This SuperSeries is composed of the SubSeries listed below.
Metabolic pathway profiling of mitochondrial respiratory chain mutants in C. elegans.
No sample metadata fields
View SamplesUtilizing C. elegans as a model of mitochondrial dysfunction provides insight into cellular adaptations which occur as a consequence of genetic alterations causative of human disease. We characterized genome-wide expression profiles of hypomorhpic C. elegans mutants in nuclear-encoded subunits of respiratory chain complexes I, II and III.
Metabolic pathway profiling of mitochondrial respiratory chain mutants in C. elegans.
No sample metadata fields
View SamplesUtilizing C. elegans as a model of mitochondrial dysfunction provides insight into cellular adaptations which occur as a consequence of genetic alterations causative of human disease. We characterized genome-wide expression profiles of hypomorphic C. ele
Metabolic pathway profiling of mitochondrial respiratory chain mutants in C. elegans.
No sample metadata fields
View SamplesWe transformed Populus trichocarpa and generated transgenics with knockdown or overexpression of monolignol genes and transcription factors Overall design: RNAseq of xylem tissue of transgenic and wildtype Populus trichocarpa. 378 samples.
Modeling cross-regulatory influences on monolignol transcripts and proteins under single and combinatorial gene knockdowns in Populus trichocarpa.
Specimen part, Subject
View SamplesWe focused on RNA-seq-based full transcriptome responses to PtrSND1-B1 overexpression at 7, 12, and 25 h in stem defferentiating xylem (SDX) protoplasts Overall design: We transfected PtrSND1-B1 and sGFP into stem differentiating xylem protoplasts and performed RNA-seq to reveal the whole transcriptome.
SND1 transcription factor-directed quantitative functional hierarchical genetic regulatory network in wood formation in Populus trichocarpa.
Specimen part, Subject
View SamplesWe used the stem cross-sections of P. trichocarpa and our recently developed laser capture microdissection (LCM) to collect fibers, vessels, and a combination of 3 cell types (fibers + vessels + rays). Total RNA from the three samples was isolated, amplified, and analyzed by full-transcriptome RNA-sequencing. The sequencing reads were mapped to the P. trichocarpa genome. Overall design: Different major tissues (shoot tip, leaf, phloem, primary root, stem differentiating xylem) and xylem tissue cell types (fiber, vessel, ray cells) were analyzed by RNA-seq.
Hierarchical Transcription Factor and Chromatin Binding Network for Wood Formation in Black Cottonwood (<i>Populus trichocarpa</i>).
Age, Specimen part, Subject
View SamplesPosttranscriptional regulation of mRNA levels in neutrophils and its consequences for immune responses are unexplored. By employing profiling of the neutrophil transcriptome we show that the mRNA-destabilizing protein tristetraprolin (TTP) limits the expression of hundreds of genes, including genes negatively regulating apoptosis. Elicited TTP-deficient neutrophils exhibited reduced apoptosis and were increased in numbers. The anti-apoptotic protein Mcl-1 was elevated in TTP-deficient neutrophils and Mcl1 mRNA was bound and destabilized by TTP. Ablation of TTP in macrophages and neutrophils resulted in an improved defense and survival of mice during invasive infection with Streptococcus pyogenes. Mice lacking myeloid TTP prevented dissemination of bacteria and efficiently blunted systemic disease by massive but controlled neutrophil deployment. These data identify posttranscriptional control by TTP to restrict neutrophils and antimicrobial defense. Overall design: WT and TTPKO peritoneal neutrophils stimulated with LPS for 4 h. Each condition analyzed in three replicates
The RNA-binding protein tristetraprolin schedules apoptosis of pathogen-engaged neutrophils during bacterial infection.
Subject
View SamplesPrecise control of mRNA decay is fundamental for robust yet not exaggerated inflammatory responses to pathogens. Parameters determining the specificity and extent of mRNA degradation within the entire inflammation-associated transcriptome remain incompletely understood. Using transcriptome-wide high resolution occupancy assessment of the mRNA-destabilizing protein TTP, a major inflammation-limiting factor, we qualitatively and quantitatively characterize TTP binding positions and functionally relate them to TTP-dependent mRNA decay in immunostimulated macrophages. We identify pervasive TTP binding with incompletely penetrant linkage to mRNA destabilization. A necessary but not sufficient feature of TTP-mediated mRNA destabilization is binding to 3’ untranslated regions (UTRs). Mapping of binding positions of the mRNA-stabilizing protein HuR in activated macrophages revealed that TTP and HuR binding sites in 3’ UTRs occur mostly in different transcripts implicating only a limited co-regulation of inflammatory mRNAs by these proteins. Remarkably, we identify robust and widespread TTP binding to introns of stable transcripts. Nuclear TTP is associated with spliced-out introns and maintained in the nucleus throughout the inflammatory response. Our study establishes a functional annotation of binding positions dictating TTP-dependent mRNA decay in immunostimulated macrophages. The findings allow navigating the transcriptome-wide landscape of RNA elements controlling inflammation. Overall design: Experiment comparing RNA decay rates in WT and TTP-/- macrophages at LPS 3 h and 6 h. Transcription was blocked with actinomycin D for 0, 45 or 90 min. Decay rates was calculated using linear model.
Tristetraprolin binding site atlas in the macrophage transcriptome reveals a switch for inflammation resolution.
Specimen part, Cell line, Subject, Time
View SamplesPrecise control of mRNA decay is fundamental for robust yet not exaggerated inflammatory responses to pathogens. Parameters determining the specificity and extent of mRNA degradation within the entire inflammation-associated transcriptome remain incompletely understood. Using transcriptome-wide high resolution occupancy assessment of the mRNA-destabilizing protein TTP, a major inflammation-limiting factor, we qualitatively and quantitatively characterize TTP binding positions and functionally relate them to TTP-dependent mRNA decay in immunostimulated macrophages. We identify pervasive TTP binding with incompletely penetrant linkage to mRNA destabilization. A necessary but not sufficient feature of TTP-mediated mRNA destabilization is binding to 3’ untranslated regions (UTRs). Mapping of binding positions of the mRNA-stabilizing protein HuR in activated macrophages revealed that TTP and HuR binding sites in 3’ UTRs occur mostly in different transcripts implicating only a limited co-regulation of inflammatory mRNAs by these proteins. Remarkably, we identify robust and widespread TTP binding to introns of stable transcripts. Nuclear TTP is associated with spliced-out introns and maintained in the nucleus throughout the inflammatory response. Our study establishes a functional annotation of binding positions dictating TTP-dependent mRNA decay in immunostimulated macrophages. The findings allow navigating the transcriptome-wide landscape of RNA elements controlling inflammation. Overall design: RNA-Seq of RNA isolated from murine bone marrow derived macrophages (WT or TTP-deficient) stimulated for 6 h with LPS
Tristetraprolin binding site atlas in the macrophage transcriptome reveals a switch for inflammation resolution.
No sample metadata fields
View SamplesAccute stretch and tachycardia are capable of inducing pathological excitation transcription coupling - an early invent before structural cardiac remodeling which transitions to heart failure. The sodium calcium exchanger is a key player in maintaining calcium homeostasis and is implicated in pathological signaling during heart failure.
The role of stretch, tachycardia and sodium-calcium exchanger in induction of early cardiac remodelling.
Specimen part, Treatment
View Samples