Identification of genes differentially expressed in roots of Arabidopsis Col-0 and ndr1-1 mutants 48 h post inoculation with the fungal pathogen Verticillium longisporum.
Susceptibility to Verticillium longisporum is linked to monoterpene production by TPS23/27 in Arabidopsis.
Age, Specimen part, Time
View SamplesComparison of BOLITA mutant leaves (gain-of-function mutant) vs. wild type leaves, grown in the same conditions. The BOLITA (BOL) gene (At1g24590), an AP2/ERF transcription factor, was characterized with the help of an activation tag mutant and overexpression lines in Arabidopsis and tobacco. The leaf size of plants overexpressing BOL was smaller than wild type plants due to a reduction in both cell size and cell number. Moreover, severe overexpressors showed ectopic callus formation in roots. Accordingly, global gene expression analysis using the overexpression mutant reflected the alterations in cell proliferation, differentiation and growth through expression changes in RBR, CYCD, and TCP genes, as well as genes involved in cell expansion (i.e. expansins and the actin remodeling factor ADF5). Furthermore, the expression of hormone signaling (i.e. auxin and cytokinin), biosynthesis (i.e. ethylene and jasmonic acid) and regulatory genes was found to be perturbed in bol-D mutant leaves. The gene is expressed at the shoot apical meristem, and more intensely at leaf primordia. It is also expressed at very young leaves, and flower buds. The gene is closely related to DORNROSCHEN.
BOLITA, an Arabidopsis AP2/ERF-like transcription factor that affects cell expansion and proliferation/differentiation pathways.
Age, Specimen part
View SamplesRNA was purified from lung tissue and isolated Alveolar type II cells. The "SAMPLE_ID" sample description is a sample identifier internal to Genentech. The ID of this project in Genentech''s ExpressionPlot database is PRJ0007671 Overall design: RNA from lung and Alveolar type II cells of the following mutant mice: (1) SpcCreERT2;RosatdTomato n=5 ; (2) SpcCreERT2;RosatdTomato;Etv5ko/loxp n= 5
Transcription factor Etv5 is essential for the maintenance of alveolar type II cells.
Specimen part, Subject
View SamplesRNA was purified from lung tissue and isolated Alveolar type II cells. The "SAMPLE_ID" sample description is a sample identifier internal to Genentech. The ID of this project in Genentech''s ExpressionPlot database is PRJ0005064 Overall design: RNA from lung and Alveolar type II cells of the following mutant mice: (1) KRaswt/d12;RosaCreERT2 n=4 (2) KRaswt/d12; Etv5loxp/loxp;RosaCreERT2 n=4 (3) KRaswt/d12; Etv4KO/KO; Etv5loxp/loxp;RosaCreERT2 n=4
Transcription factor Etv5 is essential for the maintenance of alveolar type II cells.
Specimen part, Subject
View SamplesCytoplasmic DNA triggers the activation of the innate immune system. While downstream signaling components have been characterized, the DNA sensing components remain largely elusive. We performed a systematic proteomics screen for proteins that associate with DNA, traversed to a screen for IFN--induced transcripts. We identified DSIRE (DNA sensor for the IL-1 response, previously called AIM2) as a candidate cytoplasmic sensor. DSIRE showed a marked selectivity for double-stranded DNA. DSIRE can recruit the inflammasome adaptor ASC and gets redistributed to ASC speckles upon coexpression of ASC. RNAi-mediated reduction of DSIRE expression led to an impairment in IL-1 maturation. Reconstitution of unresponsive cells with DSIRE, ASC, caspase 1 and IL-1 showed that DSIRE is sufficient for inflammasome activation. Overall, our data strongly suggest that DSIRE is a cytoplasmic DNA sensor for the inflammasome.
An orthogonal proteomic-genomic screen identifies AIM2 as a cytoplasmic DNA sensor for the inflammasome.
No sample metadata fields
View SamplesIdentify genes which are differentially expressed in ?Cop1ß compared to control islets and are also signficantly rescued in ?Cop1? ?ETV1/4/5ß Overall design: Islets were harvested from 5 biological replicates of the followig genotypes: Control, ?Cop1ß and ?Cop1? ?ETV1/4/5ß. Islets were individually handpicked and total RNA was isolated and purified for library preperation and Next Generation Sequencing.
β-Cell Insulin Secretion Requires the Ubiquitin Ligase COP1.
No sample metadata fields
View SamplesWe performed whole transcriptome profiling on sorted tissue macrophages from the spleen or from visceral adipose tissue (VAT) of wild-type mice that are 3-month or 24-month of age or from 24-month Nlrp3-/- mice Overall design: Profiles were generated on fluorescence-activated-cells (FACs) sorted F480+CD11b+ cells from spleen or adipose tissue, using sequencing analysis
Inflammasome-driven catecholamine catabolism in macrophages blunts lipolysis during ageing.
Sex, Age, Specimen part, Subject
View SamplesRIPK4 but not the related kinases RIPK1, RIPK2, and RIPK3 caused similar transcriptional changes to Wnt3a. Overall design: PA1 cells were transfected by 8ug RIPK1, RIPK2, RIPK3, or RIPK4 for 48h, RNA were extracted and sequenced.
Phosphorylation of Dishevelled by protein kinase RIPK4 regulates Wnt signaling.
Cell line, Subject
View SamplesMalignancies arising from mutation of tumor suppressor genes display an unexplained tissue proclivity. For example, tumor suppressor BAP1 encodes a ubiquitously expressed deubiquitinase for histone H2A but germline mutations predominantly cause uveal melanomas and mesotheliomas. We show that BAP1 inactivation causes apoptosis in mouse embryonic stem cells, fibroblasts, liver and pancreas, whereas melanocytes and mesothelial cells remain viable. E3 ligase RNF2, which silences genes by monoubiquitinating H2A, promoted apoptosis in BAP1-deficient cells by suppressing the pro-survival genes Bcl-2 and Mcl-1. Our data argue that BAP1 modulates gene expression by countering H2A ubiquitination, but its loss only promotes tumorigenesis in cells that do not engage an RNF2-dependent apoptotic program. We propose that intolerance of BAP1 loss, and perhaps the loss of other tumor suppressors, restricts the mutant tumor spectrum. Overall design: RNA was extracted from following genotypes - BAP1 wt (WT) and BAP1 knockout (BAP1 KO).
Intrinsic apoptosis shapes the tumor spectrum linked to inactivation of the deubiquitinase BAP1.
Specimen part, Subject
View SamplesWe introduced genome-wide pooled CRISPR-Cas9 libraries into primary mouse dendritic cells (DCs) to identify genes that control the induction of tumor necrosis factor (TNF) by bacterial lipopolysaccharide (LPS), a key process in the host response to pathogens, mediated by the TLR4 pathway. We found many of the known regulators of TLR4 signaling, as well as dozens of previously unknown candidates that we validated. Overall design: We used stain base phenotype (staining for TNF) in order to search for negative and positive regulators of LPS response in differentiated BMDCs
A Genome-wide CRISPR Screen in Primary Immune Cells to Dissect Regulatory Networks.
No sample metadata fields
View Samples