Ontology highlight
ABSTRACT:
PROVIDER: PRJNA529066 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Cell type specific gene expression map of Arabidopsis thaliana SAM.
| PRJNA139823 | ENA
Project description:Knowledge about an organism’s cell and tissue-specific transcriptional repertoire is essential for understanding the gene regulatory circuits that control key developmental events. The shoot apical meristem (SAM) is responsible for development of all the above ground parts of plants. Our understanding of SAM at the molecular level is far from complete. The present work investigates the global gene expression repertoire of SAMs in the garden pea (Pisum sativum). To this end, 10,346 EST sequences representing 7611 unique genes were generated from pea SAM cDNA libraries. These sequences, together with previously reported ESTs, were used to construct a 12K oligonucleotide array used to identify genes exhibiting differential SAM expression, as compared to the axillary meristem, root apical meristem, and non-meristematic tissues. We identified a number of genes that are predominantly expressed in specific cell layers or domains of the SAM, and thus are likely components of the gene networks involved in stem cell maintenance and initiation of lateral organ primordial cells. In situ hybridization confirmed the spatial localisation of some of these key genes within the SAM. Our data also indicate the diversification of some gene expression patterns and functions in legume crop plants.
2009-10-26 | GSE13451 | GEO
Project description:S-adenosylmethionine (SAM) is the principal methyl group donor of the cell, required to modify various molecules, including DNA, RNA and proteins. Inside mitochondria, SAM is associated with several steps of mitochondrial gene expression. However, the exact role and significance of these modifications remains debated. Here, we depleted mitochondria of SAM, constitutively in mouse embryonic fibroblasts or progressively in mouse skeletal muscle. Our data reveal that mitochondrial SAM is crucial for both early and late stages of mitochondrial gene expression. Direct long-read RNA sequencing demonstrated that the mitochondrial ribosomal gene cluster is particularly sensitive to perturbed mitochondrial methylation potential, leading to the accumulation of unprocessed RNA precursors. Stable isotope labelling of amino acids in culture (SILAC) followed by mass spectrometry on ribosome fractions shows that these precursors are associated with processing and ribosome assembly factors. Finally, structural analysis by cryogenic electron microscopy (Cryo-EM) revealed that mitochondrial ribosome assembly is adversely affected by the absence of mitochondrial SAM and that methylation is integral for correct peptidyl transferase centre assembly of the large ribosome subunit. Our data thus identifies two critical steps for methylation during mitochondrial gene expression.
2025-05-19 | PXD062614 | Pride
Project description:S-adenosylmethionine (SAM) is the principal methyl group donor of the cell, required to modify various molecules, including DNA, RNA and proteins. Inside mitochondria, SAM is associated with several steps of mitochondrial gene expression. However, the exact role and significance of these modifications remains debated. Here, we depleted mitochondria of SAM, constitutively in mouse embryonic fibroblasts or progressively in mouse skeletal muscle. Our data reveal that mitochondrial SAM is crucial for both early and late stages of mitochondrial gene expression. Direct long-read RNA sequencing demonstrated that the mitochondrial ribosomal gene cluster is particularly sensitive to perturbed mitochondrial methylation potential, leading to the accumulation of unprocessed RNA precursors. Stable isotope labelling of amino acids in culture (SILAC) followed by mass spectrometry on ribosome fractions shows that these precursors are associated with processing and ribosome assembly factors. Finally, structural analysis by cryogenic electron microscopy (Cryo-EM) revealed that mitochondrial ribosome assembly is adversely affected by the absence of mitochondrial SAM and that methylation is integral for correct peptidyl transferase centre assembly of the large ribosome subunit. Our data thus identifies two critical steps for methylation during mitochondrial gene expression.
2025-05-19 | PXD055907 | Pride
Project description:The aim of the study was to investigate whether environmental factors like S-adenosylmethionine (SAM) via affecting epigenome could alter cocaine-induced gene expression and locomotor sensitization in mice. Using mouse nucleus accumbens (NAc) tissue, whole-genome gene expression profiling revealed that repeated SAM treatment affected a limited number of genes, but significantly modified cocaine-induced gene expression by blunting nonspecifically the cocaine response. At the gene level, we discovered that SAM modulated cocaine-induced DNA methylation by inhibiting both promoter-associated CpG-island hyper- and hypomethylation in the NAc but not in the reference tissue cerebellum.
2013-06-27 | GSE48365 | GEO
Project description:S-adenosylmethionine (SAM) is the principal cellular donor of methyl-moiety in methylation reaction and regulates gene expression by regulating methylation related cellular events, such as epigenetic regulation. Although SAM biosynthesis affects variety of biological phenomena including disease and aging, whether cell-specific SAM biosynthesis status present and how it contributes cellular function are largely unknow. Here, we firstly showed that Drosophila germline in gametogenesis has repressive SAM biosynthesis status through observation of SAM synthetase (Sam-S), a key enzyme for SAM biosynthesis. In addition, our study showed that germline-unique repressive SAM biosynthesis status contributes to inhibition of retrotransposon expression; enhancement of SAM biosynthesis in germline caused excessive expression of retrotransposons including HeT-A, a telomere-specific retroelement, as the most affected target. We found that promoter activity of HeT-A is enhanced in SAM increased condition with increased accumulation of 6mA DNA methylation, the major DNA methylation modification in Drosophila genome. Interestingly, the enhanced 6mA enrichment and gene expression in enriched loci was not correlated in neither other retrotransposons nor structural genes. Taken together, our results suggest SAM-deficient status in germline uniquely regulates HeT-A transcription via 6mA methylation modification. Thus, our study provides new understanding how germline unique metabolic status contributes to regulation of retrotransposon expression.
2025-04-10 | GSE294178 | GEO
Project description:S-adenosylmethionine (SAM) is the principal cellular donor of methyl-moiety in methylation reaction and regulates gene expression by regulating methylation related cellular events, such as epigenetic regulation. Although SAM biosynthesis affects variety of biological phenomena including disease and aging, whether cell-specific SAM biosynthesis status present and how it contributes cellular function are largely unknow. Here, we firstly showed that Drosophila germline in gametogenesis has repressive SAM biosynthesis status through observation of SAM synthetase (Sam-S), a key enzyme for SAM biosynthesis. In addition, our study showed that germline-unique repressive SAM biosynthesis status contributes to inhibition of retrotransposon expression; enhancement of SAM biosynthesis in germline caused excessive expression of retrotransposons including HeT-A, a telomere-specific retroelement, as the most affected target. We found that promoter activity of HeT-A is enhanced in SAM increased condition with increased accumulation of 6mA DNA methylation, the major DNA methylation modification in Drosophila genome. Interestingly, the enhanced 6mA enrichment and gene expression in enriched loci was not correlated in neither other retrotransposons nor structural genes. Taken together, our results suggest SAM-deficient status in germline uniquely regulates HeT-A transcription via 6mA methylation modification. Thus, our study provides new understanding how germline unique metabolic status contributes to regulation of retrotransposon expression.
2025-04-10 | GSE294101 | GEO