This SuperSeries is composed of the SubSeries listed below.
A fine balance: epigenetic control of cellular quiescence by the tumor suppressor PRDM2/RIZ at a bivalent domain in the cyclin a gene.
Cell line
View SamplesKnockdown of PRDM2 led to precocious differentiation. To understand the molecular basis for this phenotype, we performed microaary analysis of 28hr differentiated myoblasts.
A fine balance: epigenetic control of cellular quiescence by the tumor suppressor PRDM2/RIZ at a bivalent domain in the cyclin a gene.
Cell line
View SamplesKnockdown of PRDM2 led to precocious differentiation. To understand the molecular basis for this phenotype, we performed microaary analysis of quiescent myoblasts.
A fine balance: epigenetic control of cellular quiescence by the tumor suppressor PRDM2/RIZ at a bivalent domain in the cyclin a gene.
Cell line
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Gene Array Analyzer: alternative usage of gene arrays to study alternative splicing events.
Age, Specimen part
View SamplesThe latest version of microarrays released by Affymetrix, the GeneChip Gene 1.0 ST Arrays (gene arrays), are designed in a similar fashion as exon arrays, which enables to identify differentially expressed exons, rather than only the expression level of whole transcripts. Here, we propose an extension, Gene Array Analyzer (GAA), to our previously published Exon Array Analyzer (EAA). GAA enables to analyse gene arrays on exon level and therefore supports to identify alternative splicing with gene arrays. To show the applicability of GAA, we used gene arrays to profile alternative splice events during the development of the heart. Further re-analysis of published gene arrays could show, that some of these splice events reoccur under pathological conditions. The web interface of GAA is user friendly, functional without set up and freely available at http://GAA.mpi-bn.mpg.de.
Gene Array Analyzer: alternative usage of gene arrays to study alternative splicing events.
Age, Specimen part
View SamplesThe right ventricle (RV) differs in several aspects from the left ventricle (LV) including its embryonic origin, physiological role and anatomical design. In contrast to LV hypertrophy, little is known about the molecular circuits, which are activated upon RV hypertrophy (RVH). We established a highly reproducible model of RVH in mice using pulmonary artery clipping (PAC), which avoids detrimental RV pressure overload and thus allows long-term survival of operated mice. Magnetic resonance imaging revealed pathognomonic changes with striking similarities to human congenital heart disease- or pulmonary arterial hypertension- patients. Comparative, microarray based transcriptome analysis of right- and left-ventricular remodeling identified distinct transcriptional responses to pressure-induced hypertrophy of either ventricle, which were mainly characterized by stronger transcriptional responses of the RV compared to the LV myocardium. Hierarchic cluster analysis revealed a RV- and LV-specific pattern of gene activity after induction of hypertrophy, however, we did not find evidence for qualitatively distinct regulatory pathways in RV compared to LV. Data mining of nearly three thousand RV-enriched genes under PAC disclosed novel potential (co)-regulators of long-term RV remodeling and hypertrophy. We reason that specific inhibitory mechanisms in RV restrict excessive myocardial hypertrophy and thereby contribute to its vulnerability to pressure overload.
Identification of right heart-enriched genes in a murine model of chronic outflow tract obstruction.
Sex, Age, Specimen part
View SamplesMany of the genes coding for secreted protein effectors are arranged in gene clusters in the genome of the biotrophic plant pathogen Ustilago maydis. The largest of these gene clusters, cluster 19A, encodes 24 secreted effectors. Deletion of the entire cluster results in severe attenuation of virulence. The generation and analysis strains carrying sub-deletions identified 9 genes significantly contributing to tumor formation after seedling infection. As the individual contributions of these genes to tumor formation were small, we studied the response of maize plants to the whole cluster mutant as well as to several individual mutants by array analysis. This revealed distinct plant responses, demonstrating that the respective effectors have discrete plant targets. Many of the genes coding for secreted protein effectors are arranged in gene clusters in the genome of the biotrophic plant pathogen Ustilago maydis. The largest of these gene clusters, cluster 19A, encodes 24 secreted effectors. Deletion of the entire cluster results in severe attenuation of virulence. The generation and analysis strains carrying sub-deletions identified 9 genes significantly contributing to tumor formation after seedling infection. As the individual contributions of these genes to tumor formation were small, we studied the response of maize plants to the whole cluster mutant as well as to several individual mutants by array analysis. This revealed distinct plant responses, demonstrating that the respective effectors have discrete plant targets.
Characterization of the largest effector gene cluster of Ustilago maydis.
Specimen part, Treatment
View SamplesThe basidiomycete Ustilago maydis causes smut disease in maize. Colonization of the host plant is initiated by direct penetration of cuticle and cell wall of maize epidermis cells. The invading hyphae are surrounded by the plant plasma membrane and proliferate within the plant tissue. We identified a novel secreted protein, termed Pep1. Disruption mutants of pep1 are not affected in saprophytic growth and develop normal infection structures. However, pep1 mutants fail to penetrate the epidermal cell wall and elicit a strong plant defense response. Using Affymetrix maize arrays we identified about 110 plant genes which are differentially regulated in pep1 and wild type infections during the penetration stage.
Pep1, a secreted effector protein of Ustilago maydis, is required for successful invasion of plant cells.
No sample metadata fields
View SamplesUstilago maydis is a basidiomycete fungus that causes smut disease in maize. Most prominent symptoms of the disease are plant tumors, which can be induced by U. maydis on all aerial parts of the plant. We identified two linked genes, pit1 and pit2, which are specifically expressed during plant colonization. Deletion mutants for either pit1 or pit2 are unable to induce tumor development and elicit plant defense responses.
Two linked genes encoding a secreted effector and a membrane protein are essential for Ustilago maydis-induced tumour formation.
Specimen part, Disease, Disease stage
View SamplesPulmonary fibrosis develops as a consequence of environmentally induced lung injury and/or an inherent disease susceptibility causing fibroblast activation, proliferation and extracellular matrix deposition.
Microarray profiling reveals suppressed interferon stimulated gene program in fibroblasts from scleroderma-associated interstitial lung disease.
Specimen part, Disease
View Samples