Basilar papillae (i.e.auditory epithelia) were isolated from 4-day-old chickens and sectioned into low, middle, and high frequency segments. RNA was isolated from each segment separately, amplified using a two-cycle approach, biotinylated, and hybridized to Affymetrix chicken whole-genome arrays.
Gene expression gradients along the tonotopic axis of the chicken auditory epithelium.
Specimen part
View Samplesthe nuclear pore complex (NPC) is emerging as an important mediator of cellular processes beyond molecule transport, including control of gene expression, replication and DNA repair.
The Nup84 complex coordinates the DNA damage response to warrant genome integrity.
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View SamplesThis dataset investigates the transcriptional effect of mitochondrial 12S rRNA hypermethylation, both by overexpressing the mitochondrial methyltransferase mtTFB1 in HeLa cells and by using A1555G cybrids, where the 12S rRNA is hypermethylated. HeLa cells overexpressing a methyltransferase-deficient mtTFB1 (mtTFB1[G65A]) and wild-type A1555A cybrids were used as controls.
Mitochondrial stress engages E2F1 apoptotic signaling to cause deafness.
Cell line
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A genome-wide function of THSC/TREX-2 at active genes prevents transcription-replication collisions.
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View SamplesTranscription is a major obstacle for replication fork progression and a cause of genome instability. Such instability increases in mutants with a suboptimal assembly of the nascent messenger ribonucleo-protein particle (mRNP), as THO/TREX and the NPC-associated THSC/TREX-2 complex.
A genome-wide function of THSC/TREX-2 at active genes prevents transcription-replication collisions.
No sample metadata fields
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Excess of Yra1 RNA-Binding Factor Causes Transcription-Dependent Genome Instability, Replication Impairment and Telomere Shortening.
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View SamplesTranscription is a major obstacle for replication fork progression and a cause of genome instability. Such instability increases in mutants with an imbalance proportion of Yra1, a component of THO/TREX.
Excess of Yra1 RNA-Binding Factor Causes Transcription-Dependent Genome Instability, Replication Impairment and Telomere Shortening.
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View SamplesSide populations have recently been identified in ovarian cancers and may play an important role in post treatment relapse and resistance to chemotherapeutic drugs. In this study, we aimed to identify the differential expression between IGROV1 SP and NSP on Affymetrix HG-U133plus2 microarrays. We found ovarian tumour SP cells frequently over-express the multi-drug resistance associated P-glycoprotein (ABCB1) by Rank Product (FDR<0.05), and by geneset enrichment analysis, embryonic stem cell-associated NOS signature (Notch/Oct4/Sox2 regulated genes) and Polycomb Repressive Complex 2 (PRC2) genes were over-expressed, while PRC2-repressed target genes were significantly under-expressed in the SP from ovarian cell lines compared to non-SP (FDR<10-4).
Ovarian cancer stem cell-like side populations are enriched following chemotherapy and overexpress EZH2.
Specimen part
View SamplesMammalian genomes are organized into megabase-scale topologically associated domains (TADs) that have been proposed to represent large regulatory units. Here we demonstrate that disruption of TADs can cause rewiring of long-range regulatory architecture and result in pathogenic phenotypes. We show that distinct human limb malformations are caused by deletions, inversions, or duplications altering the structure of the TAD-spanning WNT6/IHH/EPHA4/PAX3 locus. Using CRISPR/Cas genome editing, we generated mice with corresponding rearrangements. Both in mouse limb tissue and patient-derived fibroblasts, disease-relevant structural changes cause ectopic interactions between promoters and non-coding DNA, and a cluster of limb enhancers normally associated with Epha4 is misplaced relative to TAD boundaries and drives ectopic limb expression of another gene in the locus. Our results demonstrate the functional importance of TADs for orchestrating gene expression via genome architecture and indicate criteria for predicting the pathogenicity of human structural variants, particularly in non-coding regions of the human genome. Overall design: RNA-seq profile of developing distal limbs of mutants and WT animals at E11.5
Disruptions of topological chromatin domains cause pathogenic rewiring of gene-enhancer interactions.
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View SamplesThis SuperSeries is composed of the SubSeries listed below.
The Npl3 hnRNP prevents R-loop-mediated transcription-replication conflicts and genome instability.
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