Unknown,Transcriptomics,Genomics,Proteomics

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Arabidopsis floral initiator SKB1 confers high salt tolerance by regulating transcription and pre-mRNA splicing through altering histone H4R3 and small nuclear ribonucleoprotein LSM4 methylation

ABSTRACT: This study examines how histone modification confers salt stress in Arabidopsis. The floral initiator SKB1 is found to mediate the plant’s response to salt stress by altering the methylation status of histone H4R3 and of the small nuclear ribonucleoprotein (snRNP) LSM4, and thereby affecting the expression of stress-responsive genes. Total RNA was isolated with Trizol reagent (Invitrogen) from eleven11-day-old seedlings of the wild type and skb1-1 mutant without or with 200 mM NaCl for 6 hrs. 29k Arabidopsis Genome Array hybridization was carried out by CapitalBio Corporation (Beijing, China).

ORGANISM(S): Arabidopsis thaliana

SUBMITTER: Zhaoliang Zhang

PROVIDER: E-GEOD-26398 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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.

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Arabidopsis floral initiator SKB1 confers high salt tolerance by regulating transcription and pre-mRNA splicing through altering histone H4R3 and small nuclear ribonucleoprotein LSM4 methylation

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