@article {127, title = {xcore: an R package for inference of gene expression regulators.}, journal = {BMC Bioinformatics}, volume = {24}, year = {2023}, month = {2023 Jan 11}, pages = {14}, abstract = {

BACKGROUND: Elucidating the Transcription Factors (TFs) that drive the gene expression changes in a given experiment is a common question asked by researchers. The existing methods rely on the predicted Transcription Factor Binding Site (TFBS) to model the changes in the motif activity. Such methods only work for TFs that have a motif and assume the TF binding profile is the same in all cell types.

RESULTS: Given the wealth of the ChIP-seq data available for a wide range of the TFs in various cell types, we propose that gene expression modeling can be done using ChIP-seq "signatures" directly, effectively skipping the motif finding and TFBS prediction steps. We present xcore, an R package that allows TF activity modeling based on ChIP-seq signatures and the user{\textquoteright}s gene expression data. We also provide xcoredata a companion data package that provides a collection of preprocessed ChIP-seq signatures. We demonstrate that xcore leads to biologically relevant predictions using transforming growth factor beta induced epithelial-mesenchymal transition time-courses, rinderpest infection time-courses, and embryonic stem cells differentiated to cardiomyocytes time-course profiled with Cap Analysis Gene Expression.

CONCLUSIONS: xcore provides a simple analytical framework for gene expression modeling using linear models that can be easily incorporated into differential expression analysis pipelines. Taking advantage of public ChIP-seq databases, xcore can identify meaningful molecular signatures and relevant ChIP-seq experiments.

}, keywords = {Animals, Binding Sites, Chromatin Immunoprecipitation, Chromatin Immunoprecipitation Sequencing, Gene Expression, Protein Binding, Transcription Factors}, issn = {1471-2105}, doi = {10.1186/s12859-022-05084-0}, author = {Migda{\l}, Maciej and Arakawa, Takahiro and Takizawa, Satoshi and Furuno, Masaaki and Suzuki, Harukazu and Arner, Erik and Winata, Cecilia Lanny and Kaczkowski, Bogumi{\l}} } @article {73, title = {The interaction of epithelial Ihha and mesenchymal Fgf10 in zebrafish esophageal and swimbladder development.}, journal = {Dev Biol}, volume = {359}, year = {2011}, month = {2011 Nov 15}, pages = {262-76}, abstract = {

Developmental patterning and growth of the vertebrate digestive and respiratory tracts requires interactions between the epithelial endoderm and adjacent mesoderm. The esophagus is a specialized structure that connects the digestive and respiratory systems and its normal development is critical for both. Shh signaling from the epithelium regulates related aspects of mammalian and zebrafish digestive organ development and has a prominent effect on esophageal morphogenesis. The mechanisms underlying esophageal malformations, however, are poorly understood. Here, we show that zebrafish Ihha signaling from the epithelium acting in parallel, but independently of Shh, controls epithelial and mesenchymal cell proliferation and differentiation of smooth muscles and neurons in the gut and swimbladder. In zebrafish ihha mutants, the esophageal and swimbladder epithelium is dysmorphic, and expression of fgf10 in adjacent mesenchymal cells is affected. Analysis of the development of the esophagus and swimbladder in fgf10 mutant daedalus (dae) and compound dae/ihha mutants shows that the Ihha-Fgf10 regulatory interaction is realized through a signaling feedback loop between the Ihha-expressing epithelium and Fgf10-expressing mesenchyme. Disruption of this loop further affects the esophageal and swimbladder epithelium in ihha mutants, and Ihha acts in parallel to but independently of Shha in this process. These findings contribute to the understanding of epithelial-mesenchymal interactions and highlight an interaction between Hh and Fgf signaling pathways during esophagus and swimbladder development.

}, keywords = {Air Sacs, Animals, Animals, Genetically Modified, Cell Proliferation, Embryo, Nonmammalian, Epithelium, Esophagus, Female, Fibroblast Growth Factor 10, Gastrointestinal Tract, Gene Expression Regulation, Developmental, Gene Knockdown Techniques, Green Fluorescent Proteins, Hedgehog Proteins, In Situ Hybridization, Male, Membrane Proteins, Mesoderm, Microscopy, Confocal, Mutation, Protein Binding, Receptors, Cell Surface, Signal Transduction, Zebrafish, Zebrafish Proteins}, issn = {1095-564X}, doi = {10.1016/j.ydbio.2011.08.024}, author = {Korzh, Svitlana and Winata, Cecilia Lanni and Zheng, Weiling and Yang, Shulan and Yin, Ao and Ingham, Phillip and Korzh, Vladimir and Gong, Zhiyuan} }