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accession-icon GSE17013
The sexually antagonistic genes of Drosophila melanogaster
  • organism-icon Drosophila melanogaster
  • sample-icon 120 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

Differences in the selective pressures experienced by males and females are believed to be ubiquitous in dioecious organisms and are expected to result in the evolution of sexually antagonistic alleles, thereby driving the evolution of sexual dimorphism. Negative genetic correlation for fitness between the sexes has been documented, however, the identity, number and location of loci causing this relationship are unknown.

Publication Title

The sexually antagonistic genes of Drosophila melanogaster.

Sample Metadata Fields

Specimen part

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accession-icon GSE24729
Effect of mitochondria on nuclear gene expression in Drosophila melanogaster
  • organism-icon Drosophila melanogaster
  • sample-icon 38 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

Five different mitochondrial strains were introgressed in male and female fruit flies with identical (w1118) nuclear genetic background.

Publication Title

Experimental evidence supports a sex-specific selective sieve in mitochondrial genome evolution.

Sample Metadata Fields

Sex

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accession-icon GSE37325
Expression profiles of Drosophila melanogaster males with DX mothers and X-chromosomes that were subjected to male-limited evolution
  • organism-icon Drosophila melanogaster
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

Intralocus sexual conflict, where males and females have different fitness optima for the same trait, has been suggested to potentially be resolved by genomic imprinting, whereby expression in offspring is altered according to parent-of-origin. However, this idea has not yet been empirically tested. Here, we designed an experimental evolution protocol in Drosophila melanogaster which enabled us to look for imprinting effects on the X-chromosome. We enforced father-to-son transmission of the X-chromosome for many generations, and compared fitness and gene expression levels between control males, males with a control X-chromosome that had undergone one generation of father-son transmission (CDX), and males with an X-chromosome that had undergone many generations of father-son transmission (MLX). Although fitness differences were consistent with lowered fitness of males with a paternally inherited X-chromosome, expression differences suggested that this was due to deleterious maternal effects rather than imprinting. We conclude that imprinting is unlikely to resolve intralocus sexual conflict in Drosophila melanogaster.

Publication Title

Epigenetics and sex-specific fitness: an experimental test using male-limited evolution in Drosophila melanogaster.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon GSE27076
Female Drosophila melanogaster gene expression and mate choice: candidate genes underlying sexual isolation
  • organism-icon Drosophila melanogaster
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

Background The evolution of female choice mechanisms favouring males of their own kind is considered as crucial step during the early stages of speciation. However, although the genomics of mate choice may influence both the likelihood and speed of speciation, the identity and location of genes underlying assortative mating remain largely unknown.

Publication Title

Female Drosophila melanogaster gene expression and mate choice: the X chromosome harbours candidate genes underlying sexual isolation.

Sample Metadata Fields

Age, Specimen part, Treatment

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accession-icon SRP013644
CpG islands and GC content dictate nucleosome depletion in a transcription independent manner at mammalian promoters (RNA-seq)
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II

Description

One clear hallmark of mammalian promoters is the presence of CpG islands (CGIs) at more than two thirds of genes whereas TATA boxes are only present at a minority of promoters. Using genome-wide approaches, we show that GC content and CGIs are major promoter elements in mammalian cells, able to govern open chromatin conformation and support paused transcription. First, we define three classes of promoters with distinct transcriptional directionality and pausing properties which correlate with their GC content. We further analyze the direct influence of GC content on nucleosome positioning and depletion, and show that CGIs correlate with nucleosome depletion both in vivo and in vitro. We also show that transcription is not essential for nucleosome exclusion but influences both a weak +1 and a well-positioned nucleosome at CGI borders. Altogether our data support the idea that CGIs have become an essential feature of promoter structure defining novel regulatory properties in mammals. Overall design: Nucleosome density and positioning were studied by high-throughput sequencing of DNA previously treated with Mnase. In parallel, chIPseq for PolII and H3K27ac were performed in mouse and human with different conditions to assess a potential effect of transcription on nucleosomes properties. To investigate transcription at promoters, we analyzed together with genome-wide Pol II accumulation by ChIP-Seq, paused bidirectional transcripts associated with transcription start sites (TSS RNAs).

Publication Title

CpG islands and GC content dictate nucleosome depletion in a transcription-independent manner at mammalian promoters.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP125472
Knockout of the Arp2/3 complex in epidermis causes a psoriasis-like disease hallmarked by hyperactivation of transcription factor Nrf2 [Epidermis ssRNA-Seq]
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Arp2/3 complex assembles branched actin filaments key to many cellular processes, but its organismal roles remain poorly understood. Here we employed conditional arpc4 knockout mice to study the function of the Arp2/3 complex in the epidermis.We found that depletion of the Arp2/3 complex by knockout of arpc4 results in skin abnormalities at birth that evolve into a severe psoriasis-like disease hallmarked by hyperactivation of transcription factor Nrf2. Knockout of arpc4 in cultured keratinocytes was sufficient to induce nuclear accumulation of Nrf2, upregulation of Nrf2-target genes and decreased filamentous actin levels. Furthermore, pharmacological inhibition of the Arp2/3 complex unmasked the role of branched actin filaments in Nrf2 regulation. Consistently, we unveiled that Nrf2 associates with the actin cytoskeleton in cells and binds to filamentous actin in vitro Finally, we discovered that Arpc4 is downregulated in both human and mouse psoriatic epidermis. Thus, the Arp2/3 complex affects keratinocytes'' shape and transcriptome through an actin-based cell-autonomous mechanism that influences epidermal morphogenesis and homeostasis. Overall design: Gene expression profile of wt and ARPC4 ko epidermis

Publication Title

Knockout of the Arp2/3 complex in epidermis causes a psoriasis-like disease hallmarked by hyperactivation of transcription factor Nrf2.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP125471
Knockout of the Arp2/3 complex in epidermis causes a psoriasis-like disease hallmarked by hyperactivation of transcription factor Nrf2 [Keratinocytes ssRNA-Seq]
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Arp2/3 complex assembles branched actin filaments key to many cellular processes, but its organismal roles remain poorly understood. Here we employed conditional arpc4 knockout mice to study the function of the Arp2/3 complex in the epidermis.We found that depletion of the Arp2/3 complex by knockout of arpc4 results in skin abnormalities at birth that evolve into a severe psoriasis-like disease hallmarked by hyperactivation of transcription factor Nrf2. Knockout of arpc4 in cultured keratinocytes was sufficient to induce nuclear accumulation of Nrf2, upregulation of Nrf2-target genes and decreased filamentous actin levels. Furthermore, pharmacological inhibition of the Arp2/3 complex unmasked the role of branched actin filaments in Nrf2 regulation. Consistently, we unveiled that Nrf2 associates with the actin cytoskeleton in cells and binds to filamentous actin in vitro Finally, we discovered that Arpc4 is downregulated in both human and mouse psoriatic epidermis. Thus, the Arp2/3 complex affects keratinocytes'' shape and transcriptome through an actin-based cell-autonomous mechanism that influences epidermal morphogenesis and homeostasis. Overall design: Gene expression profile of wt, ARPC4 ko and EGFP-Nrf2 expressing keratinocytes.

Publication Title

Knockout of the Arp2/3 complex in epidermis causes a psoriasis-like disease hallmarked by hyperactivation of transcription factor Nrf2.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon SRP092132
Metformin RNA-seq
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Transcriptomic response to metfromin treatment.

Publication Title

Genomic Characterization of Metformin Hepatic Response.

Sample Metadata Fields

Sex, Age, Specimen part, Cell line

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accession-icon GSE17907
Molecular profiling of ERBB2-amplified breast cancers
  • organism-icon Homo sapiens
  • sample-icon 55 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

15-25% of breast cancers (BC) show ERBB2-amplification and overexpression of the encoded ERBB2 tyrosine kinase receptor. They are associated with a poor prognosis but can benefit from targeted therapy. A better knowledge of these BCs may help understand their behavior and design new therapeutic strategies. In this study, we defined the high resolution genome and gene expression profiles of 54 ERBB2-amplified BCs using 244K oligonucleotide array-comparative genomic hybridization and whole-genome DNA microarrays. We first identified the ERBB2-C17orf37-GRB7 genomic segment as the minimal common amplicon, and CRKRS and IKZF3 as the most frequent centromeric and telomeric amplicon borders, respectively. Second, we identified 17 genome regions affected by copy number aberration (CNA). The expression of 37 genes of these regions was deregulated. Third, two types of heterogeneity were observed in ERBB2-amplified BCs. The genomic profiles of estrogen receptor-postive (ER+) and negative (ER-) ERBB2-amplified BCs were different. The WNT/-catenin signaling pathway was involved in ER- ERBB2-amplified BCs, and PVT1 and TRPS1 were candidate oncogenes associated with ER+ ERBB2-amplified BCs. The size of the ERBB2-amplicon was different in inflammatory (IBC) and non inflammatory BCs. ERBB2-amplified IBCs were characterized by the downregulated and upregulated mRNA expression of ten and two genes in proportion to CNA, respectively. We have shown that ERBB2 BCs are heterogeneous and identified genomic features that may be useful in the design of therapeutical strategies

Publication Title

Genome profiling of ERBB2-amplified breast cancers.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE26679
comparison of powdery mildew-induced gene expression between Col-0 and the edr1 mutant
  • organism-icon Arabidopsis thaliana
  • sample-icon 32 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

The edr1 mutant of Arabidopsis thaliana displays enhanced resistance to the powdery mildew Golovinomyces cichoracearum, resulting in cell death and an absence of visible disease symptoms. To better characterize and understand the defense response of edr1, a time course of early signaling responses was performed after inoculation with powdery mildew and compared to the responses of wild-type Col-0. These time points represent early stages in the infection process, before any signs of susceptibility or resistance are visible.

Publication Title

Negative regulation of defence signalling pathways by the EDR1 protein kinase.

Sample Metadata Fields

No sample metadata fields

View Samples

refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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