Plants typically contain two different types of cell walls: a primary wall that is being deposited around all growing cells, and a secondary wall that is produced in cells with specialized functions once they have ceased to grow. In Arabidopsis, VND7 is a transcription factor that is sufficient to activate secondary cell wall synthesis. To artificially turn on the secondary cell wall synthesis, VND7 was fused to the activation domain of the herpes virus VP16 protein and the glucocorticoid receptor (GR) domain. Thus, the transgenic plants harbouring the constructs can then be treated with dexamethasone (DEX), a glucocorticoid derivative, to induce the secondary cell wall formation.
A Transcriptional and Metabolic Framework for Secondary Wall Formation in Arabidopsis.
Specimen part, Treatment
View SamplesAlternative polyadenylation has been implicated as an important regulator of gene expression. In some cases, alternative polyadenylation is known to couple with alternative splicing to influence last intron removal. However, it is unknown whether alternative polyadenylation events influence alternative splicing decisions at upstream exons. Knockdown of the polyadenylation factors CFIm25 or CstF64 was used as an approach in identifying alternative polyadenylation and alternative splicing events on a genome-wide scale. Although hundreds of alternative splicing events were found to be differentially spliced in the knockdown of CstF64, genes associated with alternative polyadenylation did not exhibit an increased incidence of alternative splicing. These results demonstrate that the coupling between alternative polyadenylation and alternative splicing is usually limited to defining the last exon. The striking influence of CstF64 knockdown on alternative splicing can be explained through its effects on UTR selection of known splicing regulators such as hnRNP A2/B1, thereby indirectly influencing splice site selection. We conclude that changes in the expression of the polyadenylation factor CstF64 influences alternative splicing through indirect effects. Overall design: HeLa cell line was stably transfected with shRNA plasmids targeting CstF64. Total RNA was isolated from CstF64 KD cells and wild-type control cells using Trizol according to manufacturer’s protocols. Samples were deep sequenced in duplicate using the Illumina GAIIx system.
Coupling between alternative polyadenylation and alternative splicing is limited to terminal introns.
No sample metadata fields
View SamplesThe lncRNA LOC100130476 (named as WAKMAR2) was found to be down-regulated in epidermal keratinocytes in human chronic non-healing wounds compared to normal acute wounds and the intact skin. However, its biological role in keratinocytes during wound repair has not been studied.
WAKMAR2, a Long Noncoding RNA Downregulated in Human Chronic Wounds, Modulates Keratinocyte Motility and Production of Inflammatory Chemokines.
Specimen part
View SamplesGene expression in larval, early third instar eye-antenna discs was assessed to reveal an ATF4 contribution to target gene induction following COX7a knockdown. As hypothesised, these COX7a-RNAi induced target genes require the transcription factor ATF4 for induction, irrespective of concomitant Notch pathway activation through Delta over-expression.
ATF4-Induced Warburg Metabolism Drives Over-Proliferation in Drosophila.
No sample metadata fields
View SamplesGene expression in larval, early third instar eye-antenna discs was assesed in genotypes with Notch Gain-of-Function (UAS-Delta or UAS-Notch[intra2]) over-expression or mitochondrial COX7a Loss-of-function (UAS-COX7a-RNAi) or a combination of both (UAS-Delta, UAS-COX7a-RNAi). The analysis revealed that, despite a strong genetic interaction between Notch pathway activation and knockdown of COX7a, no transcriptional cooperation or synergy was detectable in early L3 eye-antenna discs. Rather, COX7a knockdown induced a unique transcriptional signature, which further experiments revealed to be mediated by the transcription factor ATF4.
ATF4-Induced Warburg Metabolism Drives Over-Proliferation in Drosophila.
No sample metadata fields
View SamplesUnsupervised hierarchical clustering revealed a strong similarity in gene modulation resulting from either compound treatment or BRAF ablation mediated by RNA interference relative to DMSO-treated control samples .
Antitumor efficacy of the novel RAF inhibitor GDC-0879 is predicted by BRAFV600E mutational status and sustained extracellular signal-regulated kinase/mitogen-activated protein kinase pathway suppression.
No sample metadata fields
View SamplesCoilin iCLIP data revealed 42 novel human snoRNAs of intronic origin. To validate their expression and estimate abundance of novel and annotated snoRNAs, we performed RNA-seq on polyA- and rRNA-depleted RNA isolated from HeLa cells. Results show that expression of novel snoRNAs is comparable to the previously annotated snoRNAs. Overall design: 1 replicate of RNA depleted of polyA and ribosomal RNA.
The coilin interactome identifies hundreds of small noncoding RNAs that traffic through Cajal bodies.
No sample metadata fields
View SamplesAnalysis of differences in gene expression between different cell types of the vascular niche. Looking for candidates, that could potentially be up-or downregualted in the different cell types
Pericyte-expressed Tie2 controls angiogenesis and vessel maturation.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Loss of Lkb1 and Pten leads to lung squamous cell carcinoma with elevated PD-L1 expression.
Specimen part
View SamplesLung squamous cell carcinoma (SCC) is a deadly disease for which current treatments are inadequate. We demonstrate that bi-allelic inactivation of Lkb1 and Pten in the mouse lung led to SCC that recapitulated the histology, gene expression and microenvironment found in human disease. Lkb1/Pten-null (LP) tumors expressed the squamous markers Krt5, p63 and Sox2, and transcriptionally resembled the basal subtype of human SCC. In contrast to mouse adenocarcinomas, the LP tumors contained immune populations enriched for tumor-associated neutrophils. Sca1+/Ngfr+ fractions were enriched for tumor propagating cells (TPCs) that could serially transplant the disease in orthotopic assays. TPCs in the LP model and Ngfr+ cells in human SCCs highly expressed Pdl1, suggesting a novel mechanism of immune escape for TPCs.
Loss of Lkb1 and Pten leads to lung squamous cell carcinoma with elevated PD-L1 expression.
Specimen part
View Samples