Effect of either FLO8 or MSS11 deletion and -overexpression on yeast transcript profiles compared to wild type in laboratory yeast strains 1278b and S288c - also the effect of FLO11 (MUC1) overexpression in the 1278b genetic background
Many Saccharomyces cerevisiae Cell Wall Protein Encoding Genes Are Coregulated by Mss11, but Cellular Adhesion Phenotypes Appear Only Flo Protein Dependent.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
PHABULOSA Mediates an Auxin Signaling Loop to Regulate Vascular Patterning in Arabidopsis.
Specimen part
View SamplesThe class III HD-ZIPtranscription factors regulate vascular patterning in Arabidopsis thaliana roots. In this expression study we compare the expression profile in root tips upon miR165 induction, after 6h, 10h and 24h. The results are presented in PHABULOSA mediates an auxin signaling loop to regulate vascular patterning in Arabidopsis by Christina Joy Mller, Ana Elisa Valds, Guodong Wang, Prashanth Ramachandran, Lisa Beste, Daniel Uddenberg, and Annelie Carlsbecker, accepted for publication in Plant Physiology Nov. 2015.
PHABULOSA Mediates an Auxin Signaling Loop to Regulate Vascular Patterning in Arabidopsis.
Specimen part
View SamplesThe class III HD-ZIP transcription factors regulate vascular patterning in Arabidopsis thaliana roots. In this expression study we compare the expression profile of the cna-2 phb-13 phv-11 and cna-2 phb-13 phv-11 rev-6 mutants to their wild type. The results are presented in PHABULOSA mediates an auxin signaling loop to regulate vascular patterning in Arabidopsis by Christina Joy Mller, Ana Elisa Valds, Guodong Wang, Prashanth Ramachandran, Lisa Beste, Daniel Uddenberg, and Annelie Carlsbecker, accepted for publication in Plant Physiology Nov. 2015.
PHABULOSA Mediates an Auxin Signaling Loop to Regulate Vascular Patterning in Arabidopsis.
No sample metadata fields
View SamplesThe class III HD-ZIP transcription factors regulate vascular patterning in Arabidopsis thaliana roots. In this expression study we compare the expression profile of the athb8 cna phb phv quadruple mutant to its wild type. The results are presented in PHABULOSA mediates an auxin signaling loop to regulate vascular patterning in Arabidopsis by Christina Joy Mller, Ana Elisa Valds, Guodong Wang, Prashanth Ramachandran, Lisa Beste, Daniel Uddenberg, and Annelie Carlsbecker, accepted for publication in Plant Physiology Nov. 2015.
PHABULOSA Mediates an Auxin Signaling Loop to Regulate Vascular Patterning in Arabidopsis.
No sample metadata fields
View SamplesChromosomal instability in early cancer stages is caused by stress on DNA replication. The molecular basis for replication perturbation in this context is currently unknown. We studied the replication dynamics in cells in which a regulator of S-phase entry and cell proliferation, the Rb-E2F pathway, is aberrantly activated. Aberrant activation of this pathway by HPV-16 E6/E7 or cyclin E oncogenes, significantly decreased the cellular nucleotide levels in the newly transformed cells. Exogenously supplied nucleosides rescued the replication stress and DNA damage, and dramatically decreased oncogene-induced transformation. Increased transcription of nucleotide biosynthesis genes, mediated by expressing the transcription factor c-Myc, increased the nucleotide pool and also rescued the replication-induced DNA damage. Our results suggest a model for early oncogenesis in which uncoordinated activation of factors regulating cell proliferation leads to insufficient nucleotides that fail to support normal replication and genome stability.
Nucleotide deficiency promotes genomic instability in early stages of cancer development.
Sex, Specimen part
View SamplesAcetate, propionate and butyrate are the main short-chain fatty acids (SCFAs) that arise from the fermentation of fibers by the colonic microbiota. While many studies focus on the regulatory role of SCFAs, their quantitative role as a catabolic or anabolic substrate for the host has received relatively little attention. To investigate this aspect, we infused conscious mice with physiological quantities of stable isotopes [1-13C]acetate, [2-13C]propionate or [2,4-13C2]butyrate directly into the cecum, which is the natural production site in mice, and analyzed their interconversion by the microbiota as well as their metabolism by the host. Cecal interconversion - pointing to microbial cross-feeding - was high between acetate and butyrate, low between butyrate and propionate and almost absent between acetate and propionate. As much as 62% of infused propionate was used in whole-body glucose production, in line with its role as gluconeogenic substrate. Conversely, glucose synthesis from propionate accounted for 69% of total glucose production. The synthesis of palmitate and cholesterol in the liver was high from cecal acetate (2.8% and 0.7%, respectively) and butyrate (2.7% and 0.9%, respectively) as substrates, but low or absent from propionate (0.6% and 0.0%, respectively). Label incorporation due to chain elongation of stearate was approximately 8-fold higher than de novo synthesis of stearate. Microarray data suggested that SCFAs exert only a mild regulatory effect on the expression of genes involved in hepatic metabolic pathways during the 6h infusion period. Altogether, gut-derived acetate, propionate and butyrate play important roles as substrates for glucose, cholesterol and lipid metabolism.
Gut-derived short-chain fatty acids are vividly assimilated into host carbohydrates and lipids.
Sex, Specimen part, Treatment
View SamplesThe FBXL10 protein (also known as KDM2B, JHDM1B, CXXC2, and NDY1) is bound to essentially all CpG-rich promoters in the mammalian genome. FBXL10 is expressed as two isoforms: FBXL10-1, a longer form that contains an N-terminal JmjC domain with C- terminal F-box, CXXC, PHD, RING, and leucine rich repeat (LRR) domains, and FBXL10-2, a shorter form that initiates at an alternative internal exon and which lacks the JmjC domain but retains the other domains. Selective deletion of Fbxl10-1 had been reported to produce a minor and variable phenotype, and most mutant animals were essentially normal. We show here that deletion of Fbxl10-2 (in a manner that does not perturb expression of Fbxl10-1) resulted in a very different phenotype with craniofacial abnormalities, greatly increased lethality, and female sterility in surviving homozygous mutants. The phenotype of the Fbxl10-2 deletion was more severe in female mutants. We found that mutants that lacked both FBXL10-1 and -2 showed embryonic lethality and even more extreme sexual dimorphism, with more severe gene dysregulation in mutant female embryos. X-linked genes were most severely dysregulated, and there was marked overexpression of Xist in mutant females although genes that encode factors that bind to Xist RNA were globally down-regulated in mutant female as compared to male embryos. FBXL10 is the first factor shown to be required both for the normal expression and function of the Xist gene. Overall design: Expression analysis using RNA-seq was performed on WT and Fbxl10T/T male and female embryos.
Abnormal X chromosome inactivation and sex-specific gene dysregulation after ablation of FBXL10.
Sex, Specimen part, Cell line, Subject
View SamplesWe report RNA-sequencing data of 80 tumor-educated blood platelet (TEP) samples isolated from 39 patients with lower-grade glioma (LGG) and 41 healthy donors (HD). This dataset can be employed as input for the thromboSeq source code (available via GitHub: https://github.com/MyronBest/) to reproduce the thromboSeq drylab pipeline. Overall design: Blood platelets were isolated from whole blood in purple-cap BD Vacutainers containing EDTA anti-coagulant by standard centrifugation. Total RNA was extracted from the platelet pellet, subjected to cDNA synthesis and SMARTer amplification, fragmented by Covaris shearing, and prepared for sequencing using the Truseq Nano DNA Sample Preparation Kit. Subsequently, pooled sample libraries were sequenced on the Illumina Hiseq 2500 platform. All steps were quality-controlled using Bioanalyzer 2100 with RNA 6000 Picochip, DNA 7500 and DNA High Sensitivity chips measurements. For further downstream analyses, reads were quality-controlled using Trimmomatic, mapped to the humane reference genome using STAR, and intron-spanning reads were summarized using HTSeq.
RNA sequencing and swarm intelligence-enhanced classification algorithm development for blood-based disease diagnostics using spliced blood platelet RNA.
Specimen part, Disease stage, Subject
View SamplesCD8+ T cells play a crucial role in the clearance of intracellular pathogens through the generation of cytotoxic effector cells that eliminate infected cells and long-lived memory cells that provide enhanced protection against reinfection. We have previously shown that the inhibitor of E protein transcription factors, Id2, is necessary for accumulation of effector and memory CD8+ T cells during infection. Here we show that CD8+ T cells lacking Id2 did not generate a robust terminally-differentiated KLRG1hi effector population, but displayed a cell-surface phenotype and cytokine profile consistent with memory precursors, raising the question as to whether loss of Id2 impairs the differentiation and/or survival of effector-memory cells. We found that deletion of Bim rescued Id2-deficient CD8+ cell survival during infection. However, the dramatic reduction in KLRG1hi cells caused by loss of Id2 remained in the absence of Bim, such that Id2/Bim double-deficient cells form an exclusively KLRG1loCD127hi memory precursor population. Thus we describe a role for Id2 in both the survival and differentation of normal CD8+ effector and memory populations.
Id2 influences differentiation of killer cell lectin-like receptor G1(hi) short-lived CD8+ effector T cells.
Specimen part
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