We have reported previously that when chromosome Y (chrY) from the mouse strain C57BL/6J (abbreviated as B) was substituted for that of A/J mice (ChrY<A>), cardiomyocytes from the resulting 'chromosome substitution' C57BL/6J-chrY<A> strain (abbreviated as B.Y) were smaller than that of their C57BL/6J counterparts. In reverse, when chrY<A> from A/J mice was substituted for that of chrY<B>, cardiomyocytes from the resulting A/J-chrY<C57> strain were larger than in their A/J counterparts. We further used these strains (B and the consomic B.Y) to test whether the origin of chrY could also be linked to differences in the profile of gene expression in their cardiac left ventricles in adult mice where either sham surgery (intact animals) or castration has been performed at 3-4 weeks of age..
Chromosome Y variants from different inbred mouse strains are linked to differences in the morphologic and molecular responses of cardiac cells to postpubertal testosterone.
Sex
View SamplesNext to the two-component and quorum sensing systems, cell-surface signaling (CSS) has been recently identified as an important regulatory system in Pseudomonas aeruginosa. CSS senses signals from outside the cell and transmits them into the cytoplasm. It consists of a TonB-dependent outer membrane receptor, a cytoplasmic membrane-localized sigma factor regulator (or anti-sigma factor), and an extracytoplasmic function (ECF) sigma factor. Upon perception of the extracellular signal by the receptor the ECF sigma factor is activated and promotes the transcription of a specific set of gene(s). Although most P. aeruginosa ECF sigma factors are involved in the regulation of iron uptake, we have identified a novel ECF sigma factor (PA0675) involved in the regulation of virulence. By microarray analysis of cells overexpressing PA0675 from the pMUM3 plasmid we have identified the genes regulated by this sigma factor.
A Novel extracytoplasmic function (ECF) sigma factor regulates virulence in Pseudomonas aeruginosa.
No sample metadata fields
View SamplesWe used single cell RNA-seq to probe the transcriptional responses of utricle supporting cells to damage and Atoh1 transduction. Overall design: mRNA profiles of 4-6 weeks old mice utricle supporting cell cultured for 10 days and supporting cells with overexpression of Atoh1 cultured for 10 days were generated by deep sequencing, using Illumina Nextseq 500.
Transcriptomic and epigenetic regulation of hair cell regeneration in the mouse utricle and its potentiation by Atoh1.
Specimen part, Cell line, Subject
View SamplesWe used RNA-seq to probe the transcriptional and epigenetic responses of utricle supporting cells to damage and Atoh1 transduction. Overall design: mRNA profiles of 4-6 weeks old mice utricle endogenous hair cell, supporting cells, supporting cell cultured for 10 days and supporting cells with overexpression of Atoh1 cultured for 10 days were generated by deep sequencing, in duplicate or triplicate, using Illumina Nextseq500 instrument
Transcriptomic and epigenetic regulation of hair cell regeneration in the mouse utricle and its potentiation by Atoh1.
Cell line, Subject
View SamplesPrecursor T-cell lymphoblastic neoplasms are aggressive haematological neoplasm that most often manifest with extensive marrow and blood affectation (T-cell acute lymphoblastic leukaemia or T-ALL) or less commonly as a thymic mass with limited bone marrow infiltration (T-cell lymphoblastic lymphoma or T-LBL). Here we show data from RNA-Seq in a sample series of T-LBL from Spanish patients.The goal was to determine the levels of expression of coding genes and microRNAs, and to identify all genetic variants including SNVs, indels, and fusion transcripts. Overall design: Expression data were determined by comparson of each tumour sample with two control thymuses (404 and 405). Genetic variants were determined by comparison of tumour sequences with canonical ENSEMBL normal-references of each gene.
RNA-Seq reveals the existence of a CDKN1C-E2F1-TP53 axis that is altered in human T-cell lymphoblastic lymphomas.
Specimen part, Subject
View SamplesMutants in the Drosophila gene lethal (3) malignant brain tumor cause malignant growth in the larval brain. This data shows the changes in gene expression profile associated to mutations in l(3)mbt, both in situ in third instar larval brains and in tumors cultured for 1 5 and 10 (T1, T5, T10) rounds of allograft culture
Ectopic expression of germline genes drives malignant brain tumor growth in Drosophila.
No sample metadata fields
View SamplesAdamts12-deficient mice undergo more severe colitis than WT mice after induction with DSS.
ADAMTS-12 metalloprotease is necessary for normal inflammatory response.
Specimen part, Treatment
View SamplesIdentification of a NVS-ZP7-3 response signature in T-ALL cell lines to understand the transcriptional response in both Notch pathway active cell lines and Notch pathway inactive lines.
Discovery of a ZIP7 inhibitor from a Notch pathway screen.
Cell line, Treatment
View SamplesAcute quadriplegic myopathy (AQM) or critical illness myopathy (CIM) is frequently observed in intensive care unit (ICU) patients. In order to elucidate duration-dependent effects of the ICU intervention on molecular and functional networks that control the muscle wasting and weakness in AQM, gene expression profile was analyzed at time points varying from 6 hours to 14 days in a unique experimental rat model mimicking ICU conditions, i.e., post-synaptically paralyzed, mechanically ventilated and extensively monitored animals.
Muscle wasting and the temporal gene expression pattern in a novel rat intensive care unit model.
Sex, Specimen part, Disease, Disease stage
View SamplesDiamond-Blackfan anemia (DBA) is characterized by anemia and cancer susceptibility, and is caused by mutations in ribosomal genes, including Rpl11. Here, we report that Rpl11-heterozygous embryos are not viable, and homozygous deletion of Rpl11 in adult mice results in death within a few weeks, accompanied by bone marrow aplasia and intestinal atrophy. Importantly, deletion of a single Rpl11 allele in adult mice results in anemia associated to decreased erythroid progenitors and defective erythroid maturation. These phenotypes are also present in mice transplanted with inducible heterozygous Rpl11 bone marrow, indicating a cell-autonomous role of RPL11 in erythropoiesis. Additionally, fibroblasts lacking one or both Rpl11 alleles show defective p53 activation upon ribosomal stress or DNA damage. Furthermore, fibroblasts and hematopoietic tissues from heterozygous Rpl11 mice present higher basal cMYC levels. Accordingly, heterozygous Rpl11 mice are highly susceptible to radiation-induced lymphomagenesis. We conclude that Rpl11-deficient mice recapitulate DBA disorder, including cancer predisposition. Overall design: RNAseq profiles of bone marrow hematopoietic progenitors cells from WT (Rpl11+/+:: Tg.UbC-CreERT2) and LOX (Rpl11+/lox::Tb.Ub-CreERT2) mice, n=4 independent animals per genotype
Partial Loss of Rpl11 in Adult Mice Recapitulates Diamond-Blackfan Anemia and Promotes Lymphomagenesis.
Sex, Age, Specimen part, Cell line, Subject
View Samples