Talk:Zebrafish Development

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Cite this page: Hill, M.A. (2024, May 3) Embryology Zebrafish Development. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Zebrafish_Development

2011

Multifactorial Origins of Heart and Gut Defects in nipbl-Deficient Zebrafish, a Model of Cornelia de Lange Syndrome

Muto A, Calof AL, Lander AD, Schilling TF.Source Department of Developmental and Cell Biology, University of California, Irvine, California, United States of America.

Abstract

Cornelia de Lange Syndrome (CdLS) is the founding member of a class of multi-organ system birth defect syndromes termed cohesinopathies, named for the chromatin-associated protein complex cohesin, which mediates sister chromatid cohesion. Most cases of CdLS are caused by haploinsufficiency for Nipped-B-like (Nipbl), a highly conserved protein that facilitates cohesin loading. Consistent with recent evidence implicating cohesin and Nipbl in transcriptional regulation, both CdLS cell lines and tissues of Nipbl-deficient mice show changes in the expression of hundreds of genes. Nearly all such changes are modest, however-usually less than 1.5-fold-raising the intriguing possibility that, in CdLS, severe developmental defects result from the collective action of many otherwise innocuous perturbations. As a step toward testing this hypothesis, we developed a model of nipbl-deficiency in zebrafish, an organism in which we can quantitatively investigate the combinatorial effects of gene expression changes. After characterizing the structure and embryonic expression of the two zebrafish nipbl genes, we showed that morpholino knockdown of these genes produces a spectrum of specific heart and gut/visceral organ defects with similarities to those in CdLS. Analysis of nipbl morphants further revealed that, as early as gastrulation, expression of genes involved in endodermal differentiation (sox32, sox17, foxa2, and gata5) and left-right patterning (spaw, lefty2, and dnah9) is altered. Experimental manipulation of the levels of several such genes-using RNA injection or morpholino knockdown-implicated both additive and synergistic interactions in causing observed developmental defects. These findings support the view that birth defects in CdLS arise from collective effects of quantitative changes in gene expression. Interestingly, both the phenotypes and gene expression changes in nipbl morphants differed from those in mutants or morphants for genes encoding cohesin subunits, suggesting that the transcriptional functions of Nipbl cannot be ascribed simply to its role in cohesin loading.

PMID 22039349

2010

The zebrafish transcriptome during early development

BMC Dev Biol. 2011 May 24;11(1):30.

Vesterlund L, Jiao H, Unneberg P, Hovatta O, Kere J. Source Department of Biosciences and Nutrition, and Science for Life Laboratory, Karolinska Institutet, Stockholm, Sweden. liselotte.vesterlund@ki.se.

Abstract ABSTRACT: BACKGROUND: The transition from fertilized egg to embryo is accompanied by a multitude of changes in gene expression, and the transcriptional events that underlie these processes have not yet been fully characterized. In this study RNA-Seq is used to compare the transcription profiles of four early developmental stages in zebrafish (Danio rerio) on a global scale. RESULTS: An average of 79 M total reads were detected from the different stages. Out of the total number of reads 65% - 73% reads were successfully mapped and 36% - 44% out of those were uniquely mapped. The total number of detected unique gene transcripts was 11187, of which 10096 were present at 1-cell stage. The largest number of common transcripts was observed between 1-cell stage and 16-cell stage. An enrichment of gene transcripts with molecular functions of DNA binding, protein folding and processing as well as metal ion binding was observed with progression of development. The sequence data (accession number ERP000635) is available at the European Nucleotide Archive. CONCLUSION: Clustering of expression profiles shows that a majority of the detected gene transcripts are present at steady levels, and thus a minority of the gene transcripts clusters as increasing or decreasing in expression over the four investigated developmental stages. The three earliest developmental stages were similar when comparing highly expressed genes, whereas the 50% epiboly stage differed from the other three stages in the identity of highly expressed genes, number of uniquely expressed genes and enrichment of GO molecular functions. Taken together, these observations indicate a major transition in gene regulation and transcriptional activity taking place between the 512-cell and 50% epiboly stages, in accordance with previous studies.

PMID: 21609443

B1 SOX coordinate cell specification with patterning and morphogenesis in the early zebrafish embryo

PLoS Genet. 2010 May 6;6:e1000936.

Okuda Y, Ogura E, Kondoh H, Kamachi Y.

Graduate School of Frontier Biosciences, Osaka University, Suita, Japan. Abstract The B1 SOX transcription factors SOX1/2/3/19 have been implicated in various processes of early embryogenesis. However, their regulatory functions in stages from the blastula to early neurula remain largely unknown, primarily because loss-of-function studies have not been informative to date. In our present study, we systematically knocked down the B1 sox genes in zebrafish. Only the quadruple knockdown of the four B1 sox genes sox2/3/19a/19b resulted in very severe developmental abnormalities, confirming that the B1 sox genes are functionally redundant. We characterized the sox2/3/19a/19b quadruple knockdown embryos in detail by examining the changes in gene expression through in situ hybridization, RT-PCR, and microarray analyses. Importantly, these phenotypic analyses revealed that the B1 SOX proteins regulate the following distinct processes: (1) early dorsoventral patterning by controlling bmp2b/7; (2) gastrulation movements via the regulation of pcdh18a/18b and wnt11, a non-canonical Wnt ligand gene; (3) neural differentiation by regulating the Hes-class bHLH gene her3 and the proneural-class bHLH genes neurog1 (positively) and ascl1a (negatively), and regional transcription factor genes, e.g., hesx1, zic1, and rx3; and (4) neural patterning by regulating signaling pathway genes, cyp26a1 in RA signaling, oep in Nodal signaling, shh, and mdkb. Chromatin immunoprecipitation analysis of the her3, hesx1, neurog1, pcdh18a, and cyp26a1 genes further suggests a direct regulation of these genes by B1 SOX. We also found an interesting overlap between the early phenotypes of the B1 sox quadruple knockdown embryos and the maternal-zygotic spg embryos that are devoid of pou5f1 activity. These findings indicate that the B1 SOX proteins control a wide range of developmental regulators in the early embryo through partnering in part with Pou5f1 and possibly with other factors, and suggest that the B1 sox functions are central to coordinating cell fate specification with patterning and morphogenetic processes occurring in the early embryo.

PMID: 20463883

The gastric mucosa development and differentiation

Prog Mol Biol Transl Sci. 2010;96:93-115.

Khurana S, Mills JC.

Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri, USA; Department of Developmental Biology, Washington University School of Medicine, St. Louis, Missouri, USA. Abstract The development and differentiation of the gastric mucosa are controlled by a complex interplay of signaling proteins and transcriptional regulators. This process is complicated by the fact that the stomach is derived from two germ layers, the endoderm and the mesoderm, with the first giving rise to the mature epithelium and the latter contributing the smooth muscle required for peristalsis. Reciprocal epithelial-mesenchymal interactions dictate the formation of the stomach during fetal development, and also contribute to its continuous regeneration and differentiation throughout adult life. In this chapter, we discuss the discoveries that have been made in different model systems, from zebrafish to human, which show that the Hedgehog, Wnt, Notch, bone morphogenetic protein, and fibroblast growth factor (FGF) signaling systems play essential roles during various stages of stomach development.

Copyright © 2010 Elsevier Inc. All rights reserved. PMID: 21075341

Genetic analysis of fin development in zebrafish identifies furin and hemicentin1 as potential novel fraser syndrome disease genes

Carney TJ, Feitosa NM, Sonntag C, Slanchev K, Kluger J, Kiyozumi D, Gebauer JM, Coffin Talbot J, Kimmel CB, Sekiguchi K, Wagener R, Schwarz H, Ingham PW, Hammerschmidt M. PLoS Genet. 2010 Apr 15;6(4):e1000907. PMID: 20419147 [PubMed - indexed for MEDLINE]Free PMC ArticleFree text

Modes of developmental outgrowth and shaping of a craniofacial bone in zebrafish

Kimmel CB, DeLaurier A, Ullmann B, Dowd J, McFadden M. PLoS One. 2010 Mar 5;5(3):e9475.

PLoS One. 2010 Mar 5;5(3):e9475. Modes of developmental outgrowth and shaping of a craniofacial bone in zebrafish. Kimmel CB, DeLaurier A, Ullmann B, Dowd J, McFadden M.

Institute of Neuroscience, University of Oregon, Eugene, Oregon, United States of America. kimmel@uoneuro.uoregon.edu Abstract The morphologies of individual bones are crucial for their functions within the skeleton, and vary markedly during evolution. Recent studies have begun to reveal the detailed molecular genetic pathways that underlie skeletal morphogenesis. On the other hand, understanding of the process of morphogenesis itself has not kept pace with the molecular work. We examined, through an extended period of development in zebrafish, how a prominent craniofacial bone, the opercle (Op), attains its adult morphology. Using high-resolution confocal imaging of the vitally stained Op in live larvae, we show that the bone initially appears as a simple linear spicule, or spur, with a characteristic position and orientation, and lined by osteoblasts that we visualize by transgenic labeling. The Op then undergoes a stereotyped sequence of shape transitions, most notably during the larval period occurring through three weeks postfertilization. New shapes arise, and the bone grows in size, as a consequence of anisotropic addition of new mineralized bone matrix along specific regions of the pre-existing bone surfaces. We find that two modes of matrix addition, spurs and veils, are primarily associated with change in shape, whereas a third mode, incremental banding, largely accounts for growth in size. Furthermore, morphometric analyses show that shape development and growth follow different trajectories, suggesting separate control of bone shape and size. New osteoblast arrangements are associated with new patterns of matrix outgrowth, and we propose that fine developmental regulation of osteoblast position is a critical determinant of the spatiotemporal pattern of morphogenesis.

PMID 20221441

2009

Fishing for the genetic basis of cardiovascular disease

Tillman Dahme, Hugo A. Katus, and Wolfgang Rottbauer Dis Model Mech. 2009 Jan–Feb; 2(1-2): 18–22. doi: 10.1242/dmm.000687. PMCID: PMC2615162


1981

Morphogenesis and synaptogenesis of the zebrafish Mauthner neuron

Kimmel CB, Sessions SK, Kimmel RJ. J Comp Neurol. 1981 May 1;198(1):101-20. PMID: 7229136