SEARCH · PubMed Health

Results for “Zebrafish development”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,297 records · Page 72Linked to original sources

PubMed2002

Isolation of three zebrafish dachshund homologues and their expression in sensory organs, the central nervous system and pectoral fin buds.

Drosophila dachshund (dac) interacts with sine oculis (so), eyes absent (eya) and eyeless (ey) to control compound eye development. We have cloned three zebrafish dac homologues, dachA, dachB and dachC, which are expressed widely, in distinct but overlapping patterns. Expression of all three is found in sensory organs, the central nervous system and pectoral fin buds. dachA is also expressed strongly in the somites and dachC in the neural crest and pronephros. These expression domains overlap extensively with those of zebrafish pax, eya and six family members, the homologues of Drosophila ey, eya and so, respectively. This is consistent with the proposal that Dach, Eya, Six and Pax family members may form networks, similar to that found in the fly eye, in the development of many vertebrate organs.

Amino Acid Sequence↗

PubMed2007

Genetic screen for mutations affecting development and function of the enteric nervous system.

An intact enteric nervous system is required for normal gastrointestinal tract function. Several human conditions result from decreased innervation by enteric neurons; however, the genetic basis of enteric nervous system development and function is incompletely understood. In an effort to increase our understanding of the mechanisms underlying enteric nervous system development, we screened mutagenized zebrafish for changes in the number or distribution of enteric neurons. We also established a motility assay and rescreened mutants to learn whether enteric neuron number is correlated with gastrointestinal motility in zebrafish. We describe mutations isolated in our screen that affect enteric neurons specifically, as well as mutations that affect other neural crest derivatives or have pleiotropic effects. We show a correlation between the severity of enteric neuron loss and gastrointestinal motility defects. This screen provides biological tools that serve as the basis for future mechanistic studies.

Animals↗

PubMed2001

Xiphophorus genetic linkage map: beginnings of comparative gene mapping in fishes.

The explosive expansion of gene maps of mouse and man has provided strong support for hypotheses first advanced from comparing fish and mammalian genomes that the vertebrate genome was derived from multiple ancestral tetraploidizations with subsequent preferential translocations among paralogous chromosomes. At least two genome duplication events have become widely accepted in lineages leading to vertebrates, and a third has been proposed either before, or after, divergence of fishes and tetrapods. Cytogenetic and comparative gene mapping studies suggest that teleost gene maps have diverged more slowly from gene arrangements in the vertebrate ancestor than have those of mammals. The recent assembly of extensive maps of >100 genes in three fish species, medaka (Beloniformes), Xiphophorus swordtails and platyfishes (Cyprinodontiformes), and zebrafish (Cypriniformes) and the development of less extensive maps in several other fish orders provides the first salient opportunity to assess homology of most or all chromosomes among fishes.

Journal Article↗

PubMed2006

A role for extracellular and transmembrane domains of Sef in Sef-mediated inhibition of FGF signaling.

Sef (similar expression to fgf genes) is a member of the fibroblast growth factor (FGF) synexpression group that negatively regulates FGF receptor (FGFR) signaling in zebrafish during early embryonic development and in mammalian cell culture systems. The mechanism by which Sef exerts its inhibitory effect remains controversial. It has been reported that Sef functions either through binding to and inhibiting FGFR1 activation or by acting downstream of FGF receptors at the level of MEK/ERK kinases. In both cases, the intracellular domain of Sef was found to play a role in the inhibitory function of Sef. Here we demonstrated that both extracellular and transmembrane domains of Sef contributed to Sef-mediated negative regulation of FGF signaling. In fact, over-expression studies in NIH3T3 cells showed that a truncated mutant of Sef, which lacks the intracellular domain (SefECTM), exerted the inhibitory activity on FGF signaling by inhibiting FGFR1 tyrosine phosphorylation and subsequent activation of the Raf/MEK/ERK signaling cascade. We also showed that SefECTM associated with FGFR1, and inhibited FGF-induced ERK activation in HEK293T cells. Furthermore, we demonstrated that the over-expression of SefECTM was able to inhibit the function of a constitutively activated form of FGFR1, FGFR1-C289R, but not FGFR1-K562E. Finally, we found that SefECTM reduced cell viability when over-expressed in human umbilical vein endothelial cells (HUVEC). These data provide additional insight into the structure-activity relationship in the mechanism of inhibitory action of Sef on FGFR1-mediated signaling.

Animals↗

PubMed2005

Regulation of tissue-specific and extracellular matrix-related genes by a class I histone deacetylase.

Class I histone deacetylases (HDACs) repress transcription by deacetylating histones and have been shown to play crucial roles in mouse, Xenopus, zebrafish, and C. elegans development. To identify the molecular networks regulated by a class I HDAC in a multicellular organism, we carried out a global gene expression profiling study using C. elegans embryos, and identified tissue-specific and extracellular matrix (ECM)-related genes as major HDA-1 targets. Ectopic expression of HDA-1 or C. elegans cystatin, an HDA-1 target identified from the microarray, significantly perturbed mammalian cell invasion. Similarly, RNAi depletion or overexpression of human HDAC-1 also affected cell migration. These findings suggest that HDA-1/HDAC-1 may play a critical, evolutionarily conserved role in regulating the extracellular microenvironment. Because human HDACs are targets for cancer therapy, these findings have significant implications in cancer treatment.

Animals↗

PubMed2005

Regulation of axon growth in vivo by activity-based competition.

The formation of functional neural networks requires precise regulation of the growth and branching of the terminal arbors of axons, processes known to be influenced by early network electrical activity. Here we show that a rule of activity-based competition between neighbouring axons appears to govern the growth and branching of retinal ganglion cell (RGC) axon arbors in the developing optic tectum of zebrafish. Mosaic expression of an exogenous potassium channel or a dominant-negative SNARE protein was used to suppress electrical or neurosecretory activity in subsets of RGC axons. Imaging in vivo showed that these forms of activity suppression strongly inhibit both net growth and the formation of new branches by individually transfected RGC axon arbors. The inhibition is relieved when the activity of nearby 'competing' RGC axons is also suppressed. These results therefore identify a new form of activity-based competition rule that might be a key regulator of axon growth and branch initiation.

Animals↗

PubMed2003

Calcium signalling during embryonic development.

Consider a hypothetical design specification for an integrated communication-control system within an embryo. It would require short-range (subcellular) and long-range (pan-embryonic) abilities, it would have to be flexible and, at the same time, robust enough to operate in a dynamically changing environment without information being lost or misinterpreted. Although many signalling elements appear, disappear and sometimes reappear during development, it is becoming clear that embryos also depend on a ubiquitous, persistent and highly versatile signalling system that is based around a single messenger, Ca2+.

Animals↗

PubMed2003

Myotome meanderings. Cellular morphogenesis and the making of muscle.

The formation of muscles within the vertebrate embryo is a tightly orchestrated and complex undertaking. Beyond the initial specification of cells to become muscle are several complex cellular movements and migrations, which lead to the positioning of muscle precursors at specific locations within the embryo. The consequent differentiation, elongation and striation of these cells results in the formation of individual muscles. Investigation of the in vivo morphogenesis of individual vertebrate muscle cells has only recently begun, and is being approached through the use of sophisticated cell labelling and lineage analysis techniques. However, a consensus about the mechanisms involved has yet to be achieved. This review outlines vertebrate embryonic muscle formation in chick, fish and mice, focusing on the embryonic myotome, which generates both the axial musculature and the appendicular muscle of the fins and limbs. We highlight the points of consensus about, and the complexity of, this developmental system, and propose an evolutionary context for the basis of these understandings.

Animals↗

PubMed1996

Retinoid X receptor-selective ligands produce malformations in Xenopus embryos.

Retinoids exert pleiotropic effects on the development of vertebrates through the action of retinoic acid receptors (RAR) and retinoid X receptors (RXR). We have investigated the effect of synthetic retinoids selective for RXR and RAR on the development of Xenopus and zebrafish embryos. In Xenopus, both ligands selective for RAR and RXR caused striking malformations along the anterior-posterior axis, whereas in zebrafish only ligands specific for RAR caused embryonic malformations. In Xenopus, RAR- and RXR-selective ligands regulated the expression of the Xlim-1, gsc, and HoxA1 genes similarly as all-trans-retinoic acid. Nevertheless, RXR-selective ligands activated only an RXR responsive reporter but not an RAR responsive reporter introduced by microinjection into the Xenopus embryo, consistent with our failure to detect conversion of an RXR-selective ligand to different derivatives in the embryo. These results suggest that Xenopus embryos possess a unique response pathway in which liganded RXR can control gene expression. Our observations further illustrate the divergence in retinoid responsiveness between different vertebrate species.

Animals↗

PubMed2025

Complimentary vertebrate Wac models exhibit phenotypes relevant to DeSanto-Shinawi Syndrome.

Monogenic syndromes are associated with neurodevelopmental changes that result in cognitive impairments, neurobehavioral phenotypes including autism and seizures. Limited studies and resources are available to make meaningful headway into the underlying molecular mechanisms that result in these symptoms. One such example is DeSanto-Shinawi Syndrome (DESSH), a rare disorder caused by pathogenic variants in the WAC gene. Individuals with DESSH syndrome exhibit a recognizable craniofacial gestalt, developmental delay/intellectual disability, neurobehavioral symptoms that include autism, ADHD, behavioral difficulties and seizures. However, no thorough studies from a vertebrate model exist to understand how these changes occur. To overcome this, we developed both murine and zebrafish Wac/wac deletion mutants and studied whether their phenotypes recapitulate those described in individuals with DESSH syndrome. We first show that the two Wac models exhibit craniofacial and behavioral changes, reminiscent of abnormalities found in DESSH syndrome. In addition, each model revealed impacts to GABAergic neurons and further studies showed that the mouse mutants are susceptible to seizures, changes in brain volumes that are different between sexes and relevant behaviors. Finally, we uncovered transcriptional impacts of Wac loss of function in mice that will pave the way for future molecular studies into DESSH. These studies present two new animals that begin to uncover some biological underpinnings of DESSH syndrome and elucidate the biology of Wac.

Journal Article↗

PubMed2001

GLI-2 modulates retroviral gene expression.

GLI proteins are involved in the development of mice, humans, zebrafish, Caenorhabditis elegans, Xenopus, and Drosophila. While these zinc finger-containing proteins bind to TG-rich promoter elements and are known to regulate gene expression in C. elegans and Drosophila, mechanistic understanding of how regulation is mediated through naturally occurring transcriptional promoters is lacking. One isoform of human GLI-2 appears to be identical to a factor previously called Tax helper protein (THP), thus named due to its ability to interact with a TG-rich element in the human T-lymphotropic virus type 1 (HTLV-1) enhancer thought to mediate transcriptional stimulation by the Tax protein of HTLV-1. We now demonstrate that, working through its TG-rich binding site and adjacent elements, GLI-2/THP actually suppresses gene expression driven by the HTLV-1 promoter. GLI-2/THP has no effect on the HTLV-2 promoter, activates expression from the promoters of human immunodeficiency virus types 1 and (HIV-1 and -2), and stimulates HIV-1 replication. Both effective suppression and activation of gene expression and viral replication require the first of the five zinc fingers, which is not necessary for DNA binding, to be intact. Thus, not only can GLI-2/THP either activate or suppress gene expression, depending on the promoter, but the same domain (first zinc finger) mediates both effects. These findings suggest a role for GLI-2 in retroviral gene regulation and shed further light on the mechanisms by which GLI proteins regulate naturally occurring promoters.

Animals↗

PubMed2005

Epigenetic histone modification and cardiovascular lineage programming in mouse embryonic stem cells exposed to laminar shear stress.

Experimental evidence indicates that shear stress (SS) exerts a morphogenetic function during cardiac development of mouse and zebrafish embryos. However, the molecular basis for this effect is still elusive. Our previous work described that in adult endothelial cells, SS regulates gene expression by inducing epigenetic modification of histones and activation of transcription complexes bearing acetyltransferase activity. In this study, we evaluated whether SS treatment could epigenetically modify histones and influence cell differentiation in mouse embryonic stem (ES) cells. Cells were exposed to a laminar SS of 10 dyne per cm2/s(-1), or kept in static conditions in the presence or absence of the histone deacetylase inhibitor trichostatin A (TSA). These experiments revealed that SS enhanced lysine acetylation of histone H3 at position 14 (K14), as well as serine phosphorylation at position 10 (S10) and lysine methylation at position 79 (K79), and cooperated with TSA, inducing acetylation of histone H4 and phosphoacetylation of S10 and K14 of histone H3. In addition, ES cells exposed to SS strongly activated transcription from the vascular endothelial growth factor (VEGF) receptor 2 promoter. This effect was paralleled by an early induction of cardiovascular markers, including smooth muscle actin, smooth muscle protein 22-alpha, platelet-endothelial cell adhesion molecule-1, VEGF receptor 2, myocyte enhancer factor-2C (MEF2C), and alpha-sarcomeric actin. In this condition, transcription factors MEF2C and Sma/MAD homolog protein 4 could be isolated from SS-treated ES cells complexed with the cAMP response element-binding protein acetyltransferase. These results provide molecular basis for the SS-dependent cardiovascular commitment of mouse ES cells and suggest that laminar flow may be successfully applied for the in vitro production of cardiovascular precursors.

Acetylation↗

PubMed2002

Distinct functions of TBP and TLF/TRF2 during spermatogenesis: requirement of TLF for heterochromatic chromocenter formation in haploid round spermatids.

TLF (TBP-like factor) is a protein commonly thought to belong to the general transcription initiation complex. TLF is evolutionarily conserved and has been shown to be essential for early development in C. elegans, zebrafish and Xenopus. In mammals however, TLF has a specialised function, as revealed by targeted mutation of the gene in the mouse germline. The TLF mutation elicits a complete arrest of late spermiogenesis and increased haploid cell apoptosis. We explored in more detail the molecular function that TLF plays in the differentiation program of male germ cells. A comparison of TBP and TLF reveals drastic differences, both in their temporal expression pattern and in their intracellular location. While TBP is ubiquitously expressed, TLF expression is strictly developmentally regulated, being very high in late pachytene spermatocytes, suggesting a function prior to the apoptosis of the haploid cells. A refined study of TLF-deficient mice reveals defective acrosome formation in early stage spermatids. Most importantly, our results uncover an unsuspected function of TLF in chromatin organisation. Indeed, early spermatids in TLF-deficient mice display a fragmentation of the chromocenter, a condensed structure formed by the association of centromeric heterochromatin and containing the HP1 proteins. This defect is likely to be the primary cause of spermatogenic failure in the TLF mutant mice.

Acrosome↗

PubMed2026

Complementary vertebrate Wac models exhibit phenotypes relevant to DeSanto-Shinawi Syndrome.

Monogenic syndromes are associated with neurodevelopmental changes that result in cognitive impairments and neurobehavioral phenotypes, including autism and seizures. Limited studies and resources are available to make meaningful headway into the underlying molecular mechanisms that result in these symptoms. One such example is DeSanto-Shinawi Syndrome (DESSH), a rare disorder caused by pathogenic variants in the WAC gene. Individuals with DESSH syndrome exhibit a recognizable craniofacial gestalt, developmental delay/intellectual disability, neurobehavioral symptoms that include autism, ADHD, behavioral difficulties, and seizures. However, no thorough studies from a vertebrate model exist to understand how these changes occur. To overcome this, we developed both murine and zebrafish Wac/wac deletion mutants and studied whether their phenotypes recapitulate those described in individuals with DESSH syndrome. We first show that the two Wac models exhibit craniofacial and behavioral changes, reminiscent of abnormalities found in DESSH syndrome. In addition, each model revealed impacts on GABAergic neurons and further studies showed that the mouse mutants are susceptible to seizures, changes in brain volumes that are different between sexes and relevant behaviors. Finally, we uncovered transcriptional impacts of Wac loss-of-function in mice that will pave the way for future molecular studies into DESSH. These studies present two new vertebrate models that begin to uncover biological underpinnings of DESSH syndrome and elucidate the biology of Wac.

Animals↗

PubMed1995

The first retinal axons and their microenvironment in zebrafish: cryptic pioneers and the pretract.

The initial development of the optic tract was studied with light and electron microscopy in the zebrafish (Danio rerio). Intraocular injections of the fluorescent marker, 1,1'-dioctadecyl-3,3,3',3' tetramethylindocarbocyanine perchlorate (dil), labeled retinal axons and growth cones anterogradely, and injections of dil into the optic chiasm labeled retinal ganglion cells retrogradely. Labeled tissue was photoconverted and examined electron microscopically. The ventronasal retinal quadrant produced the first growth cones. They were the first growth cones in the optic stalk. The leading retinal growth cones, typically 4-10 in number, advanced alongside the tract of the postoptic commissure but rarely sent filopodia into it and never wrapped its axons. Instead, the retinal growth cones followed a pretract, a subpial region that was morphologically distinct from its surroundings and extended out in front of the leading growth cones, presaging the optic tract. Thus, the retinal growth cones, previously thought to be followers of preexisting axons, are actually cryptic pioneers whose proximity to the earlier axons masks their pioneering nature. We suggest that cryptic pioneers and pretracts are probably common elsewhere in the nervous system.

Aging↗

PubMed2006

Learning from small fry: the zebrafish as a genetic model organism for aquaculture fish species.

In recent years, the zebrafish has become one of the most prominent vertebrate model organisms used to study the genetics underlying development, normal body function, and disease. The growing interest in zebrafish research was paralleled by an increase in tools and methods available to study zebrafish. While zebrafish research initially centered on mutagenesis screens (forward genetics), recent years saw the establishment of reverse genetic methods (morpholino knock-down, TILLING). In addition, increasingly sophisticated protocols for generating transgenic zebrafish have been developed and microarrays are now available to characterize gene expression on a near genome-wide scale. The identification of loci underlying specific traits is aided by genetic, physical, and radiation hybrid maps of the zebrafish genome and the zebrafish genome project. As genomic resources for aquacultural species are increasingly being generated, a meaningful interaction between zebrafish and aquacultural research now appears to be possible and beneficial for both sides. In particular, research on nutrition and growth, stress, and disease resistance in the zebrafish can be expected to produce results applicable to aquacultural fish, for example, by improving husbandry and formulated feeds. Forward and reverse genetics approaches in the zebrafish, together with the known conservation of synteny between the species, offer the potential to identify and verify candidate genes for quantitative trait loci (QTLs) to be used in marker-assisted breeding. Moreover, some technologies from the zebrafish field such as TILLING may be directly transferable to aquacultural research and production.

Animals↗

PubMed1999

Tenascin-C expression in the trunk of wild-type, cyclops and floating head zebrafish embryos.

The function and the regulation of the expression of the extracellular matrix molecule tenascin-C during embryonic development are still unclear. In the present study, the expression of tenascin-C was analyzed in the trunk of zebrafish at the end of the first embryonic day. An antiserum raised against a zebrafish tenascin-C (TN-C) fusion protein reacted with 220 (doublet), 200, and 160 KD peptides. In situ hybridization showed that in the zebrafish wild-type embryo, tn-c mRNA was expressed by somites, neural crest cells, roof plate, notochord, hypochord, and tail fin bud. Thus, the expression of tn-c mRNA is an excellent marker for the differentiation of most zebrafish trunk structures. Immunolabelling with the anti-TN-C antibody was detected in the migratory pathway of neural crest cells and in the intersomitic furrows. In situ hybridization analysis of the zebrafish cyclops mutants, lacking the midline floor plate cells, showed normal expression of tn-c mRNA in all trunk structures. Analysis of the floating-head mutant, lacking the notochord, showed that tn-c mRNA expression in neural crest cells, roof plate, and tail fin bud is normal, but it is defective in the somites. By showing that the notochord, but not the floor plate, cells are required for normal tn-c expression in the trunk, this work provides new information on the role played by the embryonic axial structures in the regulation of the expression of tn-c during the development of zebrafish and allows new conclusions about somite patterning in the cyclops and floating-head zebrafish mutants.

Animals↗

PubMed2005

Supernumerary neuromasts in the posterior lateral line of zebrafish lacking peripheral glia.

The lateral line and its associated sensory nerves develop from cephalic epithelial thickenings called neurogenic placodes. In the zebrafish, the transcription factor neurogenin 1 is essential for the generation of the sensory ganglion from the placode, but is dispensable for the migration of the primordium and the initial development of neuromasts. We find that inactivation of the gene encoding neurogenin 1 leads to the development of over twice the normal number of neuromasts along the posterior lateral line of zebrafish larvae. Mutation of the gene encoding another transcription factor, sox10, has a similar effect. After a normal number of proneuromasts is initially deposited by the migrating primordia, interneuromast cells divide and differentiate to form the extra neuromasts. Our results indicate that the development of these intercalary neuromasts occurs principally because of the absence of neural crest-derived peripheral glia, which evidently inhibit the assembly of interneuromast cells into neuromasts.

Animals↗