E-MTAB-5044
Ontology highlight
ABSTRACT:
PROVIDER: E-MTAB-5044 | ExpressionAtlas | 2016-12-15
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-MTAB-5044-analysis-methods.tsv | Tabular | |||
| E-MTAB-5044-analytics.tsv | Tabular | |||
| E-MTAB-5044-atlasExperimentSummary.Rdata | Rdata | |||
| E-MTAB-5044-configuration.xml | Xml | |||
| E-MTAB-5044-g2_g1-mvaPlot.png | Other |
Items per page: 5 1 - 5 of 21 |
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Project description:Thioredoxin DCC1 regulates shoot regeneration through modulating multiple genes expression by RNA-seq analyses in Arabidopsis
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Project description:AtPRMT5 regulates shoot regeneration through modulating multiple genes expression analyzed by RNA-seq
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Project description:Thioredoxin DCC1 regulates shoot regeneration through modulating multiple genes expression by RNA-seq analyses in Arabidopsis
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Project description:The interplay between multiple transcription factors precisely regulates eukaryotic transcription. Here, we report that the protein methyltransferases, MLL2 and PRMT1, interact directly and act collectively to regulate gene expression. PRMT1 binds to the N-terminal region of MLL2, considered an intrinsically disordered region, and methylates multiple arginine residues within its RGG/RG motifs. Notably, overexpression of PRMT1 decreased poly-ubiquitylation of MLL2, whereas mutations on methylation sites in MLL2 increased MLL2 poly-ubiquitylation, suggesting that PRMT1-mediated methylation stabilizes MLL2. MLL2 and PRMT1 cooperatively stimulated the expression of a chromosomal reporter gene in a PRMT1-mediated, MLL2-methylation–dependent manner. RNA-seq analysis found that MLL2 and PRMT1 jointly regulate the expression of genes involved in cell membrane and extracellular matrix functions, and depletion of either resulted in impaired cell migration and invasion. Our study provides evidence that PRMT1-mediated MLL2 methylation regulates MLL2 protein stability and the expression of their target genes.
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Project description:Protein arginine methylation plays essential roles in diverse biological processes, but its role in regulating shoot regeneration remains elusive. In this study, we analyzed the function of the protein arginine methyltransferase AtPRMT5 during de novo shoot regeneration in Arabidopsis. AtPRMT5 encodes a type II PRMT that methylates proteins, including histones and RNA splicing factors. Mutation of AtPMRT5 decreased the frequency of shoot regeneration and number of shoots per callus in the atprmt5 mutant compared with those of the wild type. To understand the mechanism of AtPRMT5 regulation of shoot regeneration, we analyzed the transcript levels of wild type and the mutant atprmt5 calli during shoot regeneration by RNA-seq. Three biological repeats of wild type and the mutant atprmt5-1 calli were used for RNA sequencing. Total RNAs were isolated from the calli of wild type Col and the mutant atprmt5-1 cultured on cultured on shoot-induction medium. The RNA-seq llibraries were constructed with TruSeq Stranded mRNA Library Prep Kit and sequenced using the Illumina Hiseq 2500. The raw reads were aligned to the genome sequences of TAIR10 using Tophat software. The gene expression levels were measured in RPKM, and many critical genes regulated by AtPRMT5 were identified to be involved in shoot regeneration.
2017-06-18 | E-MTAB-5044 | biostudies-arrayexpress
Project description:The capacity of plant regeneration in different ecotypes of Arabidopsis largely varies. However, the mechanism underlying this process remains exclusive. Here, we identified a critical thioredoxin gene DCC1 in determining natural variation for shoot regeneration in Arabidopsis. Functional loss of DCC1 resulted in the repression of shoot regeneration. DCC1 encodes a thioredoxin, which was localized in mitochondria. DCC1 directly interacted with CARBONIC ANHYDRASE 2 (CA2) to regulate the mitochondrial respiratory complex activity and mediate the Reactive Oxygen Species (ROS) level. Defects of DCC1 or CA2 caused the increased ROS level. To understand the regulatory mechanism of DCC1-mediated ROS in shoot regeneration, we analyzed the transcript levels of wild type Col-0 and the mutant dcc1 calli during shoot regeneration by RNA-seq. Three biological repeats of wild type Co-0 and the mutant dcc1 calli were used for RNA sequencing. Total RNAs were isolated from the calli of wild type Col-0 and the mutant dcc1 cultured on shoot-induction medium. The RNA-seq was performed using the Illumina Hiseq 2500. The raw reads were aligned to the genome sequences of TAIR10 using Tophat2 software. The gene expression levels were measured in FPKM, and many critical genes were identified to be involved in shoot regeneration.
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Project description:De novo shoot regeneration is an essential step for massive propagation and genetic engineering of elite germplasm in forestry. Poplar that is a fast growth tree species have a very important ecologically and economically role around the world, especially in China. In this study, we found that PtWOX11 that is a homologue of AtWOX11 not only involved de novo root formation but also promote de novo shoot regeneration in poplar. We demonstrated that PtWOX11 can enhance callus regeneration competence and shoot regeneration during two-step de novo shoot regeneration. Furthermore, by using RNA-seq and qPCR, we uncovered that during callus induction stage PtWOX11 activates PtPLTs expression to promote callus formation and regeneration competence, and promote PtCUC2/3, PtWUSa and PtSTM transcription to fulfil shoot organogenesis during shoot regeneration stage. Overall, our data indicated that PtWOX11 play a new function and transcriptional regulation mechanism on de novo shoot regeneration in poplar.
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Project description:Previous studies of zebrafish caudal fin regeneration have shown that multiple genetic programs are moduled through regulatory factors. MicroRNAs are short highly conserved non-coding genes that suppress expression of target genes and thereby control multiple genetic programs. Given their important regulatory roles and evolutionary conservation, we hypothesize that microRNAs define a conserved genetic regulatory circuit important for appendage regeneration. We characterized microRNA expression during zebrafish caudal fin regeneration using small RNA sequencing. The stages of caudal fin regeneration were assayed for mRNA expression using mRNA sequencing. Small RNA and mRNA gene expression profiling during 0 and 4 days post amputation.
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Project description:Cyclin-dependent kinases (CDKs) are key regulators of the cell cycle or transcription, and are emerging as promising therapeutic targets in cancer cells. The transcriptional kinase, CDK12, is especially intriguing, as it modulates transcription elongation by phosphorylating the carboxy-terminal domain (CTD) of RNA polymerase (Pol II) with subsequent effects on expression of DNA damage response (DDR) genes. Yet the exact mechanism by which CDK12 regulates this vital process remains unclear. Using the selective inhibitor of CDK12/13, THZ5317 and transient transcriptome sequencing (TT-seq), we sought to capture the dynamic transcriptional changes linked to CDK12 by analyzing the immediate, early effects on nascent RNA production after CDK12 depletion in neuroblastoma (NB) cells. CDK12-induced inhibition resulted in gene length-dependent defects in transcription elongation, leading to a disproportionate loss of 3' reads in long genes. Short transcripts, by contrast, including those of replication-dependent histone genes, underwent 3' UTR extension. The effect on long genes was accompanied by premature cleavage and polyadenylation (PCPA), followed by early termination and loss of gene expression. DDR gene transcripts were the most prominent among those terminated by PCPA. Phosphoproteomic analysis indicated that pre-mRNA processing factors, including those involved in CPA , are direct phospho-targets of CDK12 and that CDK depletion phenocopied their effects on transcription. Importantly, sensitivity to CDK12 inhibition was predicted by a lower proportion of U1 snRNP binding sites compared to polyadenylation sites (PAS) and hence a higher propensity to intronic poly(A) site selection - a characteristic observed in most DDR genes. These results support a model in which CDK12 regulates expression of DDR genes not only by regulating transcription elongation through its effects on Pol II CTD phosphorylation, but also through direct phosphorylation of pre-mRNA processing factors. These mechanistic insights may enable the development of new anti-cancer strategies targeting multiple vulnerable steps in CDK12-dependent regulation of DNA damage repair.
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