1274 Full-Open Reading Frames of Transcripts Expressed in the Developing Mouse Nervous System

Bonaldo, Maria F.; Bair, Thomas B.; Scheetz, Todd E.; Snir, Einat; Akabogu, Ike; Bair, Jennifer; Berger, Brian; Crouch, Keith G.; Davis, A.; Eyestone, M. E.; Keppel, Catherine R.; Kucaba, Tamara A.; Lebeck, Mark; Lin, Jin-Lung; Melo, Anna Izabel R.; Rehmann, Joshua; Reiter, Rebecca S.; Schaefer, Kelly; Smith, Christina; Tack, Dylan; Trout, K.; Sheffield, Val C.; Lin, Jim Jung‐Ching; Casavant, Thomas L.; Soares, Marcelo B.

doi:10.1101/gr.2601304

Cited by 18 publications

(11 citation statements)

References 38 publications

(36 reference statements)

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“…Mouse heart in situ hybridizations were performed as previously described (34). Id1, Id2, and Id3 probe templates were made from plasmid accession numbers BE945568, AI843393, and AI839283, respectively, from the Brain Molecular Anatomy Project library (38).…”

Section: Methodsmentioning

confidence: 99%

Transcription factor genes Smad4 and Gata4 cooperatively regulate cardiac valve development

Moskowitz

Wang²,

Peterson³

et al. 2011

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

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We report that the dominant human missense mutations G303E and G296S in GATA4 , a cardiac-specific transcription factor gene, cause atrioventricular septal defects and valve abnormalities by disrupting a signaling cascade involved in endocardial cushion development. These GATA4 missense mutations, but not a mutation causing secundum atrial septal defects (S52F), demonstrated impaired protein interactions with SMAD4, a transcription factor required for canonical bone morphogenetic protein/transforming growth factor-β ( BMP / TGF-β ) signaling. Gata4 and Smad4 genetically interact in vivo: atrioventricular septal defects result from endothelial-specific Gata4 and Smad4 compound haploinsufficiency. Endothelial-specific knockout of Smad4 caused an absence of valve-forming activity: Smad4 -deficient endocardium was associated with acellular endocardial cushions, absent epithelial-to-mesenchymal transformation, reduced endocardial proliferation, and loss of Id2 expression in valve-forming regions. We show that Gata4 and Smad4 cooperatively activated the Id2 promoter, that human GATA4 mutations abrogated this activity, and that Id2 deficiency in mice could cause atrioventricular septal defects. We suggest that one determinant of the phenotypic spectrum caused by human GATA4 mutations is differential effects on GATA4/SMAD4 interactions required for endocardial cushion development.

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Section: Methodsmentioning

confidence: 99%

Transcription factor genes Smad4 and Gata4 cooperatively regulate cardiac valve development

Moskowitz

Wang²,

Peterson³

et al. 2011

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

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“…Thus, our experimental model with whole brain cannot detect expressions of specifi c genes, such as those involved in sexual diff erentiation in small hypothalamic nuclei [30] , and is not suitable for gene ontology analysis, or linkage analysis [13] . Therefore, our observations cannot be compared with gene expression fi ndings from distinct brain structures [2,15,22,24,28,30,33] .…”

Section: Discussionmentioning

confidence: 99%

“…Matoba et al [22] and Kagami and Furuichi [15] investigated correlations between gene functions and developmental expression patterns in the mouse cerebellum. Bonaldo et al [2] studied 1 274 full-open reading frames of transcripts in the developing mouse nervous system, starting at E-12.5 through E-18.5, and postnatal days P-1, P-5 and P-15. The whole brain gene expression was studied by Matsuki et al [23] at E-12, E-15, E-18 days of embryonic devel-expressions of male and female rats at birth, 3 days, and 10 days of age were measured by microarray technique ( : 10 K genes; n = 9 / category).…”

Section: Introductionmentioning

confidence: 99%

Age and Sex Differences in Brain Gene Expression in Neonatal Rats

Torbati

Totapally²,

Raszynski³

et al. 2008

Neuropediatrics

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Gene expression in the central nervous system is highly region-specific. We tested the hypothesis that certain developmental biomarkers could be detected in the whole brain or in cortical, subcortical or cerebellar structures. Brain gene expressions of male and female rats at birth, 3 days, and 10 days of age were measured by microarray technique ( approximately 10 K genes; n=9/category). We found 53 significantly up-regulated and 8 down-regulated genes at 10 days of age, relative to birth and 3 days of age. The whole brain, however, showed no significant sex differences in gene expression patterns up to 10 days of age. Ten genes with the highest up-regulation, and 5 down-regulated genes were further confirmed by quantitative real-time PCR (Q-PCR), using the whole brain, cortices, subcortical structures, and cerebellum. The Q-PCR confirmed genes are known to be involved in neuronal differentiation, axonal myelination and growth, neurotransmission and glycolytic pathways. With a few exceptions, the expression levels of Q-PCR confirmed genes were significantly different in the whole brain, compared to other regions. In a separate study, we tested the potential utility of the Q-PCR confirmed genes, as whole brain biomarkers, after a six-hour exposure to hyperoxia (>98% oxygen breathing) in 10 days old rats. This relatively mild oxidative challenge created a 3.5-fold increase in the expression of T-cell receptor beta Variable 8.3b, known to have regulatory function during development. We suggest that genes displaying significant expression in the whole brain, regardless of their origin, could be used to screen normal brain development in neonatal rat models of experimental neurology.

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“…Further ORFeome projects, or large-scale projects to collect sizeable cDNA libraries from complex organisms are proving resourceful for projects ongoing in mouse and human studies [31,32].…”

Section: Protein Interaction Networkmentioning

confidence: 99%

Biomarker discovery and compound evaluation using two-hybrid proteomic systems

Gillespie¹

2006

Expert Opinion on Drug Discovery

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Many proteomic technologies require a heavy investment in expertise and technology, which place these approaches beyond many labs and small companies. However, proteomic approaches are ideal for pilot experiments, identifying relevant biomarkers and protein pathways for development or analysis of therapeutic compounds. The two-hybrid proteomic systems are available and affordable to most researchers, requiring little more than standard microbiological equipment. The screens rapidly generate data, identifying protein interactions that can be used to construct small local protein networks. Using data from large-scale projects, these small local protein networks can be used to identify the larger cellular pathways that are being affected by therapeutic compounds in the screen. The foundation for the two-hybrid proteomic systems are commercially available, as are high quality cDNA libraries. The straightforwardness of the two-hybrid proteomic system allows smaller groups to focus their resources on critical cellular pathways and molecular targets by taking advantage of a trusted molecular assay and an ever growing set of postgenomic era databases.

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1274 Full-Open Reading Frames of Transcripts Expressed in the Developing Mouse Nervous System

Cited by 18 publications

References 38 publications

Transcription factor genes Smad4 and Gata4 cooperatively regulate cardiac valve development

Transcription factor genes Smad4 and Gata4 cooperatively regulate cardiac valve development

Age and Sex Differences in Brain Gene Expression in Neonatal Rats

Biomarker discovery and compound evaluation using two-hybrid proteomic systems

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