Mouse retina undergoes crucial changes during early postnatal development. By using Affymetrix microarrays, we analyzed gene expression profiles of wild-type 129SvEv/C57BL/6 mouse retinas at postnatal days (P) 7, 10, 14, 18, and 21 and found significantly altered expression of 355 genes. Characterization of these 355 genes provided insight into physiologic and pathologic processes of mouse retinal development during the second and third postnatal weeks, a period that corresponds to human embryogenesis between weeks 12 and 28. These genes formed 6 groups with similar change patterns. Among the genes, sixteen cause retinal diseases when mutated; most of these 16 genes were upregulated in retina during this period. Using the PathArt program, we identified the biological processes in which many of the 355 gene products function. Among the most active processes in the P7-P21 retina are those involved in neurogenesis, obesity, diabetes type II, apoptosis, growth and differentiation, and protein kinase activity. We examined the expression patterns of 58 genes in P7 and adult retinas by searching the Brain Gene Expression Map database. Although most genes were present in various cell types in retinas, many displayed high levels of expression specifically in the outer nuclear, inner nuclear, and/or ganglion cell layers. By combining our 3 analyses, we demonstrated that during this period of mouse retinal development, many genes play important roles in various cell types, multiple pathways are involved, and some genes in a pathway are expressed in coordinated patterns. Our results thus provide foundation for future detailed studies of specific genes and pathways in various genetic and environmental conditions during retinal development.
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In situ hybridization of P7 and adult retinas were obtained from the Brain Gene Expression Map (BGEM) database ( http://www.stjudebgem.org ) at the Dept. of Developmental Neurobiology and we acknowledge the help of Suraj Mukatira and Geoffery Neale at the Hartwell Center for Bioinformatics and Biotechnology, St. Jude Children's Research Hospital. This work was supported by NIH Cancer Center Support grant CA21765, the American Lebanese Syrian Associated Charities (ALSAC), and NIH grants R01 EY12950 and R01 DC06471 (to J.Z.), N01 NS02331 (to T.C.).
- In situ hybridization