[Zimmermannella] bifida NBRC 103089
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REPOSITORIES: ENA
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Project description:Investigation of whole genome gene expression level changes in a Gluconacetobacter xylinus NBRC 3288 delta-fnrG mutant, compared to the wild-type strain.
2021-07-16 | GSE41775 | GEO
Project description:Partial genome sequencing of a temperate herb, Deinanthe bifida
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Project description:Purpose:The goals of this study are to clarify the B. subtilis NBRC 16449 response to soybeans. Methods: B. subtilis NBRC 16449 cells were aerobically cultured in liquid LB, LB solidified with agar, or on surface of boiled soybeans to logarithmic growth phase. Total RNAs were extracted from bacterial cells by Hot-Phenol method. Samples for RNA-seq were prepared according to Illmina protocol available from the manufacture. The sequence reads that passed quality filters were analyzed at the transcript isoform level with bowtie v0.11.2. Results: Using an optimized data analysis workflow, we mapped around 15 million sequence reads per sample to the whole genome of B. subtilis BEST195 and identified 4271 transcripts in B. subtilis NBRC 16449 with Bowtie aligner. Read count per genome was extracted from known gene annotations with HTSeq program. Compared the transcriptomes of B. subtilis NBRC 16449 grown on LB solidified with agar to that grown on surface of boiled soybeans, about 5% of genes showed the different expression levels.
2020-11-02 | GSE109523 | GEO
Project description:The complete chloroplast genome of Cycas bifida , an extremely small population protected species
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Project description:Fetal spina bifida can associate with reduced fetal growth. However, little is known about placental development and function in pregnancies with fetal spina bifida, despite that the placenta is a critical regulator of fetal growth. We used data from a case-control study to determine how the placental transcriptome differs in fetuses with isolated spina bifida (cases), compared to fetuses without any congenital anomalies (controls).
2024-01-12 | GSE252552 | GEO
Project description:Background The vitamin A derivative, retinoic acid (RA), is a potent teratogenic agent that induces a variety of congenital abnormalities including neural tube defects. The embryopathology of RA has been extensively investigated and retinol receptors play important roles during organogenesis, development and neural tube closure. Still, the mechanisms by which RA influences these processes are not completely understood. Methods We used a custom-made mouse genome 32K oligonucleotide microarray to determine the gene expression profiles of mouse embryo spinal cord samples that had been exposed to vehicle or RA. Then, we performed a GSEA (gene set enrichment analysis) on the gene expression data by searching MSigDB (v2.5) c2 gene sets (canonical pathways) and c5 gene sets (curated GO terms), with set size restraints on the range to avoid over-narrow or over-broad categories. Results Using microarray technology, the present study identifies 85 genes in the spinal cord that exhibit at least a 1.5-fold change between control samples and samples with spina bifida aperta. A gene set enrichment analysis showed that maternal exposure to RA induced spinal bifida that were associated with altered expression of genes involved in pro- or anti-apoptosis, cell proliferation, migration, cytoskeleton components, and cell or focal adhesion, indicating that defective functions of these cell components and biological processes preceded the abnormal development of neural tube. Conclusions Maternal exposure to RA induced spinal bifida that were associated with altered expression of genes involved in pro- or anti-apoptosis, cell proliferation, migration, cytoskeleton components, and cell or focal adhesion. As shown in previous reports, defective functions of these cell components and biological processes preceded the abnormal development of the neural tube. Our study will help the understanding of the etiology and pathology of spinal bifida. However, it should be noted that the changes in gene expression induced by RA exposure may not be an effect on events other than neural tube closure; further study is required to fully understand the molecular mechanisms and consequence of neural tube defects in embryos exposed to RA. Our study provides a global analysis of gene expression patterns in spina bifida and will help the understanding of the etiology and pathology of neural tube defects. We assessed the changes in gene expression that coincide with spina bifida in RA-treated mouse fetuses. After generating an independent list of regulated genes, we analyzed samples by gene set enrichment analysis to expand our results. A pool of spinal cord tissue from spina bifida fetuses whose mothers were exposed to RA was compared to a pool of spinal cord tissue from fetuses whose mothers were exposed to olive oil vehicle. Three replicates each.
2011-05-10 | E-GEOD-28834 | biostudies-arrayexpress
Project description:Background The vitamin A derivative, retinoic acid (RA), is a potent teratogenic agent that induces a variety of congenital abnormalities including neural tube defects. The embryopathology of RA has been extensively investigated and retinol receptors play important roles during organogenesis, development and neural tube closure. Still, the mechanisms by which RA influences these processes are not completely understood. Methods We used a custom-made mouse genome 32K oligonucleotide microarray to determine the gene expression profiles of mouse embryo spinal cord samples that had been exposed to vehicle or RA. Then, we performed a GSEA (gene set enrichment analysis) on the gene expression data by searching MSigDB (v2.5) c2 gene sets (canonical pathways) and c5 gene sets (curated GO terms), with set size restraints on the range to avoid over-narrow or over-broad categories. Results Using microarray technology, the present study identifies 85 genes in the spinal cord that exhibit at least a 1.5-fold change between control samples and samples with spina bifida aperta. A gene set enrichment analysis showed that maternal exposure to RA induced spinal bifida that were associated with altered expression of genes involved in pro- or anti-apoptosis, cell proliferation, migration, cytoskeleton components, and cell or focal adhesion, indicating that defective functions of these cell components and biological processes preceded the abnormal development of neural tube. Conclusions Maternal exposure to RA induced spinal bifida that were associated with altered expression of genes involved in pro- or anti-apoptosis, cell proliferation, migration, cytoskeleton components, and cell or focal adhesion. As shown in previous reports, defective functions of these cell components and biological processes preceded the abnormal development of the neural tube. Our study will help the understanding of the etiology and pathology of spinal bifida. However, it should be noted that the changes in gene expression induced by RA exposure may not be an effect on events other than neural tube closure; further study is required to fully understand the molecular mechanisms and consequence of neural tube defects in embryos exposed to RA. Our study provides a global analysis of gene expression patterns in spina bifida and will help the understanding of the etiology and pathology of neural tube defects.
2011-05-10 | GSE28834 | GEO
Project description:Nocardia caishijiensis NBRC 108228 genome sequencing project
| PRJDB157 | ENA