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<title>Developmental_Biology RSS : Gourt</title>
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<dc:language>en-us</dc:language>
<dc:rights>Copyright 2007, Gourt.com</dc:rights>
<dc:date>2009-11-07T17:44+10:00
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  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fdvdy.22155" />
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<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22113">
<title>Normal table of postembryonic zebrafish development: Staging by externally visible anatomy of the living fish</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22113</link>
<description><![CDATA[The zebrafish is a premier model organism yet lacks a system for assigning postembryonic fish to developmental stages. To provide such a staging series, we describe postembryonic changes in several traits that are visible under brightfield illumination or through vital staining and epiflourescent illumination. These include the swim bladder, median and pelvic fins, pigment pattern, scale formation, larval fin fold, and skeleton. We further identify milestones for placing postembryonic fish into discrete stages. We relate these milestones to changes in size and age and show that size is a better indicator of developmental progress than is age. We also examine how relationships between size and developmental progress vary with temperature and density, and we document the effects of histological processing on size. To facilitate postembryonic staging, we provide images of reference individuals that have attained specific developmental milestones and are of defined sizes. Finally, we provide guidelines for reporting stages that provide information on both discrete and continuous changes in growth and development. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22129">
<title>Collagen type IV and Perlecan exhibit dynamic localization in the Allantoic Core Domain, a putative stem cell niche in the murine allantois</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22129</link>
<description><![CDATA[A body of evidence suggests that the murine allantois contains a stem cell niche, the Allantoic Core Domain (ACD), that may contribute to a variety of allantoic and embryonic cell types. Given that extracellular matrix (ECM) regulates cell fate and function in niches, the allantois was systematically examined for Collagen type IV (ColIV) and Perlecan, both of which are associated with stem cell proliferation and differentiation. Not only was localization of ColIV and Perlecan more widespread during gastrulation than previously reported, but protein localization profiles were particularly robust and dynamic within the allantois and associated visceral endoderm as the ACD formed and matured. We propose that these data provide further evidence that the ACD is a stem cell niche whose activity is synchronized with associated visceral endoderm, possibly via ECM proteins. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22155">
<title>Muscleblind-like 1 is a negative regulator of TGF-[beta]-dependent epithelial-mesenchymal transition of atrioventricular canal endocardial cells</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22155</link>
<description><![CDATA[The development of the valves and septa of the heart depends on the formation and remodeling of endocardial cushions. Here, we report that the alternative splicing regulator muscleblind-like 1 (MBNL1) exhibits a regionally restricted pattern of expression in canal region endocardium and ventricular myocardium during endocardial cushion development in chicken. Knockdown of MBNL1 in atrioventricular explants leads to a transforming growth factor [beta]-dependent increase in epithelial-mesenchymal transition (EMT) of endocardial cells. This reveals a novel role for MBNL1 during embryonic development, and represents the first evidence that an alternative splicing regulator is a key player in endocardial cushion development. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22154">
<title>Chondroitin sulfate expression is required for cardiac atrioventricular canal formation</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22154</link>
<description><![CDATA[Defects in cardiac valvulogenesis are a common cause of congenital heart disease, and the study of this process promises to provide mechanistic insights and lead to novel therapeutics. Normal valve development involves multiple signaling pathways, and recently roles have been identified for extracellular matrix components, including glycosaminoglycans. We, therefore, explored the role of the glycosaminoglycan chondroitin sulfate during zebrafish cardiac development. Beginning at 33 hr, there is a distinct zone of chondroitin sulfate expression in the atrioventricular (AV) boundary, in the cardiac jelly between the endocardium and myocardium. This expression is both spatially and temporally restricted, and is undetectable after 48 hr. Chemical as well as genetic inhibition of chondroitin synthesis results in AV canal (AVC) defects, including loss of the atrioventricular constriction, blood regurgitation, and failure of circulation. Lack of chondroitin disrupts a marker of cell migration, results in a loss of myocardial and endothelial markers of valvulogenesis, and misregulates bone morphogenetic protein expression, supporting an early role in AVC development. In summary, we have defined a requirement for chondroitin sulfate expression in the normal patterning of the AV boundary, suggesting that this component of the cardiac jelly provides a necessary signal in this critical transition in vertebrate cardiogenesis. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22150">
<title>Asator, a tau-tubulin kinase homolog in Drosophila localizes to the mitotic spindle</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22150</link>
<description><![CDATA[We have used a yeast two-hybrid interaction assay to identify Asator, a tau-tubulin kinase homolog in Drosophila that interacts directly with the spindle matrix protein Megator. Using immunocytochemical labeling by an Asator-specific mAb as well as by transgenic expression of a GFP-labeled Asator construct, we show that Asator is localized to the cytoplasm during interphase but redistributes to the spindle region during mitosis. Determination of transcript levels using qRT-PCR suggested that Asator is expressed throughout development but at relatively low levels. By P-element excision, we generated a null or strong hypomorphic Asatorexc allele that resulted in complete adult lethality when homozygous, indicating that Asator is an essential gene. That the observed lethality was caused by impaired Asator function was further supported by the partial restoration of viability by transgenic expression of Asator-GFP in the Asatorexc homozygous mutant background. The finding that Asator localizes to the spindle region during mitosis and directly can interact with Megator suggests that its kinase activity may be involved in regulating microtubule dynamics and microtubule spindle function. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22148">
<title>Characterization of molecular markers to assess cardiac cushions formation in Xenopus</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22148</link>
<description><![CDATA[The valves and septa of the mature heart are derived from the cardiac cushions, which develop from discrete swellings in two regions of developing heart tube: the atrioventricular (AV) canal and the ventricular outflow tract (OFT). In higher vertebrates, three distinct lineages contribute to the heart valves and septa, the endocardium, the myocardium, and the cardiac neural crest that will populate the cardiac jelly of the OFT. Very little is known about cardiac cushions development in amphibians. Here, we describe the expression of eight genes during key stages of cardiac cushion development in Xenopus. Among these genes, the Wnt antagonist Frzb1 and the transcription factors Xl-Fli, Sox8, Sox9, and Sox10 are differentially expressed in the mesenchyme of the OFT and AV cushions. These genes can be used in combination with lineage-tracing experiments to determine the embryonic origin of the cardiac cushions mesenchyme in Xenopus. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22143">
<title>A rapid and efficient method of genotyping zebrafish mutants</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22143</link>
<description><![CDATA[In order to facilitate high throughput genotyping of zebrafish, we have developed a novel technique that uses High Resolution Melting Analysis (HRMA) to distinguish wild-type, heterozygous mutants and homogyzous mutants. This one hour technique removes the need for restriction enzymes and agarose gels. The generated melting curve profiles are sensitive enough to detect non-specific PCR products. We have been able to reliably genotype three classes of mutations in zebrafish, including point mutants, apchu745 (apcmcr), and p53zy7 (p53I166T), a small deletion mutant (bap28y75) and a retroviral insertion mutant (wdr43hi821a). This technique can genotype individual zebrafish embryos and adults (by tail-clip) and is applicable to other model organisms. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22140">
<title>Probing events with single molecule sensitivity in zebrafish and Drosophila embryos by fluorescence correlation spectroscopy</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22140</link>
<description><![CDATA[Zebrafish and Drosophila are animal models widely used in developmental biology. High-resolution microscopy and live imaging techniques have allowed the investigation of biological processes down to the cellular level in these models. Here, using fluorescence correlation spectroscopy (FCS), we show that even processes on a molecular level can be studied in these embryos. The two animal models provide different advantages and challenges. We first characterize their autofluorescence pattern and determine usable penetration depth for FCS especially in the case of zebrafish, where tissue thickness is an issue. Next, the applicability of FCS to study molecular processes is shown by the determination of blood flow velocities with high spatial resolution and the determination of diffusion coefficients of cytosolic and membrane-bound enhanced green fluorescent protein-labeled proteins in different cell types. This work provides an approach to study molecular processes in vivo and opens up the possibility to relate these molecular processes to developmental biology questions. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22139">
<title>Cyclic Nrarp mRNA expression is regulated by the somitic oscillator but Nrarp protein levels do not oscillate</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22139</link>
<description><![CDATA[Somites are formed progressively from the presomitic mesoderm (PSM) in a highly regulated process according to a strict periodicity driven by an oscillatory mechanism. The Notch and Wnt pathways are key components in the regulation of this somitic oscillator and data from Xenopus and zebrafish embryos indicate that the Notch-downstream target Nrarp participates in the regulation of both activities. We have analyzed Nrarp/nrarp-a expression in the PSM of chick, mouse and zebrafish embryos, and we show that it cycles in synchrony with other Notch regulated cyclic genes. In the mouse its transcription is both Wnt- and Notch-dependent, whereas in the chick and fish embryo it is simply Notch-dependent. Despite oscillating mRNA levels, Nrarp protein does not oscillate in the PSM. Finally, neither gain nor loss of Nrarp function interferes with the normal expression of Notch-related cyclic genes. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22138">
<title>Robust marking of photoreceptor cells and pinealocytes with several reporters under control of the Crx gene</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22138</link>
<description><![CDATA[Crx is a member of the Otx family of homeobox genes with expression restricted to vertebrate retinal photoreceptor and bipolar cells as well as the pinealocytes of the pineal organ. To facilitate the visualization of Crx-expressing cells, we generated transgenic mice expressing several reporters under the control of the Crx regulatory sequences present within a bacterial artificial chromosome (BAC). These mice expand the transgenic mouse collection, which uses photoreceptor regulatory elements for reporter gene expression by providing a broader repertoire of reporter genes. In addition, because Crx is expressed very soon after a cell fated to be a photoreceptor cell becomes postmitotic, they provide a means for early identification of immature photoreceptor cells. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22137">
<title>Loss of Wnt8b has no overt effect on hippocampus development but leads to altered Wnt gene expression levels in dorsomedial telencephalon</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22137</link>
<description><![CDATA[Wnt signalling proteins regulate many aspects of animal development. We have investigated the function of mouse Wnt8b during forebrain development. Wnt8b is expressed in a highly restricted pattern including the prospective hippocampus and hypothalamus. Mutant mice lacking Wnt8b are viable and healthy. The size and morphology of the hippocampus appeared normal in mutant embryos and adults, and we found no evidence of hypothalamic defects in mutants. Wnt8b is also expressed in the neurogenic region of the adult dentate gyrus, however, cell proliferation was unchanged in Wnt8b-/- mutants. Mutant embryos did, however, display altered levels of expression of other Wnt genes normally expressed in forebrain. The spatial expression patterns of other Wnt genes and the overall level of canonical Wnt activity were indistinguishable from wild-types. Thus, loss of Wnt8b does not give rise to an overt morphological phenotype, but does affect expression levels of other Wnts in developing forebrain. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22126">
<title>The metalloendopeptidase gene Pitrm1 is regulated by hedgehog signaling in the developing mouse limb and is expressed in muscle progenitors</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22126</link>
<description><![CDATA[Pitrm1 is a zinc metalloendopeptidase that has been implicated in Alzheimer's disease and mitochondrial peptide degradation, but to date no major role in embryonic development has been documented. In a screen for genes regulated by hedgehog signaling in the mouse limb, we showed that expression of Pitrm1 is upregulated in response to loss of the Gli3 transcription factor. Here we confirm spatial changes in Pitrm1 expression in the Gli3 mutant mouse limb and examine Pitrm1 expression in Shh null and Ptch1 conditional deletion mouse mutants. In wild-type mice, Pitrm1 is expressed in a number of developing tissues known to be patterned by Sonic hedgehog, including the limbs, face, cortex, hippocampus, cerebellum, tectum, sub-mandibular gland, lung, genital tubercle, hair follicles, and the enamel knot of the teeth. Additionally, Pitrm1 is expressed in Pax3-expressing myoblast progenitors in the limb, the dermomyotome, and developing muscles of the face and torso. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22120">
<title>Characterization of the expression pattern of the PRC2 core subunit Suz12 during embryonic development of Xenopus laevis</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22120</link>
<description><![CDATA[The Polycomb repressive complex 2 is a multimeric aggregate that mediates silencing of a broad range of genes, and is associated with important biological contexts such as stem cell maintenance and cancer progression. PRC2 mainly trimethylates lysine 27 of histone H3 and is composed of three essential core subunits: EZH2, EED, and SUZ12. The Xenopus orthologs of PRC2 subunits Ezh2 and Eed have been described but Suz12 remained unidentified. Here, we report the cloning of the Xenopus Suz12, and determine its spatiotemporal expression during development. Xsuz12 transcript is provided maternally and continues to be expressed throughout development, particularly in the anterior part of the developing central nervous system. Importantly, comparative analysis of the expression of the PRC2 subunits Xez, Xeed, and Xrbbp4 indicates that their expression largely coincides with Xsuz12 in the nervous system, suggesting that PRC2 may have unexplored functions in the development of the frog central nervous system. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22132">
<title>Postnatal lung development of rhesus monkey airways: Cellular expression of Clara cell secretory protein</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22132</link>
<description><![CDATA[Clara cell secretory protein (CCSP) is a protective lung protein that is believed to have antioxidant, immunomodulatory, and anticarcinogenic properties. Evidence suggests that CCSP is involved in mitigating many lung disease states during development including asthma. This study's rationale is to define the distribution and abundance of CCSP in the airway epithelium of the rhesus monkey during postnatal lung development using carefully controlled site-specific morphometric approaches in defined airway regions. Immunoreactive CCSP was found in nonciliated cells and mucous cells, including glands, throughout the airway epithelium at all ages, with proximal and mid-level airways having the highest labeling. Overall airway CCSP levels were low at 1 week and 1 month, doubled between 1 and 3 months, and changed little from 3 months to 3 years. Thus, the critical developmental window for CCSP expression to reach adult levels in the rhesus conducting airways occurs between 1 and 3 months of age. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22131">
<title>Characterization of p70 S6 kinase 1 in early development of mouse embryos</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22131</link>
<description><![CDATA[The mTOR kinase controls cell growth, proliferation, and survival through two distinct multiprotein complexes mTORC1 and mTORC2. p70 S6 Kinase 1 (S6K1) is characterized as downstream effector of mTOR. Until recently, the connection between S6K1 and mTORC1 /mTORC2 during the early development of mouse embryos has not been well elucidated. Here, the expression level of total S6K1 and its phosphorylation at Thr389 was determined in four phases of one-cell embryos. S6K1 was active throughout the cell cycle especially with higher activity in G2 and M phases. Rapamycin decreased the activity of M-phase promoting factor (MPF) and delayed the first mitotic cleavage. Down-regulating mTOR and raptor reduced S6K1 phosphorylation at Thr389 in one-cell embryos. Furthermore, rapamycin and microinjection of raptor shRNA decreased the immunofluorescent staining of Thr389 phospho-S6K1. It is proposed that mTORC1 may be involved in the control of MPF by regulating S6K1 during the early development of mouse embryos. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22130">
<title>Planar cell polarity effector gene Fuzzy regulates cilia formation and Hedgehog signal transduction in mouse</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22130</link>
<description><![CDATA[Precise planar cell polarity (PCP) is critical for the development of multiple organ systems in animals. A group of core-PCP proteins are recognized to play crucial roles in convergent extension and other PCP-related processes in mammals. However, the functions of another group of PCP-regulating proteins, the PCP-effector proteins, are yet to be fully studied. In this study, the generation and characterization of a mouse mutant for the PCP effector gene Fuzzy (Fuz) is reported. Fuz homozygous mutants are embryonically lethal, with multiple defects including neural tube defects, abnormal dorsal/ventral patterning of the spinal cord, and defective anterior/posterior patterning of the limb buds. Fuz mutants also exhibit abnormal Hedgehog (Hh) signaling and inefficient proteolytic processing of Gli3. Finally, a significant decrease in cilia was found in Fuz homozygous mutants. In conclusion, Fuz plays an important role in cilia formation, Hh signal transduction, and embryonic development in mammals. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22134">
<title>Dynamic patterning at the pylorus: Formation of an epithelial intestine-stomach boundary in late fetal life</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22134</link>
<description><![CDATA[In the adult mouse, distinct morphological and transcriptional differences separate stomach from intestinal epithelium. Remarkably, the epithelial boundary between these two organs is literally one cell thick. This discrete junction is established suddenly and precisely at embryonic day (E) 16.5, by sharpening a previously diffuse intermediate zone. In the present study, we define the dynamic transcriptome of stomach, pylorus, and intestinal tissues between E14.5 and E16.5. We show that establishment of this boundary is concomitant with the induction of over a thousand genes in intestinal epithelium, and these gene products provide intestinal character. Hence, we call this process intestinalization. We identify specific transcription factors (Hnf4[gamma], Creb3l3, and Tcfec) and examine signaling pathways (Hedgehog and Wnt) that may play a role in this process. Finally, we define a unique expression domain at the pylorus itself and detect novel pylorus-specific patterns for the transcription factor Gata3 and the secreted protein nephrocan. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22133">
<title>A co-dependent requirement of xBcl9 and Pygopus for embryonic body axis development in Xenopus</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22133</link>
<description><![CDATA[The Wnt/[beta]-catenin transcriptional activation complex requires the adapter protein Pygopus (Pygo), which links the basal transcription machinery to [beta]-catenin, by its association with legless (Lgs)/ B-cell lymphoma-9 (Bcl9). Pygo was shown to be required for development in vertebrates, but the role of Lgs/Bcl9 is unknown. We identified an amphibian orthologue of Lgs/Bcl9, XBcl9, which interacted biochemically with X[beta]-catenin and XPygo2. The body axis promoting ability of X[beta]-catenin was diminished when residues required for its interaction with XBcl9 were mutated. In blastula embryos, XBcl9 was transiently preferentially expressed in nuclei of dorsoanterior cells and ectopically expressed XBcl9 required XPygo2 to localize to nuclei. Furthermore, while neither XBcl9 nor XPygo2 alone affected development when ectopically expressed, both were required to induce supernumerary axis and dorsal gene activation. Like XPygo2, depletion of maternal XBcl9 alone caused dorsal defects. These results indicated an essential role of the Pygo-Bcl9 duet in vertebrate body axis formation. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22145">
<title>Brn3a regulates the transition from neurogenesis to terminal differentiation and represses non-neural gene expression in the trigeminal ganglion</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22145</link>
<description><![CDATA[The POU-domain transcription factor Brn3a is expressed in developing sensory neurons at all levels of the neural axis, including the trigeminal ganglion, hindbrain sensory ganglia, and dorsal root ganglia. Changes in global gene expression in the trigeminal ganglion from E11.5 to E13.5 reflect the repression of early neurogenic genes, exit from the cell cycle, and initiation of the expression of definitive markers of sensory function. A majority of these developmental changes are perturbed in the trigeminal ganglia of Brn3a knockout mice. At E13.5, Brn3a-/- trigeminal neurons fail to repress a battery of developmental regulators that are highly expressed at E11.5 and are normally down-regulated as development progresses, and also fail to appropriately activate a set of definitive sensory genes. Remarkably, developing Brn3a-/- trigeminal neurons also ectopically express multiple regulatory genes associated with cardiac and/or cranial mesoderm development, although definitive myogenic programs are not activated. The majority of these genes are not ectopically expressed in the dorsal root ganglia of Brn3a null mice, perhaps due to redundant mechanisms of repression at spinal levels. These results underscore the importance of gene repression in regulating neuronal development, and the need for unbiased screens in the determination of developmental gene regulatory programs. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22144">
<title>Taste bud development and patterning in sighted and blind morphs of Astyanax mexicanus</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22144</link>
<description><![CDATA[In the blind cave-dwelling morph of A. mexicanus, the eye degenerates while other sensory systems, such as gustation, are expanded compared to their sighted (surface-dwelling) ancestor. This study compares the development of taste buds along the jaws of each morph. To determine whether cavefish have an altered onset or rate of taste bud development, we fluorescently labeled basal and receptor cells within taste buds over a developmental series. Our results show that taste bud number increases during development in both morphs. The rate of development is, however, accelerated in cavefish; a small difference in taste bud number exists at 5 dpf reaching threefold by 22 dpf. The expansion of taste buds in cavefish is, therefore, detectable after the onset of eye degeneration. This study provides important insights into the timing of taste bud expansion in cavefish as well as enhances our understanding of taste bud development in teleosts in general. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22142">
<title>Focal electroporation in ovo</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22142</link>
<description><![CDATA[Gene expression fields in embryogenesis are spatially precise and often small, so experimental gene expression often requires similar spatial definition. For in ovo electroporation, typically a gene construct is injected into a natural body cavity in the embryo prior to electroporation. Limited control of the size and location of the electroporated field can be obtained by varying electrode placement and geometry, and by altering the miscibility and viscosity of the construct vehicle but it is difficult to tightly constrain electroporation to small regions. Electroporation of different constructs in close proximity has not been possible. We show that loading the construct into an agarose bead, which is then microsurgically implanted, allows for focal electroporation. Different constructs can be electroporated in close proximity by emplacing several agarose beads. This technique is simple, cheap, rapid, and requires no more specialised equipment than that required for conventional in ovo electroporation. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22141">
<title>Kinked tail mutation results in notochord defects in heterozygotes and distal visceral endoderm defects in homozygotes</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22141</link>
<description><![CDATA[Proper formation of the anterior-posterior (AP) axis in the developing embryo is critical for the correct patterning and often survival of the organism. In the mouse, an initial step in axis establishment is the specification and migration of the distal visceral endoderm (DVE). We have identified a semi-dominant spontaneous mutation in mouse, named kinked tail (knk), which when heterozygous results in a kinky tail phenotype due to fusions and dysmorphology of the tail vertebrae. Vertebral fusions appear to be a secondary effect of notochord thickening and branching in the tail region. Homozygosity for knk results in early embryonic lethality by embryonic day 8.5 due to improper timing of DVE specification and migration, and subsequent failure to establish the AP axis. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22127">
<title>Fzd3 and Fzd6 deficiency results in a severe midbrain morphogenesis defect</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22127</link>
<description><![CDATA[Wnt/[beta]-catenin signaling controls the proper development of the mid-/hindbrain region (MHR) and of midbrain dopaminergic (mDA) neurons, but the Frizzled (Fzd) receptors transducing these signals are still unknown. Fzd3 is expressed throughout the mouse anterior neural tube, whereas Fzd6 is restricted to the MHR. We show that the MHR is properly established and mDA neurons develop normally in Fzd6-/- mutants, but the number of mDA neurons is initially reduced and recovers at later stages in Fzd3-/- embryos. Fzd3-/-; Fzd6-/- double mutants exhibit a severe midbrain morphogenesis defect consisting of collapsed brain ventricles, apparent thickening of the neuroepithelium, focal disruption of the ventricular basal lamina and protrusion of individual cells, and increased proliferation at later stages, despite a normal closure of the anterior neural tube and the rescue of the mDA defect in these embryos. Fzd3 and Fzd6 thus control proper midbrain morphogenesis by a yet unknown mechanism in the mouse. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22125">
<title>Xenopus axin-related protein: A link between its centrosomal localization and function in the Wnt/[beta]-catenin pathway</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22125</link>
<description><![CDATA[The Wnt/[beta]-catenin signaling pathway regulates cell proliferation and cell fate determination in multiple systems. However, the subcellular localization of Wnt pathway components and the significance of this localization for the pathway regulation have not been extensively analyzed. Here we report that Xenopus Axin-related protein (XARP), a component of the [beta]-catenin destruction complex, is localized to the centrosome. This localization of XARP requires the presence of the DIX domain and an adjacent region. Since other components of the Wnt pathway have also been shown to associate with the centrosome, we tested a hypothesis that the [beta]-catenin destruction complex operates at the centrosome. However, XARP mutants with poor centrosomal localization revealed an enhanced rather than decreased ability to antagonize the Wnt/[beta]-catenin pathway. Our data are consistent with the idea that the inactivation of XARP at the centrosome is an important regulatory point in Wnt signaling. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22106">
<title>Patterns of Wnt pathway activity in the mouse incisor indicate absence of Wnt/[beta]-catenin signaling in the epithelial stem cells</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22106</link>
<description><![CDATA[The Wnt pathway is crucial for tooth development as shown by dental defects caused by impaired Wnt signaling in mouse and human. We investigated Wnt signaling in continuously growing mouse incisors focusing on epithelial stem cells. Ten Wnt ligands were expressed both in the dental epithelium and mesenchyme, and were associated mainly with odontoblast and ameloblast differentiation. Wnt/[beta]-catenin activity was detected in mesenchyme in BATgal and TOPgal reporter mice while Axin2, also a reporter of Wnt/[beta]-catenin signaling, was expressed additionally in the epithelium. Axin2 was, however, excluded from the epithelial stem cells in the cervical loop. Interestingly, these cells expressed specifically Lgr5, a Wnt target gene and stem cell marker in the intestine, suggesting that Lgr5 is a marker of incisor stem cells but is not regulated by Wnt signaling in the incisor. We conclude that epithelial stem cells in the mouse incisors are not regulated directly by Wnt/[beta]-catenin signaling. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22101">
<title>Genetic interaction between Lrp6 and Wnt5a during mouse development</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22101</link>
<description><![CDATA[Lrp6 is generally described as a receptor required for signal transduction in the Wnt/[beta]-catenin pathway. Wnt5a, however, is a Wnt ligand that usually does not activate Wnt/[beta]-catenin but rather activates noncanonical Wnt signaling. We have previously shown that Lrp6 can inhibit noncanonical Wnt5a/Wnt11 signaling and that Lrp5/6 loss-of-function produces noncanonical gain-of function defects, which can be rescued by loss of Wnt5a. Here, we describe other phenotypes found in Wnt5a/Lrp6 compound mutant mice, including a worsening of individual Wnt5a or Lrp6 loss of function phenotypes. Lrp6 haploinsufficiency in a Wnt5a-/- background caused spina bifida and exacerbated posterior truncation. Wnt5a-/-Lrp6-/- embryos displayed presomitic mesoderm morphogenesis, somitogenesis, and neurogenesis defects, which are much more severe than in either of the single mutants. Interestingly these results reveal a further level of complexity in processes in which Wnt5a and LRP6 cooperate, or oppose each other, during mouse development. Developmental Dynamics, 2009. Published 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22098">
<title>Identification of responsive cells in the developing somite supports a role for [beta]-catenin-dependent Wnt signaling in maintaining the DML myogenic progenitor pool</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22098</link>
<description><![CDATA[Somitic [beta]-catenin is involved in both maintaining a stem cell population and controlling myogenic differentiation. It is unclear how [beta]-catenin-dependent Wnt signaling accomplishes these disparate roles. The present study shows that only dorsal cells in the early somite respond to [beta]-catenin-dependent Wnt signaling and as the somites compartmentalize to form the dermomyotome and myotome, responding cells are detected primarily in the dorsomedial lip (DML). Forced activation of Wnt target genes in DML cells prevents their progeny from entering the myotome, while blocking activation allows myotomal entry. This suggests a role for [beta]-catenin-dependent/Wnt signaling in maintaining progenitor cells in the DML and that if [beta]-catenin-dependent/Wnt signaling is required to induce myogenesis, the response is transitory and rapidly down-regulated. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22094">
<title>Delayed dopaminergic neuron differentiation in Lrp6 mutant mice</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22094</link>
<description><![CDATA[Wnts are known to bind and activate multiple membrane receptors/coreceptors and to regulate dopaminergic (DA) neuron development and ventral midbrain (VM) morphogenesis. The low density lipoprotein receptor-related protein (Lrp6) is a Wnt co-receptor, yet it remains unclear whether Lrp6 is required for DA neuron development or VM morphogenesis. Lrp6 is expressed ubiquitously in the developing VM. In this study, we show that Lrp6-/- mice exhibit normal patterning, proliferation and cell death in the VM, but display a delay in the onset of DA precursor differentiation. A transient 50% reduction in tyrosine hydroxylase-positive DA neurons and in the expression of DA markers such as Nurr1 and Pitx3, as well as a defect in midbrain morphogenesis was detected in the mutant embryos at embryonic day 11.5. Our results, therefore, suggest a role for Lrp6 in the onset of DA neuron development in the VM as well as a role in midbrain morphogenesis. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22072">
<title>Visualizing canonical Wnt signaling during mouse craniofacial development</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22072</link>
<description><![CDATA[Wnt signaling is critical for proper development of the head and face in the mouse embryo, playing important roles in various aspects of craniofacial development ranging from axis formation to survival of cranial neural crest cells to patterning of the brain. The signaling requirements for the development of different cell lineages in the head and face are active areas of investigation. In this study, we use a recently developed TCF/Lef-LacZ transgenic reporter mouse to characterize the expression of canonical Wnt signaling activity during craniofacial development. We present an atlas of representative sections to show embryonic craniofacial development. Our results demonstrate a pattern of sustained Wnt signaling reporter activity in most tissues which suggests sequential roles in craniofacial development. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22079">
<title>Cardiac neural crest and outflow tract defects in Lrp6 mutant mice</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22079</link>
<description><![CDATA[The role of a key Wnt coreceptor Lrp6 during heart development remains unclear. Here we show that ablation of Lrp6 in mice causes conotruncal anomalies including double-outlet right ventricle (DORV), outflow tract (OFT) cushion hypoplasia, and ventricular septal defect (VSD). Cardiac neural crest cells are specifically lost in the dorsal neural tube and caudal pharyngeal arches of the mutant embryos. We also demonstrate that Lrp6 is required for proliferation and survival of cardiac progenitors and for the expression of Isl1 in the secondary heart field. Other known cardiogenic regulators such as Msx1, Msx2, and Fgf8 are also significantly diminished in the mutant pharyngeal arches and/or OFT. Unexpectedly, the myocardium differentiation factors Mef2c and Myocardin are upregulated in the mutant OFT. Our results indicate that Lrp6 is essential for cardiac neural crest and OFT development upstream of multiple important cardiogenic genes in different cardiac lineage cells during early cardiogenesis. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22075">
<title>[beta]-catenin-mediated signaling and cell adhesion in postgastrulation mouse embryos</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22075</link>
<description><![CDATA[[beta]-Catenin plays two major roles during the development of multicellular organisms. It is the downstream effector of the canonical Wnt signaling cascade, which is involved in many developmental processes and in tumor formation. Additionally, it is linked to classic cadherins and is required for the correct assembly and function of adherens junctions. [beta]-Catenin loss of function mutants show early gastrulation lethality. To address the role of [beta]-catenin in postgastrulation stages and to overcome the early embryonic lethality, we performed conditional gene targeting, using Cdx1::Cre, a newly established mouse line. By this approach, [beta]-catenin was depleted in the entire posterior embryo after the gastrulation process at embryonic day 8.0, when the three germ layers were established. We observed defects in signaling and adhesion which are temporarily separated. At an early event, known targets of Wnt/[beta]-catenin are down-regulated in the paraxial mesoderm. Moreover, Fgf8 and Wnt3a, the key players of the segmentation process, are down-regulated in the neural ectoderm (NE). Wnt3a expression was rescued in mutant embryos by exogenous Fgf and inhibition of Fgf signaling in wild-type embryos resulted in Wnt3a down-regulation. Based on these results, we assume the existence of an autoregulatory feedback loop in the NE where Fgf8 regulates Wnt3a, which in turn, by means of [beta]-catenin, maintains Fgf8 expression. In later stages, the lack of [beta]-catenin caused a progressive posterior disintegration. We found that [beta]-catenin is required for the correct localization of N-cadherin at the membrane of neural ectodermal cells and that its absence causes a disintegration of the neural tube. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22067">
<title>A study on the interactions between heparan sulfate proteoglycans and Wnt proteins</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22067</link>
<description><![CDATA[The Wnt signaling pathway plays key roles in development and adult homeostasis. Wnt proteins are secreted, lipid-modified glycoproteins. They can form morphogen gradients that are regulated at the level of protein secretion, diffusion, and internalization. These gradients can only exist if the hydrophobic Wnt proteins are prevented from aggregating in the extracellular environment. Heparan sulfate proteoglycans (HSPGs) are necessary for proper activity of Wnt proteins and influence their distribution along the morphogenetic gradient. In this study, we show that HSPGs are able to maintain the solubility of Wnt proteins, thus stabilizing their signaling activity. Our results suggest that the role of HSPGs is not only to concentrate Wnt molecules at the cell surface but also to prevent them from aggregating in the extracellular environment. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22060">
<title>The trimeric G protein Go inflicts a double impact on axin in the Wnt/frizzled signaling pathway</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22060</link>
<description><![CDATA[The Wnt/Frizzled signaling pathway plays crucial roles in animal development and is deregulated in many cases of carcinogenesis. We and others have previously demonstrated that Frizzled proteins initiating the intracellular signaling are typical G protein-coupled receptors and rely on the trimeric G protein Go for Wnt transduction in Drosophila. However, the mode of action of Go and its interplay with other transducers of the pathway such as Dishevelled and Axin remained unclear. Here we show that the [alpha]-subunit of Go directly acts on Axin, the multidomain protein playing a negative role in the Wnt signaling. G[alpha]o physically binds Axin and re-localizes it to the plasma membrane. Furthermore, G[alpha]o suppresses Axin's inhibitory action on the Wnt pathway in Drosophila wing development. The interaction of G[alpha]o with Axin critically depends on the RGS domain of the latter. Additionally, we show that the [beta][gamma]-component of Go can directly bind and recruit Dishevelled from cytoplasm to the plasma membrane, where activated Dishevelled can act on the DIX domain of Axin. Thus, the two components of the trimeric Go protein mediate a double - direct and indirect - impact on different regions of Axin, which likely serves to ensure a robust inhibition of this protein and transduction of the Wnt signal. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22041">
<title>Organ patterning in the adult stage: The role of Wnt/[beta]-catenin signaling in liver zonation and beyond</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22041</link>
<description><![CDATA[Wnt/[beta]-catenin signaling has been found to play key roles in metabolic zonation of adult liver, regeneration, and hepatocellular carcinogenesis. In this review, recent progress in this field is summarized, in particular the rapidly growing knowledge about the various interactions of [beta]-catenin with many transcription factors involved in controlling metabolism. These interactions may provide the basis for understanding how the wide range of activities of Wnt/[beta]-catenin signaling is differentially interpreted. Based on these results, a three-level mode for the molecular interpretation of [beta]-catenin activity gradients in liver is proposed favoring cell differentiation, metabolic zonation, and proliferation. While derangement of the combinatorial interplay of the various transcription factors with [beta]-catenin at the intermediary activity level may contribute to the development of metabolic diseases, extremely high activation of [beta]-catenin may eventually lead to initiation and progression of hepatocellular tumors. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22065">
<title>Wnt signaling modulates pre- and postsynaptic maturation: Therapeutic considerations</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22065</link>
<description><![CDATA[Wnt signaling regulates a wealth of aspects of nervous system development and function in embryonic stages and in adulthood. The expression of Wnt ligands and components of the Wnt signaling machinery in early stages of neural development has been related to its role in neurite patterning and in synaptogenesis. Moreover, its expression in the mature nervous system suggests a role for this pathway in synaptic maintenance and function. Therefore, it is of crucial relevance the understanding of the mechanisms by which Wnt signaling regulates these processes. Herein, we discuss how different Wnt ligands, acting through different Wnt signaling pathways, operate in pre- and postsynaptic regions to modulate synapse structure and function. We also elaborate on the idea that Wnt signaling pathways are a target for the treatment of neurodegenerative diseases that affect synaptic integrity, such as Alzheimer's disease. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22059">
<title>Wnt to build a tube: Contributions of Wnt signaling to epithelial tubulogenesis</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22059</link>
<description><![CDATA[Epithelial tubes are crucial to the function of organ systems including the cardiovascular system, pulmonary system, gastrointestinal tract, reproductive organ systems, excretory system, and auditory system. Using a variety of animal model systems, recent studies have substantiated the role of Wnt signaling via the canonical/[beta]-catenin-mediated trajectory, the non-canonical Wnt trajectories, or both, in forming epithelial tubular tissues. This review focuses on the involvement of the Wnt pathways in the induction, specification, proliferation, and morphogenesis involved in tubulogenesis within tissues including the lungs, kidneys, ears, mammary glands, gut, and heart. The ultimate goal is to describe the developmental processes forming the various tubulogenic organ systems to determine the relationships between these processes. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22058">
<title>Wnt won the war: Antagonistic role of Wnt over Shh controls dorso-ventral patterning of the vertebrate neural tube</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22058</link>
<description><![CDATA[The spinal cord has been used as a model to dissect the mechanisms that govern the patterning of tissues during animal development, since the principles that rule the dorso-ventral patterning of the neural tube are applicable to other systems. Signals that determine the dorso-ventral axis of the spinal cord include Sonic hedgehog (Shh), acting as a bona fide morphogenetic signal to determine ventral progenitor identities, and members of the Bmp and the Wnt families, acting in the dorsal neural tube. Although Wnts have been initially recognized as important in proliferation of neural progenitor cells, their role in the dorso-ventral patterning has been controversial. In this review, we discuss recent reports that show an important contribution of the Wnt canonical pathway in dorso-ventral pattern formation. These data allow building a model by which the ventralizing activity of Shh is antagonized by Wnt activity through the expression of Gli3, a potent inhibitor of the Shh pathway. Therefore, antagonistic interactions between canonical Wnt, promoting dorsal identities, and Shh pathways, inducing ventral ones, would define the dorso-ventral patterning of the developing central nervous system. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22046">
<title>Interactions between SOX factors and Wnt/[beta]-catenin signaling in development and disease</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22046</link>
<description><![CDATA[The SOX family of transcription factors have emerged as modulators of canonical Wnt/[beta]-catenin signaling in diverse development and disease contexts. There are over 20 SOX proteins encoded in the vertebrate genome and recent evidence suggests that many of these can physically interact with [beta]-catenin and modulate the transcription of Wnt-target genes. The precise mechanisms by which SOX proteins regulate [beta]-catenin/TCF activity are still being resolved and there is evidence to support a number of models including: protein-protein interactions, the binding of SOX factors to Wnt-target gene promoters, the recruitment of co-repressors or co-activators, modulation of protein stability, and nuclear translocation. In some contexts, Wnt signaling also regulates SOX expression resulting in feedback regulatory loops that fine-tune cellular responses to [beta]-catenin/TCF activity. In this review, we summarize the examples of Sox-Wnt interactions and examine the underlying mechanisms of this potentially widespread and underappreciated mode of Wnt-regulation. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22045">
<title>Variable FZD7 expression in colorectal cancers indicates regulation by the tumour microenvironment</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22045</link>
<description><![CDATA[Recent evidence shows that a sub-population of Wnt/[beta]-catenin target genes is specifically induced in different tissue contexts. FZD7 is a putative Wnt/[beta]-catenin target gene and although it is highly expressed in well-differentiated colorectal cancer tumour cells, its expression is decreased in de-differentiated tumour cells at the invasive front despite elevated Wnt/[beta]-catenin signalling in this area. This variable expression of FZD7 implicates additional regulation by the microenvironment; however, this has not been investigated. To begin to elucidate the role of extracellular matrix in regulating FZD7 expression, we generated a FZD7 promoter reporter and analysed FZD7 promoter activity in colorectal cancer cells grown on different matrices. We demonstrate that the FZD7 promoter is regulated by [beta]-catenin in colorectal cancer cells and observed decreased promoter activity in cells grown on fibronectin but not collagen I or collagen IV. Thus, expression of FZD7 in colorectal cancer may be regulated by fibronectin in the microenvironment. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22047">
<title>Expression of Axin2 indicates a role for canonical Wnt signaling in development of the crown and root during pre- and postnatal tooth development</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22047</link>
<description><![CDATA[Previously two reporter mice, TOPgal and BATgal, have been used to uncover the spatial patterns of canonical Wnt activity up to the bell stage of tooth development. To further understand the function of this pathway, not only at the early developmental stages of odontogenesis but also in postnatal teeth, we have used Axin2-lacZ mice a direct reporter of canonical Wnt activity. As tooth development progresses, Axin2 expression becomes localized to the primary and secondary enamel knots, and the underlying mesenchyme. In postnatal teeth, Axin2 expression is observed in developing odontoblasts, in the dental pulp and concentrated around the developing roots. Expression is excluded from the ameloblasts and associated with the enamel-free zones at the tip of the molar cusps. This expression identifies new roles for Wnt signaling in defining the regions where enamel will form, and controlling root development at late stages of tooth development. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22044">
<title>Manipulating gene activity in Wnt1-expressing precursors of neural epithelial and neural crest cells</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22044</link>
<description><![CDATA[Targeted gene disruption or expression often encounters lethality. Conditional approaches, permitting manipulation at desired stages, are required to overcome this problem in order to analyze gene function in later developmental processes. Wnt1 has been shown to be expressed in neural crest precursors at the dorsal midline region. However, its expression was not detected in emigrated neural crest cells, the descendants of Wnt1-expressing precursors. We have developed mouse transgenic systems to manipulate gene activity in the Wnt1-expressing precursors and their derivatives by integrating the tetracycline-dependent activation and Cre-mediated recombination methods. A new Wnt1-rtTA strain, carrying rtTA under control of Wnt1 regulatory elements, has been created for gene manipulation in a spatiotemporal-specific fashion. Together with our previously developed Wnt1-Cre;R26STOPrtTA model, these systems permit conditional gene expression and ablation in pre-migratory and/or post-migratory neural crest cells. This study demonstrated the versatility of our mouse models to achieve gene manipulation in early neural development. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22054">
<title>Generation of Lrp6 conditional gene-targeting mouse line for modeling and dissecting multiple birth defects/congenital anomalies</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22054</link>
<description><![CDATA[Lrp6 is a key coreceptor in the canonical Wnt pathway that is widely involved in tissue/organ morphogenesis. We generated a loxP-floxed Lrp6 mouse line. Crossing with a general Cre deleter, we obtained the Lrp6-floxdel mice, in which the loxP-floxed exon 2 of Lrp6 gene has been deleted ubiquitously. The homozygotes of Lrp6-floxdel mice reproduced typical defects as seen in the conventional Lrp6-deficient mice, such as defects in eye, limb, and neural tube, and die around birth. We also found new phenotypes including cleft palate and agenesis of external genitalia in the Lrp6-floxdel mice. In addition, the Lrp6-deficient embryos are known to be defective in other systems and internal organs including the heart and brain. Thus, by selectively crossing with a lineage-specific or inducible Cre mouse line, the Lrp6 conditional gene-targeting mice will allow us to model specific types of birth defects for mechanism and prevention studies. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22020">
<title>Xwnt8 directly initiates expression of labial Hox genes</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22020</link>
<description><![CDATA[Hox transcription factors play an essential role in patterning the anteroposterior axis during embryogenesis and exhibit a complex array of spatial and temporal patterns of expression. Their earliest onset of expression in vertebrates is during gastrulation in a temporally collinear sequence in the presomitic/ventrolateral mesoderm, and it is not clear which upstream signal transduction events initiate this expression. Using Xenopus, we present evidence that Xwnt8 is necessary for initiation of this collinear sequence by activating Hox-1 expression in three Hox clusters: hoxd, hoxa, and hoxb. All three labial genes appear to be direct targets of canonical Wnt signaling through Tcf/Lef. In addition, Xwnt8 loss- and gain-of-function leads to indirect regulation of other Hox genes: Hoxb4, Hoxd4, Hoxa7, Hoxc6, and Hoxc8. These findings shed new light on the early role of Wnt8 as well as of a proposed WNT gradient in patterning the Xenopus central nervous system (Kiecker and Niehrs [] Development 128:4189-4201). Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22019">
<title>Regulation of Wnt/[beta]-catenin signaling by protein kinases</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22019</link>
<description><![CDATA[The Wnt/[beta]-catenin signaling pathway plays essential roles during development and adult tissue homeostasis. Inappropriate activation of the pathway can result in a variety of malignancies. Protein kinases have emerged as key regulators at multiple steps of the Wnt pathway. In this review, we present a synthesis covering the latest information on how Wnt signaling is regulated by diverse protein kinases. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
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<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22012">
<title>Xenopus Wnt11b is identified as a potential pronephric inducer</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22012</link>
<description><![CDATA[In this study, we aimed to establish if known wnt signaling molecules could be responsible for inducing early pronephros specification, using a novel and effective in vitro bioassay in Xenopus embryos. Anterior somites have the unique biological activity to signal to unspecified intermediate mesoderm to induce pronephros formation in Xenopus embryos. We have used a molecular candidate gene approach to analyze both canonical and noncanonical wnt expression in isolated anterior and posterior somites and dissected presumptive pronephros, pronephric anlagen, and pronephros from stage 12.5-35 embryos. We have identified potential candidate wnt genes expressed in the right time and place to specify pronephric development. These candidates were then directly tested in an in vitro pronephrogenesis assay based on Holtfreter sandwich cultures. Results revealed that noncanonical wnt11b and wnt11 can induce pronephros formation in vitro. Loss-of-function experiments confirmed that these genes are necessary for normal pronephros development. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
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<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22009">
<title>Crosstalk between Wnt and bone morphogenic protein signaling: A turbulent relationship</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22009</link>
<description><![CDATA[The Wnt and the bone morphogenic protein (BMP) pathways are evolutionarily conserved and essentially independent signaling mechanisms, which, however, often regulate similar biological processes. Wnt and BMP signaling are functionally integrated in many biological processes, such as embryonic patterning in Drosophila and vertebrates, formation of kidney, limb, teeth and bones, maintenance of stem cells, and cancer progression. Detailed inspection of regulation in these and other tissues reveals that Wnt and BMP signaling are functionally integrated in four fundamentally different ways. The molecular mechanism evolved to mediate this integration can also be summarized in four different ways. However, a fundamental aspect of functional and mechanistic interaction between these pathways relies on tissue-specific mechanisms, which are often not conserved and cannot be extrapolated to other tissues. Integration of the two pathways contributes toward the sophisticated means necessary for creating the complexity of our bodies and the reliable and healthy function of its tissues and organs. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
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<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.22003">
<title>Role of Wnt signaling in the biology of the periodontium</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.22003</link>
<description><![CDATA[Continuously erupting teeth have associated with them a continuously regenerating periodontal ligament, but the factors that control this amazing regenerative potential are unknown. We used genetic strategies to show that the periodontal ligament arises from the cranial neural crest. Despite their histological similarity, the periodontal ligament of continuously erupting incisor teeth differs dramatically from the periodontal ligament of molar teeth. The most notable difference was in the distribution of Wnt responsive cells in the incisor periodontal ligament, which coincided with regions of periodontal ligament cell proliferation. We discuss these findings in the context of dental tissue regeneration. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
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<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.21991">
<title>Ror-family receptor tyrosine kinases in noncanonical Wnt signaling: Their implications in developmental morphogenesis and human diseases</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.21991</link>
<description><![CDATA[The Ror-family receptor tyrosine kinases (RTKs) play crucial roles in the development of various organs and tissues. In mammals, Ror2, a member of the Ror-family RTKs, has been shown to act as a receptor or coreceptor for Wnt5a to mediate noncanonical Wnt signaling. Ror2- and Wnt5a-deficient mice exhibit similar abnormalities during developmental morphogenesis, reflecting their defects in convergent extension movements and planar cell polarity, characteristic features mediated by noncanonical Wnt signaling. Furthermore, mutations within the human Ror2 gene are responsible for the genetic skeletal disorders dominant brachydactyly type B and recessive Robinow syndrome. Accumulating evidence demonstrate that Ror2 mediates noncanonical Wnt5a signaling by inhibiting the [beta]-catenin-TCF pathway and activating the Wnt/JNK pathway that results in polarized cell migration. In this article, we review recent progress in understanding the roles of noncanonical Wnt5a/Ror2 signaling in developmental morphogenesis and in human diseases, including heritable skeletal disorders and tumor invasion. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
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<item rdf:about="http://dx.doi.org/10.1002%2Fdvdy.21963">
<title>GSK3[beta] affects apical-basal polarity and cell-cell adhesion by regulating aPKC levels</title>
<link>http://dx.doi.org/10.1002%2Fdvdy.21963</link>
<description><![CDATA[The dynamic rearrangement of cell-cell contacts is required for the establishment of functional epithelial cell sheets. However, the signaling pathways and cellular mechanisms that initiate and maintain this polarity are not well understood. We show that loss of the Wnt signaling component GSK3[beta] results in increased levels of aPKC and leads to defects in apical-basal polarity. We find that GSK3[beta] directly phosphorylates aPKC, which likely promotes its ubiquitin-mediated proteosomal degradation. aPKC increases the levels of Armadillo and stabilizes adherens junctions. These results suggest that the Wnt pathway component GSK3[beta] regulates the polarity determinant aPKC, which in turn affects cell-cell contacts during the development of polarized tissues. Developmental Dynamics, 2009. © 2009 Wiley-Liss, Inc.]]></description>
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