Academic literature on the topic 'Embryo patterning; Fish'
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Journal articles on the topic "Embryo patterning; Fish"
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Kishimoto, Y., K. H. Lee, L. Zon, M. Hammerschmidt, and S. Schulte-Merker. "The molecular nature of zebrafish swirl: BMP2 function is essential during early dorsoventral patterning." Development 124, no. 22 (November 15, 1997): 4457–66. http://dx.doi.org/10.1242/dev.124.22.4457.
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Early dorsoventral pattern formation in vertebrate embryos is regulated by opposing activities of ventralizing bone morphogenetic proteins (BMPs) and dorsal-specific BMP antagonists such as Chordin, Noggin and Follistatin. Specific defects in early dorsoventral patterning have been recently found in a number of zebrafish mutants, which exhibit either a ventralized or dorsalized phenotype. One of these, the ventralized mutant chordino (originally called dino) is caused by a mutation in the zebrafish chordin homologue and interacts genetically with the dorsalized mutant swirl. In swirl mutant embryos, dorsal structures such as notochord and somites are expanded while ventral structures such as blood and nephros are missing. Here we demonstrate that the swirl phenotype is caused by mutations in the zebrafish bmp2 gene (zbmp2). While injection of mRNAs encoded by the mutant alleles has no ventralizing effect, injection of wild-type zbmp2 mRNA leads to a complete rescue of the swirl mutant phenotype. Fertile adult mutant fish were obtained, showing that development after gastrulation is not dependent on zbmp2 function. In addition zBMP2 has no maternal role in mesoderm induction. Our analysis shows that swirl/BMP2, unlike mouse BMP2 but like mouse BMP4, is required for early dorsoventral patterning of the zebrafish embryo.
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Shih, J., and S. E. Fraser. "Characterizing the zebrafish organizer: microsurgical analysis at the early-shield stage." Development 122, no. 4 (April 1, 1996): 1313–22. http://dx.doi.org/10.1242/dev.122.4.1313.
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The appearance of the embryonic shield, a slight thickening at the leading edge of the blastoderm during the formation of the germ ring, is one of the first signs of dorsoventral polarity in the zebrafish embryo. It has been proposed that the shield plays a role in fish embryo patterning similar to that attributed to the amphibian dorsal lip. In a recent study, we fate mapped many of the cells in the region of the forming embryonic shield, and found that neural and mesodermal progenitors are intermingled (Shih, J. and Fraser, S.E. (1995) Development 121, 2755–2765), in contrast to the coherent region of mesodermal progenitors found at the amphibian dorsal lip. Here, we examine the fate and the inductive potential of the embryonic shield to determine if the intermingling reflects a different mode of embryonic patterning than that found in amphibians. Using the microsurgical techniques commonly used in amphibian and avian experimental embryology, we either grafted or deleted the region of the embryonic shield. Homotopic grafting experiments confirmed the fates of cells within the embryonic shield region, showing descendants in the hatching gland, head mesoderm, notochord, somitic mesoderm, endoderm and ventral aspect of the neuraxis. Heterotopic grafting experiments demonstrated that the embryonic shield can organize a second embryonic axis; however, contrary to our expectations based on amphibian research, the graft contributes extensively to the ectopic neuraxis. Microsurgical deletion of the embryonic shield region at the onset of germ ring formation has little effect on neural development: embryos with a well-formed and well-patterned neuraxis develop in the complete absence of notochord cells. While these results show that the embryonic shield is sufficient for ectopic axis formation, they also raise questions concerning the necessity of the shield region for neural induction and embryonic patterning after the formation of the germ ring.
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Fekany, K., Y. Yamanaka, T. Leung, H. I. Sirotkin, J. Topczewski, M. A. Gates, M. Hibi, et al. "The zebrafish bozozok locus encodes Dharma, a homeodomain protein essential for induction of gastrula organizer and dorsoanterior embryonic structures." Development 126, no. 7 (April 1, 1999): 1427–38. http://dx.doi.org/10.1242/dev.126.7.1427.
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The dorsal gastrula organizer plays a fundamental role in establishment of the vertebrate axis. We demonstrate that the zebrafish bozozok (boz) locus is required at the blastula stages for formation of the embryonic shield, the equivalent of the gastrula organizer and expression of multiple organizer-specific genes. Furthermore, boz is essential for specification of dorsoanterior embryonic structures, including notochord, prechordal mesendoderm, floor plate and forebrain. We report that boz mutations disrupt the homeobox gene dharma. Overexpression of boz in the extraembryonic yolk syncytial layer of boz mutant embryos is sufficient for normal development of the overlying blastoderm, revealing an involvement of extraembryonic structures in anterior patterning in fish similarly to murine embryos. Epistatic analyses indicate that boz acts downstream of beta-catenin and upstream to TGF-beta signaling or in a parallel pathway. These studies provide genetic evidence for an essential function of a homeodomain protein in beta-catenin-mediated induction of the dorsal gastrula organizer and place boz at the top of a hierarchy of zygotic genes specifying the dorsal midline of a vertebrate embryo.
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Cleaver, O., D. W. Seufert, and P. A. Krieg. "Endoderm patterning by the notochord: development of the hypochord in Xenopus." Development 127, no. 4 (February 15, 2000): 869–79. http://dx.doi.org/10.1242/dev.127.4.869.
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The patterning and differentiation of the vertebrate endoderm requires signaling from adjacent tissues. In this report, we demonstrate that signals from the notochord are critical for the development of the hypochord, which is a transient, endodermally derived structure that lies immediately ventral to the notochord in the amphibian and fish embryo. It appears likely that the hypochord is required for the formation of the dorsal aorta in these organisms. We show that removal of the notochord during early neurulation leads to the complete failure of hypochord development and to the elimination of expression of the hypochord marker, VEGF. Removal of the notochord during late neurulation, however, does not interfere with hypochord formation. These results suggest that signals arising in the notochord instruct cells in the underlying endoderm to take on a hypochord fate during early neural stages, and that the hypochord does not depend on further notochord signals for maintenance. In reciprocal experiments, when the endoderm receives excess notochord signaling, a significantly enlarged hypochord develops. Overall, these results demonstrate that, in addition to patterning neural and mesodermal tissues, the notochord plays an important role in patterning of the endoderm.
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Richardson, M. K., A. Hornbruch, and L. Wolpert. "Mechanisms of pigment pattern formation in the quail embryo." Development 109, no. 1 (May 1, 1990): 81–89. http://dx.doi.org/10.1242/dev.109.1.81.
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One hypothesis to account for pigment patterning in birds is that neural crest cells migrate into all feather papillae. Local cues then act upon the differentiation of crest cells into melanocytes. This hypothesis is derived from a study of the quail-chick chimaera (Richardson et al., Development 107, 805–818, 1989). Another idea, derived from work on larval fish and amphibia, is that pigment patterns arise from the differential migration of crest cells. We want to know which of these mechanisms can best account for pigment pattern formation in the embryonic plumage of the quail wing. Most of the feather papillae on the dorsal surface of the wing are pigmented, while many on the ventral surface are white. When ectoderm from unpigmented feather papillae is grown in culture, it gives rise to melanocytes. This indicates that neural crest cells are present in white feathers but that they fail to differentiate. If the wing tip is inverted experimentally then the pigment pattern is inverted also. This is difficult to explain in terms of a model based on migratory pathways, unless one assumes that the pathways became re-routed. When an extra polarizing region is grafted to the anterior margin of the wing bud, a duplication develops in: (1) the pattern of skeletal elements; (2) the pattern of feather papillae; (3) the feather pigment pattern. The pigment pattern was not a precise mirror image although some groups of papillae showed a high degree of symmetry in their pigmentation. Both the tip inversions and the duplications produce discontinuities in the feather and pigment patterns. No evidence of intercalation was found in these cases. We conclude that pigment patterning in birds is determined by local cues acting on melanocyte differentiation, rather than by the differential migration of crest cells. Positional values along the anteroposterior axis of the pigment pattern are determined by a gradient of positional information. Thus the pigment patterns, feather patterns and cartilage patterns of the wing may all be specified by a similar mechanism.
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Koster, R., R. Stick, F. Loosli, and J. Wittbrodt. "Medaka spalt acts as a target gene of hedgehog signaling." Development 124, no. 16 (August 15, 1997): 3147–56. http://dx.doi.org/10.1242/dev.124.16.3147.
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In vertebrates, pattern formation in the eye, central nervous system, somites, and limb depends on hedgehog activity, but a general target gene controlled by hedgehog in all these signaling centers has remained largely elusive. The medaka fish gene spalt encodes a zinc-finger transcription factor, which is expressed in all known hedgehog signaling centers of the embryo and in the organizer region at the midbrain-hindbrain boundary. We show that the spalt expression domains expand in response to ectopic hedgehog activity and narrow in the presence of protein kinase A activity, an antagonist of hedgehog signaling, indicating that spalt is a hedgehog target gene. Our results also suggest a signaling mechanism for anterior-posterior patterning of the vertebrate brain that controls spalt expression at the midbrain-hindbrain boundary in a protein kinase A dependent manner likely to involve an unknown member of the hedgehog family.
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Xue, Rui, Armand Keating, Youdong Wang, Duncan Stewart, and Xiao-Yan Wen. "A Chemical Genetic Screen Identified Small Molecules Modulating Zebrafish Vascular Development and Angiogenesis." Blood 110, no. 11 (November 16, 2007): 3721. http://dx.doi.org/10.1182/blood.v110.11.3721.3721.
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Abstract The zebrafish has emerged as an important model for studying vascular development and angiogenesis. Advantages over other models include rapid embryonic development and optical clarity of the embryos. Abnormal angiogenesis is linked to over 70 health conditions and inhibition of angiogenesis is an excellent target for cancer therapy (including hematopoietic malignancies) as tumor growth requires new blood vessels. In this study, we performed a chemical genetic screen in developing zebrafish embryos to identify compounds that modulate zebrafish vascular development and angiogenesis. A zebrafish transgenic line with the Flk1 promoter controlling the GFP (green fluorescent protein) reporter was used. The entire vascular network of the Flk1:GFP fish was marked by GFP and could be visualized under fluorescence microscopy. Screens were performed in 96 well plates with three embryos/well. The outer membranes of healthy zebrafish embryos expressing green fluorescent vasculature were removed by enzymatic digestion with protease at the 16–18 somite stages. Small molecules/compounds were then added to the water at concentrations of 0.1 μM, 1 μM, and 5 μM for 72 hrs. After 24, 48 and 72 hrs of exposure to the compound, the embryos were visually inspected for viability, gross morphological defects, heartbeating rate and circulation. The known angiogenic inhibitor, PD173074 was used as control. An initial screening of 780 compounds in a small molecule compound library identified four small molecules with potent activities in inhibiting zebrafish vascular development. Notably, 1–5 μM of Hit #1 inhibited the growth of cranial vessels and disrupted vascular patterning, which resulted in uneven spacing between intersegmental vessels. While Hit #2 and #5 also inhibited the growth of cranial vessels, the vascular patterning remained unaffected, however, the drug-treated embryos had weak or missing intersegmental vessels. Fish embryos treated by Hit #3 had an enlarged heart and thinner vessels. Interestingly, this screen also identified one compound (Hit #4) with pro-angiogenic activity. Embryos treated with Hit #4 had increased numbers of intersegmental vessels. Hit #2 is a known inhibitor of c-Jun N-terminal kinase and angiogenesis (SP600125), was recently reported to inhibit the proliferation and migration of human endothelial cells in vitro as well as inhibit solid tumor growth in mice. This observation lends validity to the zebrafish screen and the potential utility of the other hits. Experiments are currently in progress to investigate the detailed time course of the angiogenic inhibition and the potential molecular mechanism. Studies of these angiogenic inhibitors may lead to the development of potent anti-cancer drugs while the pro-angiogenic compound may prove useful in facilitating tissue/organ regeneration. We conclude that the zebrafish model is likely to yield valuable information regarding vasculogenesis and its manipulation.
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Buchner, David A., Jordan A. Shavit, Fengyun Su, Jennifer S. Yamaoka, Makoto Kamei, Beth Mcgee, Andrew W. Hanosh, Brant M. Weinstein, David Ginsburg, and Susan E. Lyons. "pak2a Mutations Cause Cerebral Hemorrhage in Redhead Zebrafish." Blood 108, no. 11 (November 16, 2006): 142. http://dx.doi.org/10.1182/blood.v108.11.142.142.
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Abstract Zebrafish are a powerful vertebrate model system for the study of human disease as they share many molecular pathways with mammals. Of note, nearly all of the mammalian coagulation factors are also highly conserved in fish. As part of a whole genome ENU mutagenesis screen, we identified a mutant zebrafish which displayed intraventricular hemorrhage between 2–3 days post fertilization (dpf), which we named redhead. Using an F2 intercross strategy, we mapped this recessive mutant to a 100 kilobase interval on chromosome 2 and identified a splice site mutation in the gene for an ortholog of the p21-activated kinase Pak2. This IVS9 T+2A mutation renders greater than 90% of transcripts nonfunctional, resulting in a hypomorphic allele. Surveying zebrafish expressed sequence tag databases, we identified two Pak2 orthologs in zebrafish, designated Pak2a and Pak2b, with the redhead mutation in pak2a. Central nervous system (CNS) hemorrhage in redhead embryos was rescued by injection of wild type pak2a mRNA. Morpholino knockdown of pak2a in wild type fish phenocopies the redhead mutant, but with an increase in penetrance and severity, including hydrocephalus and pericardial edema secondary to severe hemorrhage. Injection of either pak2a or pak2b mRNA was able to rescue this phenotype. In addition, pak2b knockdown worsened the bleeding phenotype in redhead embryos, with no effect on wild type fish. These results suggest a partial overlap in function between Pak2a and Pak2b. Confocal microscopy was performed at 2.5 dpf in pak2a knockdown embryos transgenic for Gata1-dsRED and Flk1-eGFP, distinctively labeling erythrocytes and endothelial cells, respectively. The sites and magnitude of hemorrhage were variable between individual embryos, but there were no obvious abnormalities in vessel patterning. In summary, we have identified a critical role for Pak2 in maintaining CNS vessel integrity in zebrafish, without apparent effects on other vascular beds. Further analysis of this signaling pathway in the vessel wall may provide novel insight into the mechanisms underlying vascular heterogeneity in mammals, and the tissue specific function of Pak2 in the CNS vasculature.
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O'Reilly, M. A., J. C. Smith, and V. Cunliffe. "Patterning of the mesoderm in Xenopus: dose-dependent and synergistic effects of Brachyury and Pintallavis." Development 121, no. 5 (May 1, 1995): 1351–59. http://dx.doi.org/10.1242/dev.121.5.1351.
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Widespread expression of the DNA-binding protein Brachyury in Xenopus animal caps causes ectopic mesoderm formation. In this paper, we first show that two types of mesoderm are induced by different concentrations of Brachyury. Animal pole explants from embryos injected with low doses of Xbra RNA differentiate into vesicles containing mesothelial smooth muscle and mesenchyme. At higher concentrations somitic muscle is formed. The transition from smooth muscle formation to that of somitic muscle occurs over a two-fold increase in Brachyury concentration. Brachyury is required for differentiation of notochord in mouse and fish embryos, but even the highest concentrations of Brachyury do not induce this tissue in Xenopus animal caps. Co-expression of Brachyury with the secreted glycoprotein noggin does cause notochord formation, but it is difficult to understand the molecular basis of this phenomenon without knowing more about the noggin signal transduction pathway. To overcome this difficulty, we have now tested mesoderm-specific transcription factors for the ability to synergize with Brachyury. We find that co-expression of Pintallavis, but not goosecoid, with Brachyury causes formation of dorsal mesoderm, including notochord. Furthermore, the effect of Pintallavis, like that of Brachyury, is dose-dependent: a two-fold increase in Pintallavis RNA causes a transition from ventral mesoderm formation to that of muscle, and a further two-fold increase induces notochord and neural tissue. These results suggest that Pintallavis cooperates with Brachyury to pattern the mesoderm in Xenopus.
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Conlon, F. L., S. G. Sedgwick, K. M. Weston, and J. C. Smith. "Inhibition of Xbra transcription activation causes defects in mesodermal patterning and reveals autoregulation of Xbra in dorsal mesoderm." Development 122, no. 8 (August 1, 1996): 2427–35. http://dx.doi.org/10.1242/dev.122.8.2427.
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The Brachyury (T) gene is required for formation of posterior mesoderm and for axial development in both mouse and zebrafish embryos. In this paper, we first show that the Xenopus homologue of Brachyury, Xbra, and the zebrafish homologue, no tail (ntl), both function as transcription activators. The activation domains of both proteins map to their carboxy terminal regions, and we note that the activation domain is absent in two zebrafish Brachyury mutations, suggesting that it is required for gene function. A dominant-interfering Xbra construct was generated by replacing the activation domain of Xbra with the repressor domain of the Drosophila engrailed protein. Microinjection of RNA encoding this fusion protein allowed us to generate Xenopus and zebrafish embryos which show striking similarities to genetic mutants in mouse and fish. These results indicate that the function of Brachyury during vertebrate gastrulation is to activate transcription of mesoderm-specific genes. Additional experiments show that Xbra transcription activation is required for regulation of Xbra itself in dorsal, but not ventral, mesoderm. The approach described in this paper, in which the DNA-binding domain of a transcription activator is fused to the engrailed repressor domain, should assist in the analysis of other Xenopus and zebrafish transcription factors.
Dissertations / Theses on the topic "Embryo patterning; Fish"
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Blader, Patrick. "Analysis of gene expression during early development of the zebrafish, Brachydanio rerio." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.282415.
Full textBook chapters on the topic "Embryo patterning; Fish"
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Hild, M., A. Dick, H. Bauer, S. Schulte-Merker, P. Haffter, T. Bouwmeester, and M. Hammerschmidt. "The Roles of BMPs, BMP Antagonists, and the BMP Signaling Transducers Smad1 and Smad5 During Dorsoventral Patterning of the Zebrafish Embryo." In Of Fish, Fly, Worm, and Man, 81–106. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-662-04264-9_6.
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Maden, Malcolm, and John Pizzey. "The Role of Retinoids in Patterning Fish, Amphibian, and Chick Embryos." In Retinoids: Their Physiological Function and Therapeutic Potential, 93–139. Elsevier, 1997. http://dx.doi.org/10.1016/s1569-2590(08)60054-3.
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