Panicum virgatum
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ABSTRACT:
PROVIDER: PRJNA386182 | ENA |
REPOSITORIES: ENA
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Project description:Switchgrass (Panicum virgatum) has been developed into a model lignocellulosic bioenergy crop. Downregulation of caffeic acid O-methyltransferase (COMT), a key enzyme in lignin biosynthesis, led to altered lignification and increased biofuel yield in switchgrass. Methylenetetrahydrofolate reductase (MTHFR) mediated C1 metabolism provides methyl units consumed by COMT. It was predicted that co-silencing of MTHFR and COMT would have a more significant impact on lignification than either of the single genes. However, our results showed that strong downregulation of MTHFR in a COMT-deficient background led to altered plant growth and development, but no significant change in lignin content or composition was found when compared with COMT plants. Another unexpected finding is that the double MTHFR/COMT downregulated plants showed a novel lesion-mimic leaf phenotype. Molecular analyses revealed that the lesion-mimic phenotype was caused by the synergistic effect of MTHFR and COMT genes, with MTHFR playing a predominant role. Microarray analysis showed significant induction of genes involved in oxidative and defenserelated processes. The results demonstrated the lack of additive effects of MTHFR and COMT on lignification. Furthermore, this research revealed an unexpected role of the two genes in the modulation of lesion-mimic cell death as well as their synergetic effects on agronomic performance.
2018-05-01 | GSE98676 | GEO
Project description:COMT Switchgrass Root Associated Metagenome and Metatranscriptome
| PRJNA254830 | ENA
Project description:Catechol-O-methyl transferase (COMT) is involved in detoxification of catechol estrogens, playing cancer-protective role in cells producing or utilizing estrogen. Moreover, COMT suppressed migration potential of breast cancer (BC) cells. To delineate COMT role in metastasis of estrogen receptor (ER) dependent BC, we investigated the effect of COMT overexpression on invasion, transcriptome, proteome and interactome of MCF7 cells, a luminal A BC model, stably transduced with lentiviral vector carrying COMT gene (MCF7-COMT). We performed comparative gene expression analysis using data obtained from RNA-seq of COMT-overexpressing and control cells in biological duplicates.
2023-02-01 | GSE203435 | GEO
Project description:Supplementation with high doses of folic acid, an important mediator of one-carbon transfers for DNA methylation, is used clinically to improve sperm parameters in infertile men. We recently detected an unexpected loss of DNA methylation in the sperm of idiopathic infertile men after 6 months of daily supplementation with 5mg folic acid (>10× the daily recommended intake-DRI), exacerbated in men homozygous for a common variant in the gene encoding an important enzyme in folate metabolism, methylenetetrahydrofolate reductase (MTHFR 677C>T). To investigate the epigenomic impact and mechanism underlying effects of folic acid on male germ cells, wildtype and heterozygote mice for a targeted inactivation of the Mthfr gene were fed high-dose folic acid (10× the DRI) or control diets for six months. No changes were detected in general health, sperm counts or methylation of imprinted genes. Reduced representation bisulfite sequencing revealed sperm DNA hypomethylation in Mthfr+/- mice on the 10× diets. Wildtype mice demonstrated sperm hypomethylation only with a very high dose (20×) of folic acid for 12 months. Testicular MTHFR protein levels decreased significantly in wildtype mice on the 20× diet but not in those on the 10× diet, suggesting a possible role for MTHFR deficiency in sperm DNA hypomethylation. In-depth analysis of the folic acid-exposed sperm DNA methylome suggested mouse/human susceptibility of sequences with potential importance to germ cell and embryo development. Our data provide evidence for a similar cross-species response to high dose folic acid supplementation, of sperm DNA hypomethylation, and implicate MTHFR downregulation as a possible mechanism.
2018-01-23 | GSE100849 | GEO
Project description:Catechol-O-methyl transferase (COMT) is involved in detoxification of catechol estrogens, playing cancer-protective role in cells producing or utilizing estrogen. Moreover, COMT suppressed migration potential of breast cancer cells. To delineate COMT role in metastasis of estrogen receptor dependent BC, we investigated the effect of COMT overexpression on invasion, transcriptome, proteome and interactome of MCF7 cells, a luminal A breast cancer model, stably transduced with lentiviral vector carrying COMT gene (MCF7-COMT). This PRIDE project includes quantitative analysis results for the total proteome LC-DIA-MS/MS experiment evaluating COMT overexpression in MCF7 breast cancer cell line, and results of pulldown analysis of COMT-interacting proteins in MCF7 cells.
2023-01-31 | PXD033833 | Pride
Project description:Previous studies in our laboratory have shown that low folate diet (control diet with 2mg folate/kg, low folate diet with 0.3mg folate/kg) can induce intestinal tumors in BALB/c mice. We used microarrays to compare MTHFR+/+ BALB/c mice fed control diet and MTHFR+/- BALB/c mice fed low folate diet. After weaning, 4 BALB/c Mthfr +/+ mice were fed with a control diet (CD, 2mg folate/kg) and 4 BALB/c Mthfr +/- mice were fed a low folate diet (FD, 0.3mg folate/kg) for 1 year. Both diets contain succinylsulfanthiozole (1%) to prevent folate synthesis by intestine microbial biota.
2013-12-03 | E-GEOD-34011 | biostudies-arrayexpress
Project description:Next-generation sequencing (NGS)-derived transcriptomic profiling was carried out to compare the transcriptomic changes mediated by COMT knockout in U87 cells. We found significant enrichment of gene signatures involving IFNa/b signaling in COMT-KO U87 cells compared to control cells. Our analysis also demonstrated that COMT deficiency interferes with mitochondrial functions and induces the expression of genes associated with the anti-viral RNA sensing pathway.
2023-10-12 | GSE237053 | GEO
Project description:Lesion mimic mutants in rice are widely known as spotted leaf (spl) mutants, of which several genotypes exhibit enhanced resistance to different races of Magnaporthe grisea. Besides naturally occurring spotted leaf mutants, tissue culture-induced reverse genetic repositories also act as sources of lesion mimic mutants in rice. We systematically evaluated a large collection of Tos17 mutant panel lines, developed and maintained at the National Institute of Agrobiological Sciences, Tsukuba, Japan, for their reaction to three different races of M. grisea and identified a lesion mimic mutant, NF4050-8, that showed lesions similar to naturally occurring spl5 mutant and enhanced resistance to all three blast races tested. Microarray analysis of ~44,000 rice genes in NF4050-8 with Nipponbare as control during the progressive lesion appearance stage revealed significant up-regulation of numerous defense/pathogenesis-related genes as well as several WRKY domain-containing genes and down-regulation of haem peroxidase gene. Subsequent real-time PCR analysis of WRKY45 and PR1b genes in NF4050-8 and spl5 suggested possible constitutive activation of a defense signaling pathway downstream of Salicylic Acid (SA) but independent of NH1 in these mutant lines of rice. We used Agilent rice oligo microarrays to identify putative defense/pathogenesis-related genes. Leaf tissues of the rice genotypes Nipponbare and NF4050-8 were used in the study. Two replications of microarray experiments were carried out by hybridizing the cRNA from control and progressive lesion appearance stage on 4 x 44k microarray.
2010-06-05 | E-GEOD-17791 | biostudies-arrayexpress