Microarray Analysis of the Transcriptional Network Controlled by the Photoreceptor Homeobox Gene

dy demonstrates that cDNA microarrays can be successfully used to define the transcriptional networks controlled by transcription factors in vertebrate tissue in vivo. Background Studiesof neural development have highlighted the role of cell- and tissue-specify transcriptionfransc in regulating both cell fly determination events and the later morphological stagesof neuronal difnaly6jAzzyT [1]. Little is known, however, about the gene expression or transcriptional networks regulated by thesefesey6 or those controlling cell fll determination. In the developing vertebrate retina, several transcription ftrans have been implicated in thedifM/6AyT--MzM/ of specif - cell types, including the paired-typefaire member Chx10 (bipolar neurons; [2]) and the POU-domain transcriptionfript fipti member Brn-3b (subtypeof ganglion cells [3]). The transcriptionfrans Crx (cone, rod homeobox) has a pivotal role in the morphologicaldifpho entiationof both rod and cone ph

dILA neurons in the dorsal spinal cord are the product of terminal and non-terminal asymmetric progenitor cell divisions, and require Mash1 for their development

dILA and dILB neurons comprise the major neuronal subtypes generated in the dorsal spinal cord, and arise in a salt-and-pepper pattern from a broad progenitor domain that expresses the bHLH factor Mash1. In this domain, Mash1-positive and Mash1-negative cells intermingle. Using a Mash1(GFP) allele in mice, we show here that Mash1+ progenitors give rise to dILA and dILB neurons. Using retroviral tracing in the chick, we demonstrate that a single progenitor can give rise to a dILA and a dILB neuron, and that dILA neurons are the product of asymmetric progenitor cell divisions. In Mash1-null mutant mice, the development of dILA, but not of dILB neurons is impaired. We provide evidence that a dual function of Mash1 in neuronal differentiation and specification accounts for the observed changes in the mutant mice. Our data allow us to assign to Mash1 a function in asymmetric cell divisions, and indicate that the factor coordinates cell cycle exit and specification in the one daughter that gives rise to a dILA neuron