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PubMed2005

Hedgehog and retinoid signalling confines nkx2.2b expression to the lateral floor plate of the zebrafish trunk.

The ventral neural tube of vertebrates consists of distinct neural progenitor domains positioned along the dorsoventral (DV) axis that develop different types of moto- and interneurons. Several signalling molecules, most notably Sonic Hedgehog (Shh), retinoic acid (RA) and fibroblast growth factor (FGF) have been implicated in the generation of these domains. Shh is secreted from the floor plate, the ventral most neural tube structure that consists of the medial (MFP) and the lateral floor plate (LFP). While the MFP is well characterized, organization and function of the LFP remains unclear. Here, we describe the novel homeobox gene nkx2.2b that is strongly expressed in the trunk LFP of zebrafish and thus represents a unique marker for the characterization of LFP formation and the identification of LFP deficient mutants. nkx2.2b and its paralog nkx2.2a (formerly known as nk2.2 and nkx2.2) arose by gene duplication in zebrafish. Both duplicates show significant differences in their expression patterns. For example, while prominent nkx2.2a expression has been described in the ventral brain [Barth, K.A., Wilson, S.W., 1995. Expression of zebrafish nk2.2 is influenced by sonic hedgehog/vertebrate hedgehog-1 and demarcates a zone of neuronal differentiation in the embryonic forebrain. Development 121, 1755-1768], hardly any expression can be found in the trunk LFP, which is in contrast to nkx2.2b. Overexpression, mutant and inhibitor analyses show that nkx2.2b expression in the LFP is up-regulated by Shh, but repressed by retinoids and ectopic islet-1 (isl1) expression. In contrast to previously described zebrafish trunk LFP markers, like e.g. tal2 or foxa2, nkx2.2b is exclusively expressed in the LFP. Thus, it represents a unique tool to analyse the mechanisms of ventral neural tube patterning in zebrafish.

Amino Acid Sequence↗

PubMed2006

bmp1 and mini fin are functionally redundant in regulating formation of the zebrafish dorsoventral axis.

Drosophila metalloproteinase Tolloid (TLD) is responsible for cleaving the antagonist Short gastrulation (SOG), thereby regulating signaling by the bone morphogenetic protein (BMP) Decapentaplegic (DPP). In mice there are four TLD-related proteinases, two of which, BMP1 and mammalian Tolloid-like 1 (mTLL1), are responsible for cleaving the SOG orthologue Chordin, thereby regulating signaling by DPP orthologues BMP2 and 4. However, although TLD mutations markedly dorsalize Drosophila embryos, mice doubly homozygous null for BMP1 and mTLL1 genes are not dorsalized in early development. Only a single TLD-related proteinase has previously been reported for zebrafish, and mutation of the zebrafish TLD gene (mini fin) results only in mild dorsalization, manifested by loss of the most ventral cell types of the tail. Here we identify and map the zebrafish BMP1 gene bmp1. Knockdown of BMP1 expression results in a mild tail phenotype. However, simultaneous knockdown of mini fin and bmp1 results in severe dorsalization resembling the Swirl (swr) and Snailhouse (snh) phenotypes; caused by defects in major zebrafish ventralizing genes bmp2b and bmp7, respectively. We conclude that bmp1 and mfn gene products functionally overlap and are together responsible for a key portion of the Chordin processing activity necessary to formation of the zebrafish dorsoventral axis.

Amino Acid Sequence↗

PubMed2006

Cloning and embryonic expression of five distinct sfrp genes in the zebrafish Danio rerio.

Recently, a new member of the secreted frizzled-related protein (sFRP) family, named tlc, has been identified as expressed by the anterior neural border (ANB) cells in the zebrafish Danio rerio. Tlc plays an important role in telencephalic induction and patterning. In absence of Tlc, formation of the telencephalon is severely delayed, but not abolished. This prompted us to clone the other zebrafish sfrp family members and analyse their expression patterns, in search of a family member that may partly functionally overlap with Tlc. Except sizzled, expression profile of sfrp genes in zebrafish has not been reported so far. Here, we describe the cloning of full-length cDNA for sfrp1a, sfrp1b, sfrp2, sfrp3 and sfrp5 gene transcripts and we examine their expression at different embryonic stages. Only sfrp1a is expressed in the anterior neural plate including the ANB cells where and when tlc is expressed. Interestingly, compared to both tlc and sfrp1a, wnt genes are complementary expressed more posteriorly in the neural plate. Later, both sfrp1a and sfrp5 expression profiles are overlapping, in particular at pharyngula stage these genes are expressed in the ventral part of the forebrain, midbrain and hindbrain. sfrp1b, sfrp2 and sfrp3 are mainly expressed in mesodermal and endodermal embryonic tissues. Expression profiles of these different genes in zebrafish gave interesting clues on the possible function and evolution of sFRPs in zebrafish and other organisms.

Animals↗

PubMed2004

Using the zebrafish model to study GATA transcription factors.

The zebrafish is an established animal model system that profits from the availability of strong experimental approaches in both genetics and embryology. As a vertebrate, zebrafish can be used to model many aspects of human development and disease. GATA transcription factors play important roles in the development of many organ systems, including those for hematopoietic, cardiovascular, reproductive, and gut-endoderm derived tissues. The six vertebrate GATA factors are highly conserved in zebrafish at the level of sequence, expression pattern, and function. The identification of mutants, establishment of transgenic GFP reporter fish, and the ease of performing loss- and gain-of-function experiments have all contributed new insight into our understanding of the regulation and function of GATA factors. We review recent advances toward this goal using the zebrafish system with a focus on hematopoiesis and cardiogenesis, and suggest how comparative genetics using the zebrafish genes might reveal core conserved properties, as well as changes in gene function that reflect different morphogenetic programs utilized by various vertebrate embryos.

Amino Acid Sequence↗

PubMed2004

Inhibition of embryonic development by microcystin-LR in zebrafish, Danio rerio.

Microcystin-LR (MC-LR), a cyanobacterial toxin, is a potent inhibitor of protein phosphatase 1 (PP1) and protein phosphatase 2A (PP2A). PP1 and PP2A are critical regulators in embryonic development. However, the effects of MC-LR in embryonic development have been controversial. MC-LR has been demonstrated to be highly toxic in medaka, but not in zebrafish or rabbit embryos. The causes of difference may be due to membrane impermeability that impaired the delivery of MC-LR into cytoplasm of zebrafish and rabbit embryos. Therefore, we microinjected MC-LR directly into developing zebrafish embryos and investigated the effects of MC-LR on embryonic development. We demonstrated that MC-LR induced the lethality of zebrafish embryos in a dose- and time-dependent manner. MC-LR also induced the loss of blastomere coherence via the interference of beta-catenin and cadherins distributions. Furthermore, the MC-LR treated fry revealed various developmental defects. These results suggested that MC-LR might affect the phosphorylation equilibrium of signaling molecules, including beta-catenin and cadherins, required early in zebrafish embryonic development.

Animals↗

PubMed2004

Myosin VI is required for structural integrity of the apical surface of sensory hair cells in zebrafish.

Unconventional myosins have been associated with hearing loss in humans, mice, and zebrafish. Mutations in myosin VI cause both recessive and dominant forms of nonsyndromic deafness in humans and deafness in Snell's waltzer mice associated with abnormal fusion of hair cell stereocilia. Although myosin VI has been implicated in diverse cellular processes such as vesicle trafficking and epithelial morphogenesis, the role of this protein in the sensory hair cells remains unclear. To investigate the function of myosin VI in zebrafish, we cloned and examined the expression pattern of myosin VI, which is duplicated in the zebrafish genome. One duplicate, myo6a, is expressed in a ubiquitous pattern during early development and at later stages, and is highly expressed in the brain, gut, and kidney. myo6b, on the other hand, is predominantly expressed in the sensory epithelium of the ear and lateral line at all developmental stages examined. Both molecules have different splice variants expressed in these tissues. Using a candidate gene approach, we show that myo6b is satellite, a gene responsible for auditory/vestibular defects in zebrafish larvae. Examination of hair cells in satellite mutants revealed that stereociliary bundles are irregular and disorganized. At the ultrastructural level, we observed that the apical surface of satellite mutant hair cells abnormally protrudes above the epithelium and the membrane near the base of the stereocilia is raised. At later stages, stereocilia fused together. We conclude that zebrafish myo6b is required for maintaining the integrity of the apical surface of hair cells, suggesting a conserved role for myosin VI in regulation of actin-based interactions with the plasma membrane.

Alternative Splicing↗

PubMed2004

Repression of nodal expression by maternal B1-type SOXs regulates germ layer formation in Xenopus and zebrafish.

B1-type SOXs (SOXs 1, 2, and 3) are the most evolutionarily conserved subgroup of the SOX transcription factor family. To study their maternal functions, we used the affinity-purified antibody antiSOX3c, which inhibits the binding of Xenopus SOX3 to target DNA sequences [Development. 130(2003)5609]. The antibody also cross-reacts with zebrafish embryos. When injected into fertilized Xenopus or zebrafish eggs, antiSOX3c caused a profound gastrulation defect; this defect could be rescued by the injection of RNA encoding SOX3DeltaC-EnR, a SOX3-engrailed repression domain chimera. In antiSOX3c-injected Xenopus embryos, normal animal-vegetal patterning of mesodermal and endodermal markers was disrupted, expression domains were shifted toward the animal pole, and the levels of the endodermal markers SOX17 and endodermin increased. In Xenopus, SOX3 acts as a negative regulator of Xnr5, which encodes a nodal-related TGFbeta-family protein. Two nodal-related proteins are expressed in the early zebrafish embryo, squint and cyclops; antiSOX3c-injection leads to an increase in the level of cyclops expression. In both Xenopus and zebrafish, the antiSOX3c phenotype was rescued by the injection of RNA encoding the nodal inhibitor Cerberus-short (CerS). In Xenopus, antiSOX3c's effects on endodermin expression were suppressed by injection of RNA encoding a dominant negative version of Mixer or a morpholino against SOX17alpha2, both of which act downstream of nodal signaling in the endoderm specification pathway. Based on these data, it appears that maternal B1-type SOX functions together with the VegT/beta-catenin system to regulate nodal expression and to establish the normal pattern of germ layer formation in Xenopus. A mechanistically conserved system appears to act in a similar manner in the zebrafish.

Amino Acid Sequence↗

PubMed2005

Combinatorial activity of Flamingo proteins directs convergence and extension within the early zebrafish embryo via the planar cell polarity pathway.

The seven-transmembrane protocadherin, Flamingo, functions in a number of processes during Drosophila development, including planar cell polarity (PCP). To assess the role(s) of Flamingo1/Celsr1 (Fmi1) during vertebrate embryogenesis we have exploited the zebrafish system, identifying two Fmi1 orthologues (zFmi1a and zFmi1b) and employing morpholinos to induce mis-splicing of zebrafish fmi1 mRNAs, to both imitate mutations identified in Drosophila flamingo and generate novel aberrant Flamingo proteins. We demonstrate that in the zebrafish gastrula, Fmi1 proteins function in concert with each other and with the vertebrate PCP proteins, Wnt11 and Strabismus, to mediate convergence and extension during gastrulation, without altering early dorso-ventral patterning. We show that zebrafish Fmi1a promotes extension of the entire antero-posterior axis of the zebrafish gastrula including prechordal plate and ventral diencephalic precursors. However, while we show that control over axial extension is autonomous, we find that Fmi1a is not required within lateral cells undergoing dorsal convergence.

Animals↗

PubMed2004

Delta-sarcoglycan is required for early zebrafish muscle organization.

Mutations in sarcoglycans (alpha-, beta-, gamma-, and delta-) have been linked with limb girdle muscular dystrophy (LGMD) types 2C-F in humans. We have cloned the zebrafish orthologue encoding delta-sarcoglycan and mapped the gene to linkage group 21. The predicted zebrafish delta-sarcoglycan protein is highly homologous with its human orthologue including conservation of two of the three predicted glycosylation sites. Like other members of the dystrophin-associated protein complex (DAPC), delta-sarcoglycan localizes to the sarcolemmal membrane of the myofiber in adult zebrafish, but is more apparent at the myosepta in developing embryos. Zebrafish embryos injected with morpholinos against delta-sarcoglycan were relatively inactive at 5 dpf, their myofibers were disorganized, and swim bladders uninflated. Immunohistochemical and immunoblotting experiments show that delta-, beta-, and gamma-sarcoglycans were all downregulated in the morphants, whereas dystrophin expression was unaffected. Whereas humans lacking delta-sarcoglycan primarily show adult phenotypes, our results suggest that delta-sarcoglycan plays a role in early zebrafish muscle development.

Amino Acid Sequence↗

PubMed2005

Production and purification of recombinant somatolactin beta and its effects on melanosome aggregation in zebrafish.

A second form of somatolactin, somatolactin beta (SLbeta), was recently discovered in zebrafish (Danio rerio). This novel subtype of somatolactin is distantly related to somatolactin alpha (SLalpha) found in teleost species and is produced in a different region of the pituitary. To date, no physiological study of SLbeta has been reported. In order to study the physiological functions of SLbeta, recombinant SLbeta protein has been produced and purified. The cDNA of zebrafish SLbeta was cloned into a pET100 bacteria expression vector and His-tagged fusion proteins were produced in BL21 (DE3) Escherichia coli cells. The majority of recombinant somatolactins produced by E. coli were isolated in inclusion bodies although a small percentage of recombinant proteins (<1%) were also found in soluble form. Fusion proteins were solubilized from inclusion bodies using 6M guanidine hydrochloride. Pure recombinant somatolactins were obtained by affinity purification. The estimated molecular weight of 28 kDa by sodium dodecyl sulfate-polyacrylamide gel electrophoresis correlates with the molecular mass calculated from the deduced amino acid sequence of SLbeta. Thereafter, specific polyclonal antibodies against the recombinant SLbeta were developed. These antibodies recognized specifically a group of cells located in the anterior pars intermedia of the pituitary. The antibodies did not react with SLalpha, growth hormone or prolactin cells in the zebrafish pituitary glands. Furthermore, recombinant SLbeta induced melanosome aggregation in a concentration-dependent manner in skin of zebrafish scales. Significant melanosome aggregation was observed in zebrafish melanophores at a concentration of 1 microg/ml. These results, combined with previous reports demonstrate that the recombinant SLbeta proteins produced here are bioactive. The function of inducing melanosome aggregation is conserved among the somatolactin functions.

Animals↗

PubMed2005

Genomic annotation and expression analysis of the zebrafish Rho small GTPase family during development and bacterial infection.

The zebrafish genomic sequence database was analyzed for the presence of genes encoding members of the Rho small GTPases. The analysis shows the presence of 32 zebrafish Rho genes representing one or more homologs of the human RHOA, RND3, RHOF, RHOG, RHOH, RHOJ, RHOU, RHOV, CDC42, RAC1, RAC2, RAC3, RND1, RHOBTB1, RHOBTB2, RHOBTB3, and RHOT1 genes. By expression analysis using reverse transcriptase-PCR we show that at least 20 of the predicted zebrafish small GTPase genes are expressed in the adult stage. Interestingly, only 5 of these were found to be expressed at early embryonic stages, including rhoab, rhoad, cdc42a, cdc42c, and rac1a. We observed a strong upregulation of zebrafish rhogb expression after Mycobacterium marinum infection of adult fish. This complete annotation study provides a firm basis for the use of zebrafish as a model for analysis of Rho GTPase function in vertebrate development and the innate immune system.

Amino Acid Sequence↗

PubMed2003

Induction of cytochrome P450 1A is required for circulation failure and edema by 2,3,7,8-tetrachlorodibenzo-p-dioxin in zebrafish.

The mechanism of toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is thought to result from changes in gene expression via the aryl hydrocarbon receptor (AHR). The induction of cytochrome P450 1A (CYP1A) in various organs is a cardinal effect of TCDD. However, whether CYP1A is involved in endpoints of TCDD toxicity is controversial. We investigated the role of CYP1A in TCDD-induced developmental toxicities using gene knock-down with morpholino antisense oligos. Exposure of zebrafish embryos to TCDD, at concentrations eliciting the hallmark endpoints of developmental toxicity, induced CYP1A in the heart and vascular endothelium throughout the body. This induction by TCDD was markedly inhibited by morpholinos to zebrafish arylhydrocarbon receptor 2 (zfAHR2-MO) and to zebrafish CYP1A (zfCYP1A-MO). The zfAHR2-MO but not the zfCYP1A-MO inhibited zfCYP1A mRNA expression, indicating the specificities of these morpholinos. Injection of either zfAHR2-MO or zfCYP1A-MO blocked the representative signs of TCDD developmental toxicity in zebrafish, pericardial edema and trunk circulation failure. The morpholinos appeared do not affect normal development in TCDD-untreated embryos. These results suggest a mediatory role of zfCYP1A induction through zfAHR2 activation in causing circulation failure by TCDD in zebrafish. This is the first molecular evidence demonstrating an essential requirement for CYP1A induction in TCDD-evoked developmental toxicities in any vertebrate species.

Animals↗

PubMed1997

Overexpression of neurogenin induces ectopic expression of HuC in zebrafish.

Several basic helix-loop-helix (bHLH) transcription factors are known to be involved in vertebrate neurogenesis. To investigate their roles in zebrafish neurogenesis, we isolated cDNAs for homologues of neurogenin and Math(-1)/atonal. The transcription of neurogenin was first detectable in zebrafish nervous system at late gastrulation stage. The expression of zebrafish neurogenin precedes and overlaps that of HuC, one of the earliest neuronal precursor markers. Injection of neurogenin mRNA into early stage zebrafish embryos induced ectopic expression of HuC. These results suggest that neurogenin may participate in the generation of HuC-expressing cells, implying its role in neuronal determination in zebrafish.

Amino Acid Sequence↗

PubMed2000

Cloning and characterization of zebrafish smad2, smad3 and smad4.

smad genes encode transcription factors involved in the signal transduction of members of the TGFbeta superfamily. We report here the cloning, characterization and genomic mapping of smad2, smad3 and smad4 from the zebrafish, Danio rerio. In Xenopus, smad2 overexpression has been shown to interfere with gastrulation and dorsal cell fate specification. However, full-length zebrafish smad2, although functionally active in Xenopus explants, has no effect when overexpressed in zebrafish embryos. In contrast, an N-terminally truncated, constitutively active version of Smad2 protein causes severe dorsalization or partial secondary axis formation, pointing to a role of Smad2 during mesoderm and axis formation. The temporal and spatial expression patterns of zebrafish smad2, 3 and 4 were investigated by developmental RT-PCR and whole mount in-situ hybridization. All three genes show strong and ubiquitous maternal expression. Zygotic expression is weak and ubiquitous in the case of smad2, and strong and ubiquitious in the case of smad4, while smad3 shows a spatially restricted zygotic expression pattern. It is expressed in migrating neural crest cells of the trunk and a subset of cells in the diencephalon in close proximity to the expression domain of the Nodal-related protein Cyclops/Ndr2/Znr1, a potential signal upstream of Smad2/3 required for eye-field separation and floor plate specification. Overexpression of truncated smad2 in cyclops mutant embryos leads to a rescue of the eye and floorplate defects. These data suggest that Smad2 acts as a mediator of Nodal signals during zebrafish midline signaling, while Smad3 might be involved in later steps of eye field separation.

Amino Acid Sequence↗

PubMed1999

A molecular pathway leading to endoderm formation in zebrafish.

BACKGROUND: Several potentially important regulators of vertebrate endoderm development have been identified, including Activin-related growth factors and their receptors; transcriptional regulators encoded by the genes Mixer, Xsox17, and HNF3beta; zebrafish One-eyed pinhead (Oep), a member of the Cripto/FRL-1/Cryptic family of epidermal growth factor related proteins (EGF-CFC); and the product of the zebrafish locus casanova, which plays an essential cell-autonomous role in endoderm formation. RESULTS: Using overexpression studies and the analysis of different zebrafish mutants, we have assembled a molecular pathway that leads to endoderm formation. We report that a zebrafish Sox17 homologue is expressed during gastrulation exclusively in the endoderm and that casanova mutants lack all sox17 expression. Overexpression of mixer induces ectopic sox17-expressing cells in wild-type embryos and promotes endoderm formation in oep mutants, but does not rescue sox17 expression or endoderm formation in casanova mutants. Overexpression of a constitutively active form of the type I transforming growth factor beta (TGF-beta) receptor TARAM-A also promotes sox17 expression in wild-type and oep mutant embryos, but not in casanova mutants. We also show that the Nodal-related molecules Cyclops and Squint and the transmembrane protein Oep are essential for normal mixer expression. CONCLUSIONS: The data indicate that the following pathway leads to zebrafish endoderm formation: Cyclops and Squint activate receptors such as TARAM-A; Oep also appears to act upstream of such receptors; signals transduced by these receptors lead to the expression of mixer, Mixer then acts through casanova to promote the expression of sox17 and differentiation of the endoderm.

Amino Acid Sequence↗

PubMed2002

Zebrafish as a model organism for the identification and characterization of drugs and genes affecting p53 signaling.

p53 and its main negative regulator, Mdm2, are key players in mammalian cancer development. Activation of the transcription factor p53 through DNA damage or other stresses can result in cell cycle arrest, apoptosis, or both. Because of the absence of characterized p53 signaling in zebrafish (Danio rerio), we have studied the roles of Mdm2 and p53 in zebrafish by generating early embryonic knockdowns and examined the involvement of p53 in DNA damage-induced apoptosis. p53-deficient embryos, induced by injection of antisense morpholinos, were morphologically indistinguishable from control embryos, when unperturbed, whereas Mdm2 knockdown embryos were severely apoptotic and arrested very early in development. Double knockdowns showed that p53 deficiency rescued Mdm2-deficient embryos completely, similar to observations in mice. p53 deficiency also markedly decreased DNA damage-induced apoptosis, elicited by ultraviolet irradiation or by the anti-cancer compound camptothecin. p21/Waf/Cip-1 appeared to be a downstream target of zebrafish p53, as revealed relative p21 mRNA levels determined via TaqMan analysis. In contrast to mammals, zebrafish may regulate p53 activity by using an internal polyA signal site. We conclude that zebrafish represents a promising model organism for future compound-based and genetic screens and believe that it will help to identify and characterize new anticancer drugs and new targets for cancer treatment.

Animals↗

PubMed2005

Zebrafish (Danio rerio) matrilins: shared and divergent characteristics with their mammalian counterparts.

We have cloned the cDNAs of the zebrafish (Danio rerio) members of the matrilin family of extracellular adaptor proteins. In contrast to mammals, no orthologue of matrilin-2 was found in zebrafish, either by RT (reverse-transcriptase) PCR using degenerated primers or by screening the databases (Ensembl and NCBI); however, two forms of matrilin-3, matrilin-3a and -3b, were present. The identity with the mammalian matrilins is from more than 70% for the VWA (von Willebrand factor A)-like domains to only 28% for the coiled-coil domains of matrilin-3a and -3b. In all zebrafish matrilins we found a greater variety of splice variants than in mammals, with splicing mainly affecting the number of EGF (epidermal growth factor)-like repeats. The exon-intron organization is nearly identical with that of mammals, and also the characteristic AT-AC intron interrupting the exons coding for the coiled-coil domain is conserved. In the matrilin-3b gene a unique exon codes for a proline- and serine/threonine-rich domain, possibly having mucin-like properties. The matrilin-1 and -3a genes were mapped to chromosome 19 and 20 respectively by the radiation hybrid method. The temporal and spatial expression of zebrafish matrilins is similar to that seen in the mouse. Zebrafish matrilin-4 is highly expressed as early as 24 hpf (h post fertilization), whereas the other matrilins show peak expression at 72 hpf. By immunostaining of whole mounts and sections, we found that matrilin-1 and -3a show predominantly skeletal staining, whereas matrilin-4 is more widespread, with the protein also being present in loose connective tissues and epithelia.

Alternative Splicing↗

PubMed2000

Identification of seven genes in the major histocompatibility complex class I region of the zebrafish.

Physical linkage of genes whose products are involved in similar physiological pathways may have functional significance. The identification of conserved gene linkage in distantly related organisms can therefore strengthen the hypothesis of selection acting towards keeping genes on a chromosome. We used the cDNA selection technique and the polymerase chain reaction (PCR) with generic primers for the identification of new genes on the genomic clones bearing the major histocompatibility complex (Mhc) class I genes of the zebrafish (Danio rerio). We found six new genes (BING1, DAXX, TAPBP, KNSL2, TAP2B and KE6) whose orthologues are known to be linked to the Mhc class II region in humans and mice. In addition, a new zebrafish Mhc class I gene, termed Dare-UFA, was detected. By contrast, a search for the human leucocyte antigen (HLA)-linked BING3, KE3 and SACM2L genes revealed that these loci are not located on the class I clones of the zebrafish. The zebrafish class I region contains repetitive elements with similarity to the DANA, SATA and LINE repeats, as well as Tc1 transposable elements. Our findings indicate a high degree of linkage conservation between the zebrafish class I and the mammalian class II regions.

ATP Binding Cassette Transporter, Subfamily B, Mem↗