User-friendly solutions for microarray quality control and pre-processing on ArrayAnalysis.org

Eijssen, Lars; Jaillard, Magali; Adriaens, Michiel E.; Gaj, Stan; Groot, Philip J. de; Müller, Michael; Evelo, Chris T.

doi:10.1093/nar/gkt293

Cited by 120 publications

(95 citation statements)

References 30 publications

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“…Pre-processing steps including quality control, background adjustment, and quantile normalization were performed using the array analysis tools available via www.arrayanalysis.org using the lumi package and bgAdjust function (18). Variance stabilization was managed with a log 2 transformation.…”

Section: Methodsmentioning

confidence: 99%

Transcriptional Heterogeneity of Mast Cells and Basophils upon Activation

Chhiba

Hsu

Berdnikovs

et al. 2017

The Journal of Immunology

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Mast cells and basophils are developmentally related cells whose activation is a hallmark of allergy. Functionally, mast cells and basophils overlap in their ability to produce several mediators, including histamine and granule proteases, but studies have increasingly demonstrated non-redundant roles. To characterize the transcriptional heterogeneity of mast cells and basophils upon their activation, we performed large-scale comparative microarrays of murine bone marrow–derived mast cells (BMMCs) and basophils (BMBs) at rest, upon an adaptive-type activation (IgE crosslinking), or upon an innate-type activation (IL-33 stimulation). Hierarchical clustering demonstrated that BMMCs and BMBs shared specific activation-associated transcriptional signatures but differed in others, both between cell type and between activation mode. In BMMCs, IgE crosslinking upregulated 785 genes including Egr2, Ccl1, and Fxyd6, while IL-33 stimulation induced 823 genes including Ccl1, Egr2, and Il1b. Focused bioinformatics pathway analysis demonstrated that IgE activation aligned with processes such as oxidative phosphorylation, angiogenesis, and the p53 pathway. The IL-33–activated transcriptome was enriched in genes commonly altered by NF-κB in response to TNF, by IL-6 via STAT3, and in response to IFNγ. Furthermore, BMBs activated via IgE crosslinking selectively induced immune response genes Ccl1, Il3, and Il2 compared to IL-33–stimulated BMBs. Principal-component analysis revealed key cell- and activation-specific clustering. Overall, our data demonstrate that mast cells and basophils have cell- and activation-specific transcriptional responses and suggest that context-specific gene networks and pathways may shape how the immune system responds to allergens and innate cytokines.

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Section: Methodsmentioning

confidence: 99%

Transcriptional Heterogeneity of Mast Cells and Basophils upon Activation

Chhiba

Hsu

Berdnikovs

et al. 2017

The Journal of Immunology

View full text Add to dashboard Cite

show abstract

“…After an automated process of washing and staining, absolute values of expression were calculated from the scanned array using the Affymetrix GCOS software. Data preprocessing and analysis was conducted based on scripts from ArrayAnalysis.org using R2.7.1 [101] and Bioconductor libraries (http://www.R-project.org) [102]. Data were 2log transformed and normalized (gcRMA) [103].…”

Section: Affymetrix Expression Arrays Pathway Analysismentioning

confidence: 99%

PRC1 Prevents Replication Stress during Chondrogenic Transit Amplification

et al. 2017

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Transit amplification (TA), a state of combined, rapid proliferative expansion and differentiation of stem cell-descendants, remains poorly defined at the molecular level. The Polycomb Repressive Complex 1 (PRC1) protein BMI1 has been localized to TA compartments, yet its exact role in TA is unclear. PRC1 proteins control gene expression, cell proliferation and DNA-damage repair. Coordination of such DNA-templated activities during TA is predicted to be crucial to support DNA replication and differentiation-associated transcriptional programming. We here examined whether chondrogenesis provides a relevant biological context for synchronized coordination of these chromatin-based tasks by BMI1. Taking advantage of a prominently featuring TA-phase during chondrogenesis in vitro and in vivo, we here report that TA is completely dependent on intact PRC1 function. BMI1-depleted chondrogenic progenitors rapidly accumulate double strand DNA breaks during DNA replication, present massive non-H3K27me3-directed transcriptional deregulation and fail to undergo chondrogenic TA. Genome-wide accumulation of Topoisomerase 2α and Geminin suggests a model in which PRC1 synchronizes replication and transcription during rapid chondrogenic progenitor expansion. Our combined data reveals for the first time a vital cell-autonomous role for PRC1 during chondrogenesis. We provide evidence that chondrocyte hyper-replication and hypertrophy represent a unique example of programmed senescence in vivo. These findings provide new perspectives on PRC1 function in development and disease.

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“…org/) (Maastricht University, The Netherlands) [22] for human Affymetrix gene chips, using the Robust Multichip Average (RMA) algorithm [23] and MBNI custom CDF version 15 [24]. Subsequently, normalized data was Log2 transformed.…”

Section: Data Analysis and Statisticsmentioning

confidence: 99%