Microarray analysis of the developing cortex

Semeralul, Mawahib O.; Boutros, Paul C.; Likhodi, Olga; Okey, Allan B.; Tol, Hubert H.M. Van; Wong, Albert H.C.

doi:10.1002/neu.20302

Cited by 38 publications

(44 citation statements)

References 44 publications

(59 reference statements)

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“…The expression information suggested important functions for a number of regulatory genes, and provided strong evidence for a highly dynamic transcriptome during mouse brain development. Previous microarray work in postnatal cortical development found an increase of sox11 but decrease of sox4 expression from postnatal week 2 to week 3 (13). However, our results revealed a substantial decrease of both sox11 (10-fold) and sox4 (5-fold) from E18 to P7, suggesting that transcriptional regulation may differ significantly before and after birth.…”

Section: Resultscontrasting

confidence: 78%

“…Previous surveys of early brain development have focused on a small number of genes. More recently, microarray studies and others have revealed differential expression of groups of genes in specific brain regions or associated with brain disorders (6)(7)(8)(9)(10)(11)(12)(13)(14). Specifically, gene expression has been examined using whole brains or brain tissues from young and old, and diseased mice (7,8,12,15).…”

mentioning

confidence: 99%

“…In a microarray study of 11,000 genes and ESTs, the expression level of 1,926 genes was found to change significantly during hippocampal development from E16 through P30 (11). Also, 366 ProbeSets were found to be differentially expressed during postnatal 2-10 weeks (13). However, microarray technology has several limitations: (1) the number of genes is fixed; (2) the sensitivity is limited by background hybridization; and (3) the inaccuracy of mRNA levels because of difference in hybridization among probes.…”

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confidence: 99%

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Transcriptome of embryonic and neonatal mouse cortex by high-throughput RNA sequencing

Han

Wu²,

Chung³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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Brain structure and function experience dramatic changes from embryonic to postnatal development. Microarray analyses have detected differential gene expression at different stages and in disease models, but gene expression information during early brain development is limited. We have generated >27 million reads to identify mRNAs from the mouse cortex for >16,000 genes at either embryonic day 18 (E18) or postnatal day 7 (P7), a period of significant synaptogenesis for neural circuit formation. In addition, we devised strategies to detect alternative splice forms and uncovered more splice variants. We observed differential expression of 3,758 genes between the 2 stages, many with known functions or predicted to be important for neural development. Neurogenesis-related genes, such as those encoding Sox4, Sox11, and zinc-finger proteins, were more highly expressed at E18 than at P7. In contrast, the genes encoding synaptic proteins such as synaptotagmin, complexin 2, and syntaxin were up-regulated from E18 to P7. We also found that several neurological disorder-related genes were highly expressed at E18. Our transcriptome analysis may serve as a blueprint for gene expression pattern and provide functional clues of previously unknown genes and disease-related genes during early brain development.E18 ͉ P7 ͉ brain ͉ transcription factors ͉ neural diseases M ammalian brain development can be largely divided into 2 periods: embryonic and postnatal. Embryonic mouse brain development starts Ϸ10-11 days after gestation (E10-E11) with massive neuronal production from neural stem cells. The development of rodent cerebral cortex is a well-studied model system, where the initial neurons form the subplate layer, although subsequent neurons migrate in an inside-out pattern to form the multilayer cortical structure (1, 2). By embryonic day 18 (E18), neurons start to send out axons and dendrites to be poised for synaptic connections. After birth, the first week of postnatal brain development is characterized by elevated production of astrocytes, which are crucial for neuronal synaptogenesis (3, 4). By postnatal day 7, many neurons start to establish synaptic connections with other neurons, forming a primitive neural circuit. Early brain development is precisely controlled by transcription factors, cell adhesion molecules, receptors and channels, synaptic proteins, and other effectors. A single misstep might result in a severe deformation of the brain circuit. For example, loss of Otx2 function results in the absence of early brain development (5). Since many psychiatric disorders such as autism and mental retardation are closely associated with early brain development, understanding the gene expression profile will facilitate the search for an optimal treatment for these disorders. Previous surveys of early brain development have focused on a small number of genes. More recently, microarray studies and others have revealed differential expression of groups of genes in specific brain regions or associated with brain disorders (6-1...

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Section: Resultscontrasting

confidence: 78%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Transcriptome of embryonic and neonatal mouse cortex by high-throughput RNA sequencing

Han

Wu²,

Chung³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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“…Collagen III is a major collagen in connective tissues, with integrins α1β1 and α2β1 serving as its typical receptors (26,27). There has been only scant literature suggesting the presence of collagen III in the brain through microarray analysis (28). To establish the expression pattern of collagen III in the brain, we performed collagen III immunohistochemistry (IHC) on embryonic mouse brains.…”

Section: Gpr56mentioning

confidence: 99%

G protein-coupled receptor 56 and collagen III, a receptor-ligand pair, regulates cortical development and lamination

Luo

Jeong

Jin

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

245

338

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GPR56, an orphan G protein-coupled receptor (GPCR) from the family of adhesion GPCRs, plays an indispensable role in cortical development and lamination. Mutations in the GPR56 gene cause a malformed cerebral cortex in both humans and mice that resembles cobblestone lissencephaly, which is characterized by overmigration of neurons beyond the pial basement membrane. However, the molecular mechanisms through which GPR56 regulates cortical development remain elusive due to the unknown status of its ligand. Here we identify collagen, type III, alpha-1 (gene symbol Col3a1) as the ligand of GPR56 through an in vitro biotinylation/ proteomics approach. Further studies demonstrated that Col3a1 null mutant mice exhibit overmigration of neurons beyond the pial basement membrane and a cobblestone-like cortical malformation similar to the phenotype seen in Gpr56 null mutant mice. Functional studies suggest that the interaction of collagen III with its receptor GPR56 inhibits neural migration in vitro. As for intracellular signaling, GPR56 couples to the Gα 12/13 family of G proteins and activates RhoA pathway upon ligand binding. Thus, collagen III regulates the proper lamination of the cerebral cortex by acting as the major ligand of GPR56 in the developing brain.brain malformation | meningeal fibroblasts D uring cerebral cortical development, most cortical neurons are born deep in specialized proliferative regions near the lining of the lateral ventricles and migrate out to take up residence in the surface layer of the brain, eventually forming a highly folded sheet of six neuronal layers (1-5). Disruptions in normal neuronal migration and positioning lead to cortical disorders, one of which is cobblestone lissencephaly (6). Cobblestone lissencephaly is typically seen in three distinct human congenital muscular dystrophy syndromes: muscle-eye-brain disease, Fukuyama-type congenital muscular dystrophy, and Walker-Warburg syndrome (6). Mutant mice with deletions in some members of the integrin pathway molecules and the extracellular matrix (ECM) constituents also exhibit cortical migration defects with deficiencies in basal lamina integrity and cortical ectopias, features that resemble the human cobblestone malformation (7-12). The suggested mechanism leading to cobblestone lissencephaly has been a defective pial basement membrane (BM) (6). However, recent literature demonstrates that abnormal neuronal migration may account partially for the improper formation of the cobblestone-like cortex (13-16).GPR56 is an orphan G protein-coupled receptor (GPCR) from the family of adhesion GPCRs. Mutations in GPR56 cause a specific human brain malformation called bilateral frontoparietal polymicrogyria (BFPP), an autosomal recessively inherited developmental disorder of the brain (17)(18)(19)(20). Magnetic resonance imaging of BFPP brains shows numerous (poly) small (micro) gyri, which extend diffusely across the frontal and parietal lobes with a decreasing anterior-to-posterior gradient of severity (17)(18)(19)(20). Further studies in...

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“…A developmental increase in transcriptional repressors could decrease access of the transcriptional machinery to the ERα promoters, thus resulting in a decrease in ERα mRNA expression. A detailed analysis of transcription factors that regulate ERα expression in the brain have not been performed, although numerous transcription factors undergo developmental regulation in the cortex [25].…”

Section: Disscussionmentioning

confidence: 99%

Changes in estrogen receptor-alpha mRNA in the mouse cortex during development

Prewitt

Wilson

2007

Brain Research

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Estrogen plays a critical role in brain development and is responsible for generating sex differences in cognition and emotion. Studies in rodent models have shown high levels of estrogen binding in non-reproductive areas of the brain during development, including the cortex and hippocampus, yet binding is diminished in the same areas of the adult brain. These binding studies demonstrated that estrogen receptors decline in the cortex during development but did not identify which of the two estrogen receptors was present. In the current study, we examined the expression of estrogen receptor alpha (ERα) and estrogen receptor beta (ERβ) in the mouse cortex during the first month of life. Messenger RNA was isolated from cortical tissue taken from C57BL/6 mice on postnatal day (PND) 1, 4, 10, 18 and 25 and expression levels were determined by real-time PCR. ERα mRNA expression in the mouse cortex at PND 25 was significantly reduced as compared to PND 1 (p<0.01). ERβ mRNA expression at PND25 was significantly increased as compared to PND 1 (p<0.05). Although the increase in ERβ mRNA was statistically significant, the ERβ levels were extremely low in the isocortex compared to ERα mRNA levels, suggesting that ERα may play a more critical role in the developmental decrease of estradiol binding than ERβ. Additionally, we measured ERα mRNA expression in organotypic explant cultures of cortex taken from PND 3 mice. Explants were maintained in vitro for 3 weeks. mRNA was isolated at several time points and ERα and ERβ mRNA was measured by real-time RT-PCR. ERα and ERβ mRNA levels reflected a similar pattern in vitro and in vivo, suggesting that signals outside the cortex are not needed for this developmental change. This study lays the groundwork for an understanding of the mechanisms of the developmental regulation of ERα mRNA.

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Microarray analysis of the developing cortex

Cited by 38 publications

References 44 publications

Transcriptome of embryonic and neonatal mouse cortex by high-throughput RNA sequencing

Transcriptome of embryonic and neonatal mouse cortex by high-throughput RNA sequencing

G protein-coupled receptor 56 and collagen III, a receptor-ligand pair, regulates cortical development and lamination

Changes in estrogen receptor-alpha mRNA in the mouse cortex during development

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