Plants have evolved shoot elongation mechanisms to escape from diverse environmental stresses such as flooding and vegetative shade. The apparent similarity in growth responses suggests possible convergence of the signalling pathways. Shoot elongation is mediated by passive ethylene accumulating in flooded plant organs and by changes in light quality and quantity under vegetation shade. Here we study hypocotyl elongation as a proxy for shoot elongation and delineated Arabidopsis hypocotyl length kinetics in response to ethylene and shade. Based on these kinetics, we further investigated ethylene and shade-induced genome-wide gene expression changes in hypocotyls and cotyledons separately. Both treatments induced a more extensive transcriptome reconfiguration in the hypocotyls compared to the cotyledons. Bioinformatics analyses suggested contrasting regulation of growth promotion- and photosynthesis-related genes. These analyses also suggested an induction of auxin, brassinosteroid and gibberellin signatures and the involvement of several candidate regulators in the elongating hypocotyls. Pharmacological and mutant analyses confirmed the functional involvement of several of these candidate genes and physiological control points in regulating stress-escape responses to different environmental stimuli. We discuss how these signaling networks might be integrated and conclude that plants, when facing different stresses, utilise a conserved set of transcriptionally regulated genes to modulate and fine tune growth.
Ethylene- and Shade-Induced Hypocotyl Elongation Share Transcriptome Patterns and Functional Regulators.
Specimen part, Treatment, Time
View SamplesThis study profiles transcriptomic changes of Arabidopsis thaliana Col-0 in response to submergence. This dataset includes CEL files, RMA signal values and MAS5 P/M/A calls from total mRNA populations of plants at 9 to 10 leaf rosette stage. Biological replicates of root and shoot tissues were harvested after 7 h and 24 h of submergence in darkness along with corresponding non-submerged dark controls. To characterize the dark response, non-submerged light controls plants were harvested at the 0 h time point. Quantitative profiling of cellular mRNAs was accomplished with the Affymetrix ATH1 platform. Changes in the transcriptome in response to submergence and early darkness were evaluated, and the data led to identification of genes co-regulated at the conditional and organ-specific level.
Molecular characterization of the submergence response of the Arabidopsis thaliana ecotype Columbia.
Specimen part, Treatment
View SamplesGrowth in dense stands induces shade avoidance responses. Early responses to neighbors seem to be assoctaed with touch, not light signalling.
Plant neighbor detection through touching leaf tips precedes phytochrome signals.
Specimen part
View SamplesIn rice (Oryza sativa L.), the haplotype at the multigenic SUBMERGENCE 1 (SUB1) locus determines survival of prolonged submergence. SUB1 encodes two or three group VII Ethylene Response Factor (ERF) family transcription factors, SUB1A, SUB1B and SUB1C. A highly submergence-inducible SUB1A allele is present in lines that are submergence tolerant. This gene is the determinant of submergence tolerance. Here, the heterologous ectopic expression of rice SUB1A and SUB1C in Arabidopsis thaliana was employed to assess the transcriptional network mobilized by ectopic expression of SUB1A and SUB1C.
Expression of rice SUB1A and SUB1C transcription factors in Arabidopsis uncovers flowering inhibition as a submergence tolerance mechanism.
Specimen part
View SamplesIn this study we analyzed the effect of overexpression of an HA-tagged version of the ERF RAP2.12 on the transcriptome levels in aerobic and hypoxic-treated (O2 21% and 1%, respectively) Arabidopsis thaliana rosettes.
Oxygen sensing in plants is mediated by an N-end rule pathway for protein destabilization.
Treatment
View SamplesLow R:FR signaling through phytochromes induces shade avoidance responses, including petiole elongation. Salicylic acid-mediated defense against pathogens is inhibited under these conditions.
Perception of low red:far-red ratio compromises both salicylic acid- and jasmonic acid-dependent pathogen defences in Arabidopsis.
Age, Specimen part, Treatment
View SamplesIn this study we studied the presence of tumor cells that underwent epithelial-to-mesenchymal transition within polyoma middle T antigen (PyMT) breast tumors. For this we dissociated tumors and isolated Ecad positive tumor cells by FACS sorting. We confirmed that PyMT tumors contain a small set of tumor cells that have undergone EMT in the primary tumor and that E-cadherin can be used as a marker on single cell level for mesenchymal status in this model. Overall design: (i) We isolated primary tumors from mice, dissociated the tumors and FACS-sorted for single Ecad positive tumor cells, after this we performed single cell sequencing of the cells. (ii) We isolated CTCs and solid tumor cells from mice, dissociated the tumors and FACS-sorted for single Ecad positive and negative cells, after this we performed single cell sequencing of the cells.
Plasticity between Epithelial and Mesenchymal States Unlinks EMT from Metastasis-Enhancing Stem Cell Capacity.
Specimen part, Subject
View SamplesThe polycomb repressive complex 2 (PRC2) regulates epigenetic gene repression in eukaryotes. Mechanisms controlling its developmental specificity and signal-responsiveness are poorly understood. Here, we identify an oxygen-sensitive N-terminal (N-) degron in the plant PRC2 subunit VERNALIZATION(VRN)2, a homolog of animal Su(z)12, that promotes its degradation via the N-end rule pathway. We provide evidence that this N-degron arose early during angiosperm evolution via gene duplication and N-terminal truncation, facilitating expansion of PRC2 function in flowering plants. We show that proteolysis via the N-end rule pathway prevents ectopic VRN2 accumulation, and that hypoxia and long-term cold exposure lead to increased VRN2 abundance, which we propose may be due to inhibition of VRN2 turnover via its N-degron. Furthermore, we identify an overlap in the transcriptional responses to hypoxia and prolonged cold, and show that VRN2 promotes tolerance to hypoxia. Our work reveals a mechanism for post-translational regulation of VRN2 stability that could potentially link environmental inputs to the epigenetic control of plant development. Overall design: RNA was extracted from non-vernalized (0v; C) or 4 week vernalized (4v; V) seedlings. Three biological replicates for each treatment were used for subsequent RNA sequencing
Oxygen-dependent proteolysis regulates the stability of angiosperm polycomb repressive complex 2 subunit VERNALIZATION 2.
Specimen part, Treatment, Subject
View SamplesThe therapeutic landscape of melanoma is rapidly changing. While targeted inhibitors yield significant responses, their clinical benefit is often limited by the early onset of drug resistance. This motivates the pursuit to establish more durable clinical responses, by developing combinatorial therapies. But while potential new combinatorial targets steadily increase in numbers, they cannot possibly all be tested in patients. Similarly, while genetically engineered mouse melanoma models have great merit, they do not capture the enormous genetic diversity and heterogeneity typical in human melanoma. Furthermore, whereas in vitro studies have many advantages, they lack the presence of micro-environmental factors, which can have a profound impact on tumor progression and therapy response. This prompted us to develop an in vivo model for human melanoma that allows for studying the dynamics of tumor progression and drug response, with concurrent evaluation and optimization of new treatment regimens. Here, we present a collection of patient-derived xenografts (PDX), derived from BRAFV600E, NRASQ61 or BRAFWT/NRASWT melanoma metastases. The BRAFV600E PDX melanomas were acquired both prior to treatment with the BRAF inhibitor vemurafenib and after resistance had occurred, including six matched pairs. We find that PDX resemble their human donors’ melanomas regarding biomarkers, chromosomal aberrations, RNA expression profiles, mutational spectrum and targeted drug resistance patterns. Mutations, previously identified to cause resistance to BRAF inhibitors, are captured in PDX derived from resistant melanomThis melanoma PDX platform represents a comprehensive public resource to study both fundamental and translational aspects of melanoma progression and treatment in a physiologically relevant setting. Overall design: RNA sequencing of 4 melanoma PDX samples to validate the effects of a structural variant on BRAF mRNA in BRAF inhibitor resistant melanoma.
BRAF(V600E) Kinase Domain Duplication Identified in Therapy-Refractory Melanoma Patient-Derived Xenografts.
No sample metadata fields
View SamplesWe used microarrays to find Stat6 dependent genes in control and IL-4 exposed bone marrow derived macrophages.
Alternatively activated macrophages inhibit T-cell proliferation by Stat6-dependent expression of PD-L2.
Specimen part
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