilitate these studies and yield large datasets for analysis of transcription factor-dependent networks of genes at distinct developmental stages.