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        <title>Editor's picks</title>
        <link>http://www.biomedcentral.com/bmcdevbiol/</link>
        <description>The editor's pick of recent articles published by BMC Developmental Biology</description>
        <dc:date>2012-04-27T00:00:00Z</dc:date>
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                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-213X/12/14" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-213X/12/10" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-213X/12/9" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-213X/12/8" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-213X/11/76" />
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        <item rdf:about="http://www.biomedcentral.com/1471-213X/12/14">
        <title>Histamine is a modulator of metamorphic competence in Strongylocentrotus purpuratus (Echinodermata: Echinoidea)</title>
        <description>Background:
A metamorphic life-history is present in the majority of animal phyla. This developmental mode is particularly prominent among marine invertebrates with a bentho-planktonic life cycle, where a pelagic larval form transforms into a benthic adult. Metamorphic competence (the stage at which a larva is capable to undergo the metamorphic transformation and settlement) is an important adaptation both ecologically and physiologically. The competence period maintains the larval state until suitable settlement sites are encountered, at which point the larvae settle in response to settlement cues. The mechanistic basis for metamorphosis (the morphogenetic transition from a larva to a juvenile including settlement), i.e. the molecular and cellular processes underlying metamorphosis in marine invertebrate species, is poorly understood. Histamine (HA), a neurotransmitter used for various physiological and developmental functions among animals, has a critical role in sea urchin fertilization and in the induction of metamorphosis. Here we test the premise that HA functions as a developmental modulator of metamorphic competence in the sea urchin Strongylocentrotus purpuratus.
Results:
Our results provide strong evidence that HA leads to the acquisition of metamorphic competence in S. purpuratus larvae. Pharmacological analysis of several HA receptor antagonists and an inhibitor of HA synthesis indicates a function of HA in metamorphic competence as well as programmed cell death (PCD) during arm retraction. Furthermore we identified an extensive network of histaminergic neurons in pre-metamorphic and metamorphically competent larvae. Analysis of this network throughout larval development indicates that the maturation of specific neuronal clusters correlates with the acquisition of metamorphic competence. Moreover, histamine receptor antagonist treatment leads to the induction of caspase mediated apoptosis in competent larvae.
Conclusions:
We conclude that HA is a modulator of metamorphic competence in S. purpuratus development and hypothesize that HA may have played an important role in the evolution of settlement strategies in echinoids. Our findings provide novel insights into the evolution of HA signalling and its function in one of the most important and widespread life history transitions in the animal kingdom - metamorphosis.</description>
        <link>http://www.biomedcentral.com/1471-213X/12/14</link>
                <dc:creator>Josh Sutherby</dc:creator>
                <dc:creator>Jamie-Lee Giardini</dc:creator>
                <dc:creator>Julia Nguyen</dc:creator>
                <dc:creator>Gary Wessel</dc:creator>
                <dc:creator>Mariana Leguia</dc:creator>
                <dc:creator>Andreas Heyland</dc:creator>
                <dc:source>BMC Developmental Biology 2012, 12:14</dc:source>
        <dc:date>2012-04-27T00:00:00Z</dc:date>
        <dc:identifier>10.1186/1471-213X-12-14</dc:identifier>
                            <dc:title>Sea urchin development modulated by histamine</dc:title>
                            <dc:description>Histamine modulates the development of purple sea urchins, Strongylocentrotus purpuratus, from larva to settled adult apparently through inhibition of programmed cell death, an essential process of the metamorphic transition.</dc:description>
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                <prism:publicationName>BMC Developmental Biology</prism:publicationName>
        <prism:issn>1471-213X</prism:issn>
        <prism:volume>12</prism:volume>
        <prism:startingPage>14</prism:startingPage>
        <prism:publicationDate>2012-04-27T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.biomedcentral.com/1471-213X/12/10">
        <title>Genetic and physical interaction of Meis2, Pax3 and Pax7 during dorsal midbrain development</title>
        <description>Background:
During early stages of brain development, secreted molecules, components of intracellular signaling pathways and transcriptional regulators act in positive and negative feed-back or feed-forward loops at the mid-hindbrain boundary. These genetic interactions are of central importance for the specification and subsequent development of the adjacent mid- and hindbrain. Much less, however, is known about the regulatory relationship and functional interaction of molecules that are expressed in the tectal anlage after tectal fate specification has taken place and tectal development has commenced.
Results:
Here, we provide experimental evidence for reciprocal regulation and subsequent cooperation of the paired-type transcription factors Pax3, Pax7 and the TALE-homeodomain protein Meis2 in the tectal anlage. Using in ovo electroporation of the mesencephalic vesicle of chick embryos we show that (i) Pax3 and Pax7 mutually regulate each other&apos;s expression in the mesencephalic vesicle, (ii) Meis2 acts downstream of Pax3/7 and requires balanced expression levels of both proteins, and (iii) Meis2 physically interacts with Pax3 and Pax7. These results extend our previous observation that Meis2 cooperates with Otx2 in tectal development to include Pax3 and Pax7 as Meis2 interacting proteins in the tectal anlage.
Conclusion:
The results described here suggest a model in which interdependent regulatory loops involving Pax3 and Pax7 in the dorsal mesencephalic vesicle modulate Meis2 expression. Physical interaction with Meis2 may then confer tectal specificity to a wide range of otherwise broadly expressed transcriptional regulators, including Otx2, Pax3 and Pax7.</description>
        <link>http://www.biomedcentral.com/1471-213X/12/10</link>
                <dc:creator>Zsuzsa Agoston</dc:creator>
                <dc:creator>Naixin Li</dc:creator>
                <dc:creator>Anja Haslinger</dc:creator>
                <dc:creator>Andrea Wizenmann</dc:creator>
                <dc:creator>Dorothea Schulte</dc:creator>
                <dc:source>BMC Developmental Biology 2012, 12:10</dc:source>
        <dc:date>2012-03-05T00:00:00Z</dc:date>
        <dc:identifier>10.1186/1471-213X-12-10</dc:identifier>
                            <dc:title>Pax3 and Pax7 influence midbrain development</dc:title>
                            <dc:description>The transcription factors Pax3 and Pax7 regulate each other&apos;s expression in the dorsal midbrain of chick embryos and modulate the expression of Meis2, a TALE-homeodomain protein, required for normal development of this brain region</dc:description>
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                <prism:publicationName>BMC Developmental Biology</prism:publicationName>
        <prism:issn>1471-213X</prism:issn>
        <prism:volume>12</prism:volume>
        <prism:startingPage>10</prism:startingPage>
        <prism:publicationDate>2012-03-05T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.biomedcentral.com/1471-213X/12/9">
        <title>Skeletal muscle regeneration in &lt;it&gt;Xenopus &lt;/it&gt;tadpoles and zebrafish larvae</title>
        <description>Background:
Mammals are not able to restore lost appendages, while many amphibians are. One important question about epimorphic regeneration is related to the origin of the new tissues and whether they come from mature cells via dedifferentiation and/or from stem cells. Several studies in urodele amphibians (salamanders) indicate that, after limb or tail amputation, the multinucleated muscle fibres do dedifferentiate by fragmentation and proliferation, thereby contributing to the regenerate. In Xenopus laevis tadpoles, however, it was shown that muscle fibres do not contribute directly to the tail regenerate. We set out to study whether dedifferentiation was present during muscle regeneration of the tadpole limb and zebrafish larval tail, mainly by cell tracing and histological observations.
Results:
Cell tracing and histological observations indicate that zebrafish tail muscle do not dedifferentiate during regeneration. Technical limitations did not allow us to trace tadpole limb cells, nevertheless we observed no signs of dedifferentiation histologically. However, ultrastructural and gene expression analysis of regenerating muscle in tadpole tail revealed an unexpected dedifferentiation phenotype. Further histological studies showed that dedifferentiating tail fibres did not enter the cell cycle and in vivo cell tracing revealed no evidences of muscle fibre fragmentation. In addition, our results indicate that this incomplete dedifferentiation was initiated by the retraction of muscle fibres.
Conclusions:
Our results show that complete skeletal muscle dedifferentiation is less common than expected in lower vertebrates. In addition, the discovery of incomplete dedifferentiation in muscle fibres of the tadpole tail stresses the importance of coupling histological studies with in vivo cell tracing experiments to better understand the regenerative mechanisms.</description>
        <link>http://www.biomedcentral.com/1471-213X/12/9</link>
                <dc:creator>Alexandre Rodrigues</dc:creator>
                <dc:creator>Bea Christen</dc:creator>
                <dc:creator>Mercé Martí</dc:creator>
                <dc:creator>Juan Carlos Izpisúa Belmonte</dc:creator>
                <dc:source>BMC Developmental Biology 2012, 12:9</dc:source>
        <dc:date>2012-02-27T00:00:00Z</dc:date>
        <dc:identifier>10.1186/1471-213X-12-9</dc:identifier>
                            <dc:title>Dedifferention not enough for regeneration</dc:title>
                            <dc:description>Regenerating limbs in lower amphibians, such as tadpoles and zebrafish, show no evidence of myofibre dedifferentiation indicating that this process is less important to regeneration than previously thought and implicating progenitor cells as the major players.</dc:description>
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                <prism:publicationName>BMC Developmental Biology</prism:publicationName>
        <prism:issn>1471-213X</prism:issn>
        <prism:volume>12</prism:volume>
        <prism:startingPage>9</prism:startingPage>
        <prism:publicationDate>2012-02-27T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.biomedcentral.com/1471-213X/12/8">
        <title>Integrins are required for cardioblast polarisation in &lt;it&gt;Drosophila&lt;/it&gt;</title>
        <description>Background:
The formation of a tubular organ, such as the heart, requires the communication of positional and polarity signals between migratory cells. Key to this process is the establishment of a new luminal domain on the cell surface, generally from the apical domain of a migratory cell. This domain will also acquire basal properties, as it will produce a luminal extracellular matrix. Integrin receptors are the primary means of cell adhesion and adhesion signaling with the extracellular matrix. Here we characterise the requirement of Integrins in a genetic model of vasculogenesis, the formation of the heart in Drosophila.
Results:
As with vertebrates, the Drosophila heart arises from lateral mesoderm that migrates medially to meet their contralateral partners, to then assemble a midline vessel. During migration, Integrins are among the first proteins restricted to the presumptive luminal domain of cardioblasts. Integrins are required for normal levels of leading edge membrane motility. Apical accumulation of Integrins is enhanced by Robo, and reciprocally, apicalisation of luminal factors like Slit and Robo requires Integrin function. Integrins may provide a template for the formation of a lumen by stabilising lumen factors like Robo. Subsequent to migration, Integrin is required for normal cardioblast alignment and lumen formation. This phenotype is most readily modified by other mutations that affect adhesion, such as Talin and extracellular matrix ligands.
Conclusion:
Our findings reveal an instructive role for Integrins in communicating polarising information to cells during migration, and during transition to an epithelial tube structure.</description>
        <link>http://www.biomedcentral.com/1471-213X/12/8</link>
                <dc:creator>Jessica Vanderploeg</dc:creator>
                <dc:creator>L Lourdes Vazquez Paz</dc:creator>
                <dc:creator>Allison MacMullin</dc:creator>
                <dc:creator>J Roger Jacobs</dc:creator>
                <dc:source>BMC Developmental Biology 2012, 12:8</dc:source>
        <dc:date>2012-02-21T00:00:00Z</dc:date>
        <dc:identifier>10.1186/1471-213X-12-8</dc:identifier>
                            <dc:title>Integrins integral for heart development</dc:title>
                            <dc:description>Drosphila lacking integrin receptors show abnormal dorsal vessel tube closure and incorrect distribution of Slit, Robo and Dg, all required for this process, revealing the importance of these proteins in heart development.</dc:description>
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                <prism:publicationName>BMC Developmental Biology</prism:publicationName>
        <prism:issn>1471-213X</prism:issn>
        <prism:volume>12</prism:volume>
        <prism:startingPage>8</prism:startingPage>
        <prism:publicationDate>2012-02-21T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.biomedcentral.com/1471-213X/11/76">
        <title>Targeting the hemangioblast with a novel cell type-specific enhancer</title>
        <description>Background:
Hemangioblasts are known as the common precursors for primitive hematopoietic and endothelial lineages. Their existence has been supported mainly by the observation that both cell types develop in close proximity and by in vitro differentiation and genetic studies. However, more compelling evidence will arise from tracking their cell fates using a lineage-specific marker.
Results:
We report the identification of a hemangioblast-specific enhancer (Hb) located in the cis-regulatory region of chick Cerberus gene (cCer) that is able to direct the expression of enhanced green fluorescent protein (eGFP) to the precursors of yolk sac blood and endothelial cells in electroporated chick embryos. Moreover, we present the Hb-eGFP reporter as a powerful live imaging tool for visualizing hemangioblast cell fate and blood island morphogenesis.
Conclusions:
We hereby introduce the Hb enhancer as a valuable resource for genetically targeting the hemangioblast population as well as for studying the dynamics of vascular and blood cell development.</description>
        <link>http://www.biomedcentral.com/1471-213X/11/76</link>
                <dc:creator>Vera Teixeira</dc:creator>
                <dc:creator>Natacha Arede</dc:creator>
                <dc:creator>Rui Gardner</dc:creator>
                <dc:creator>Joaquín Rodríguez-León</dc:creator>
                <dc:creator>Ana T Tavares</dc:creator>
                <dc:source>BMC Developmental Biology 2011, 11:76</dc:source>
        <dc:date>2011-12-28T00:00:00Z</dc:date>
        <dc:identifier>10.1186/1471-213X-11-76</dc:identifier>
                            <dc:title>Hemangioblast targeting</dc:title>
                            <dc:description>The identification of a hemangioblast-specific enhancer (Hb) allows live imaging of hemangioblast cells by expression of green fluorescent protein and will facilitate study of hemangioblast cell fate and blood island morphogenesis.</dc:description>
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                <prism:publicationName>BMC Developmental Biology</prism:publicationName>
        <prism:issn>1471-213X</prism:issn>
        <prism:volume>11</prism:volume>
        <prism:startingPage>76</prism:startingPage>
        <prism:publicationDate>2011-12-28T00:00:00Z</prism:publicationDate>
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                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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