@article {34, title = {Prepatterning of developmental gene expression by modified histones before zygotic genome activation.}, journal = {Dev Cell}, volume = {21}, year = {2011}, month = {2011 Dec 13}, pages = {993-1004}, abstract = {

A hallmark of anamniote vertebrate development is a window of embryonic transcription-independent cell divisions before onset of zygotic genome activation (ZGA). Chromatin determinants of ZGA are unexplored; however, marking of developmental genes by modified histones in sperm suggests a predictive role of histone marks for ZGA. In zebrafish, pre-ZGA development for ten cell cycles provides an opportunity to examine whether genomic enrichment in modified histones is present before initiation of transcription. By profiling histone H3 trimethylation on all zebrafish promoters before and after ZGA, we demonstrate here an epigenetic prepatterning of developmental gene expression. This involves pre-ZGA marking of transcriptionally inactive genes involved in homeostatic and developmental regulation by permissive H3K4me3 with or without repressive H3K9me3 or H3K27me3. Our data suggest that histone modifications are instructive for the developmental gene expression program.

}, keywords = {Animals, Body Patterning, Chromatin, Epigenesis, Genetic, Female, Gene Expression Regulation, Developmental, Histones, Male, Methylation, Multigene Family, Promoter Regions, Genetic, Spermatozoa, Zebrafish, Zebrafish Proteins}, issn = {1878-1551}, doi = {10.1016/j.devcel.2011.10.008}, author = {Lindeman, Leif C and Andersen, Ingrid S and Reiner, Andrew H and Li, Nan and Aanes, H{\r a}vard and {\O}strup, Olga and Winata, Cecilia L and Mathavan, Sinnakaruppan and M{\"u}ller, Ferenc and Alestr{\"o}m, Peter and Collas, Philippe} } @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} } @article {65, title = {Transcriptome kinetics of arsenic-induced adaptive response in zebrafish liver.}, journal = {Physiol Genomics}, volume = {27}, year = {2006}, month = {2006 Nov 27}, pages = {351-61}, abstract = {

Arsenic is a prominent environmental toxicant and carcinogen; however, its molecular mechanism of toxicity and carcinogenicity remains poorly understood. In this study, we performed microarray-based expression profiling on liver of zebrafish exposed to 15 parts/million (ppm) arsenic [As(V)] for 8-96 h to identify global transcriptional changes and biological networks involved in arsenic-induced adaptive responses in vivo. We found that there was an increase of transcriptional activity associated with metabolism, especially for biosyntheses, membrane transporter activities, cytoplasm, and endoplasmic reticulum in the 96 h of arsenic treatment, while transcriptional programs for proteins in catabolism, energy derivation, and stress response remained active throughout the arsenic treatment. Many differentially expressed genes encoding proteins involved in heat shock proteins, DNA damage/repair, antioxidant activity, hypoxia induction, iron homeostasis, arsenic metabolism, and ubiquitin-dependent protein degradation were identified, suggesting strongly that DNA and protein damage as a result of arsenic metabolism and oxidative stress caused major cellular injury. These findings were comparable with those reported in mammalian systems, suggesting that the zebrafish liver coupled with the available microarray technology present an excellent in vivo toxicogenomic model for investigating arsenic toxicity. We proposed an in vivo, acute arsenic-induced adaptive response model of the zebrafish liver illustrating the relevance of many transcriptional activities that provide both global and specific information of a coordinated adaptive response to arsenic in the liver.

}, keywords = {Adaptation, Physiological, Animals, Arsenic, Down-Regulation, Gene Expression Profiling, Gene Expression Regulation, Genomics, Liver, Male, Metabolic Networks and Pathways, Oligonucleotide Array Sequence Analysis, Transcription, Genetic, Up-Regulation, Zebrafish}, issn = {1531-2267}, doi = {10.1152/physiolgenomics.00201.2005}, author = {Lam, Siew Hong and Winata, Cecilia L and Tong, Yan and Korzh, Svetlana and Lim, Wen San and Korzh, Vladimir and Spitsbergen, Jan and Mathavan, Sinnakarupan and Miller, Lance D and Liu, Edison T and Gong, Zhiyuan} }