Previous studies have reported that microglia depletion leads to impairment of synapse formation and these cells rapidly repopulate from CNS progenitors. However, the impact of microglia depletion and repopulation on the long-term state of the CNS environment has not been characterized. Here, we found by RNA-seq analysis that acute and synchronous microglia depletion results in a type 1-interferon inflammatory signature in degenerating somatosensory cortex in microglia-depleted mice. Transcriptomic and mass cytometry analysis of repopulated microglia demonstrates an interferon regulatory factor 7-driven activation state. Minocycline and anti-IFNAR1 antibody treatment attenuate the CNS type-1 interferon-driven inflammation and restore microglia homeostasis. Together, we found that acute microglia ablation induces a type-1 interferon activation state of grey matter microglia associated with acute neurodegeneration. Overall design: RNAseq analysis of brain cortical tissue from control and microglia-depleted mice.
Acute microglia ablation induces neurodegeneration in the somatosensory system.
Specimen part, Subject
View SamplesDifferencies between groups between pre and post haematopoietic stem cell transplantation children
Genetic Background of Immune Complications after Allogeneic Hematopoietic Stem Cell Transplantation in Children.
Specimen part, Disease stage
View SamplesDifferences between groups of children with obesity and healthy controls.
Looking for new diagnostic tools and biomarkers of hypertension in obese pediatric patients.
Specimen part, Disease
View SamplesLeaf transcriptome comparison of untransformed Col-0 Arabidopsis plants with plants transformed to be anti-sense for AtAOX1a (alternative oxidase). Two bio-replicates were sampled, for a total of four microarray chipsCol-0 and anti-sense leaf tissue from a first planting (samples GSM45208 and GSM45231, respectively), and from a second planting made one week later (samples GSM45209 and GSM45278, respectively). See sample descriptions for growth conditions and microarray procedure.
Characterization of transformed Arabidopsis with altered alternative oxidase levels and analysis of effects on reactive oxygen species in tissue.
No sample metadata fields
View SamplesMurine healthy tissue samples, DCIS and invasive mammary tumors were analyzed in order to identify marker genes which show enhanced expresssion in DCIS and invasive ductal carcinomas.
Identification of early molecular markers for breast cancer.
Specimen part
View SamplesHuman healthy tissue samples, DCIS and invasive mammary tumors were analyzed in order to identify marker genes which show enhanced expresssion in DCIS and invasive ductal carcinomas.
Identification of early molecular markers for breast cancer.
Specimen part, Disease, Disease stage
View SamplesO-GlcNAcylation is an essential, nutrient-sensitive post-translational modification, but its biochemical and phenotypic effects remain incompletely understood. To address this knowledge gap, we investigated the global transcriptional response to perturbations in O-GlcNAcylation. Unexpectedly, many transcriptional effects of O-GlcNAc transferase (OGT) inhibition were due to the activation of NRF2, the master regulator of redox stress tolerance. Moreover, we found that a signature of low OGT activity strongly correlates with NRF2 activation in multiple tumor expression datasets. Guided by this information, we identified KEAP1 (also known as KLHL19), the primary negative regulator of NRF2, as a direct substrate of OGT. We show that O-GlcNAcylation of KEAP1 at serine 104 is required for the efficient ubiquitination and degradation of NRF2. Interestingly, O-GlcNAc levels and NRF2 activation co-vary in response to glucose fluctuations, indicating that KEAP1 O-GlcNAcylation links nutrient sensing to downstream stress resistance. Our results reveal a novel regulatory connection between nutrient-sensitive glycosylation and NRF2 signaling, and provide a blueprint for future approaches to discover functionally important O-GlcNAcylation events on other KLHL family proteins in various experimental and disease contexts.
Glycosylation of KEAP1 links nutrient sensing to redox stress signaling.
Specimen part, Cell line
View SamplesWe identified genes whose expression changes between stage 8 and stage 10. We also identified genes whose expression was altered in stage 10 from temperature senstive ecdysone receptor mutant flies raised at the restrictive temperature. The experiments showed a significant number of genes that are upregulated in stage 10 depend EcR-mediated signaling. Overall design: 3 samples x 3 repeats
Steroid Signaling Establishes a Female Metabolic State and Regulates SREBP to Control Oocyte Lipid Accumulation.
Sex, Specimen part, Cell line, Subject
View SamplesAnalysis of expression changes in prelabeled laser-microdissected thoracic propriospinal neurons at different times after low-thoracic spinal cord transection in adult rats.
Intrinsic response of thoracic propriospinal neurons to axotomy.
Sex, Age, Specimen part, Time
View SamplesQuiescent stem cells are periodically activated to maintain tissue homeostasis or occasionally called into action upon injury. Molecular mechanisms that constitutively maintain stem cell identity or promote stem cell proliferation and differentiation upon activation have been extensively studied. However, it is unclear how quiescent stem cells maintain identity and reinforce quiescence when they transition from quiescence to activation. Here we show mouse hair follicle stem cell compartment induces a transcription factor, Foxc1, when activated. Importantly, deletion of Foxc1 in the activated but not quiescent stem cells compromises stem cell identity, fails to re-establish quiescence and subsequently drives premature stem cell activation.These findings uncover a dynamic, cell-intrinsic mechanism employed by hair follicle stem cells to reinforce stemness in response to activation. Overall design: Poly(A)-enriched transcriptome RNA-seq on HFSCs isolated in WT and K14Cre cKO mice at anagen and early telogen stage of hair cycle.
Foxc1 reinforces quiescence in self-renewing hair follicle stem cells.
No sample metadata fields
View Samples