Slb/Wnt11 controls hypoblast cell migration and morphogenesis at the onset of zebrafish gastrulation

Slb/Wnt11 controls hypoblast cell migration and morphogenesis at the onset of zebrafish gastrulation

Florian Ulrich,1* Miguel L. Concha,2,3* Paul J. Heid,4 Ed Voss,4 Sabine Witzel,1 Henry Roehl,5 Masazumi Tada,2 Stephen W. Wilson,2 Richard J. Adams,6 David R. Soll,4 and Carl-Philipp Heisenberg1†

Development. 2003 November; 130(22): 5375–5384

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Genes Critical to Vasculogenesis as Defined by Systematic Analysis of Vascular Defects in Knockout Mice

Genes Critical to Vasculogenesis as Defined by Systematic Analysis of Vascular Defects in Knockout Mice

,

http://dx.doi.org/10.1002/ar.a.20232

Abstract
To identify genes important to the process of , we evaluated embryonic vascular anomalies from 100 mouse knockout studies using a novel meta-analysis approach. By applying this method, termed approach for ranking of embryonic vascular anomalies (), rank scores were calculated for each knockout based on the occurrence of vascular defects during periods of vasculogenesis in specific embryonic regions. As a result, 12 genes (, , , , , , , , , , , and ) were determined to play critical roles in vasculogenesis. Functional categorization of these genes revealed the fundamental importance of signaling since 10 of the 12 genes (fibronectin, VEGFR-1/Flt-1, VEGFR-2/Flk-1, alpha 5 integrin, VE-cadherin, VEGFA, ShcA, cytochrome P450 reductase, CD148/DEP-1, and EphrinB2) relate to this pathway. Furthermore, the findings highlight a potential network for regulating VEGF signaling involving integration of fibronectin, EphrinB2, Tie2, and connexin 45 signaling pathways via the ShcA/Ras/Raf/Mek/Erk cascade. In addition to retrospective application of AREVA as done herein, AREVA can be used prospectively to determine the relevancy to vasculogenesis of newly inactivated genes.

Vascular endothelial tyrosine phosphatase (VE-PTP)-null mice undergo vasculogenesis but die embryonically because of defects in angiogenesis

Vascular endothelial tyrosine phosphatase (VE-PTP)-null mice undergo vasculogenesis but die embryonically because of defects in angiogenesis

, , , , , , , , , , , , and

Abstract
Development of the vascular system depends on the highly coordinated actions of a variety of angiogenic regulators. Several of these regulators are members of the tyrosine kinase superfamily, including receptors and angiopoietin receptors, and . Tyrosine kinase signaling is counter-regulated by the activity of tyrosine phosphatases, including vascular endothelial protein tyrosine phosphatase (), which has previously been shown to modulate Tie2 activity. We generated mice in which VE-PTP is replaced with a reporter gene. We confirm that VE-PTP is expressed in endothelium and also show that VE-PTP is highly expressed in the developing outflow tract of the heart and later is expressed in developing heart valves. occurs normally in mice lacking VE-PTP; however, is abnormal. Angiogenic defects in VE-PTP-null mice were most pronounced in the yolk sac and include a complete failure to elaborate the primitive vascular scaffold into higher-order branched arteries, veins, and capillaries. VE-PTP continues to be expressed into adulthood in the vasculature and heart valves, suggesting later roles in vascular development or homeostasis. VE-PTP is also expressed in the vasculature of growing tumors, suggesting that VE-PTP may be a new potential target for angiogenic therapies.

The forkhead transcription factor Foxf1 is required for differentiation of extra-embryonic and lateral plate mesoderm

The forkhead transcription factor Foxf1 is required for differentiation of extra-embryonic and lateral plate mesoderm ([pdf]

, , and

Development 128, 155-166 (2001)

Summary
The murine gene encodes a forkhead transcription factor expressed in extra-embryonic and lateral plate mesoderm and later in splanchnic mesenchyme surrounding the gut and its derivatives. We have disrupted Foxf1 and show that mutant embryos die at midgestation due to defects in mesodermal differentiation and cell adhesion. The embryos do not turn and become deformed by the constraints of a small, inflexible amnion. Extra-embryonic structures exhibit a number of differentiation defects: no occurs in yolk sac or allantois; fails; the amnion does not expand with the growth of the embryo, but misexpresses vascular and hematopoietic markers. Separation of the bulk of yolk sac mesoderm from the endodermal layer and adherence between mesoderm of yolk sac and amnion, indicate altered cell adhesion properties and enhanced intramesodermal cohesion. A possible cause of this is misexpression of the cell-adhesion protein VCAM1 in Foxf1-deficient extra-embryonic mesoderm, which leads to co-expression of with its receptor, alpha(4)-integrin. The expression level of 4 is decreased in the posterior part of the embryo proper. Consistent with this, mesodermal proliferation in the primitive streak is reduced and somite formation is retarded. Expression of Foxf1 and the homeobox gene defines the splanchnic and somatic mesodermal layers, respectively. In Foxf1-deficient embryos incomplete separation of splanchnic and somatic mesoderm is accompanied by misexpression of Irx3 in the splanchnopleure, which implicates Foxf1 as a repressor of Irx3 and as a factor involved in coelom formation.

Defects in Yolk Sac Vasculogenesis, Chorioallantoic Fusion, and Embryonic Axis Elongation in Mice with Targeted Disruption of Yap65

Defects in Yolk Sac Vasculogenesis, Chorioallantoic Fusion, and Embryonic Axis Elongation in Mice with Targeted Disruption of Yap65

, , , , , , , , and

Mol Cell Biol. 2006 January; 26(1): 77–87.

Abstract
is a multifunctional adapter protein and transcriptional coactivator with several binding partners well described in vitro and in cell culture. To explore in vivo requirements for YAP, we generated mice carrying a targeted disruption of the Yap gene. Homozygosity for the Yaptm1Smil allele (Yap−/−) caused developmental arrest around E8.5. Phenotypic characterization revealed a requirement for YAP in yolk sac vasculogenesis. Yolk sac endothelial and erythrocyte precursors were specified as shown by histology, PECAM1 immunostaining, and alpha globin expression. Nonetheless, development of an organized yolk sac vascular plexus failed in Yap−/− embryos. In striking contrast, vasculogenesis proceeded in both the allantois and the embryo proper. Mutant embryos showed patterned gene expression domains along the anteroposterior neuraxis, midline, and streak/tailbud. Despite this evidence of proper patterning and tissue specification, Yap−/− embryos showed developmental perturbations that included a notably shortened body axis, convoluted anterior neuroepithelium, caudal dysgenesis, and failure of chorioallantoic fusion. These results reveal a vital requirement for YAP in the developmental processes of , , and .

Wnt-5A/Ror2 Regulate Expression of XPAPC through an Alternative Noncanonical Signaling Pathway

Wnt-5A/Ror2 Regulate Expression of XPAPC through an Alternative Noncanonical Signaling Pathway

, and

Developmental Cell, Volume 12, Issue 5, 8 May 2007, Pages 779-792

Summary

, a member of the nontransforming class of ligands, is required for convergent extension movements in embryos. XWnt-5A knockdown phenocopies paraxial protocadherin (XPAPC) loss of function: involuted mesodermal cells fail to align mediolaterally, which results in aberrant movements and a selective inhibition of constriction. XWnt-5A depletion was rescued by coinjection of XPAPC RNA, indicating that XWnt-5A acts upstream of XPAPC. XWnt-5A, but not XWnt-11, stimulates XPAPC expression independent of the canonical Wnt/ pathway. We show that transcriptional regulation of XPAPC by XWnt-5A requires the receptor tyrosine kinase . XWnt-5A/Xror2 signal through and to activate the with the transcription factors and . The Wnt-5A/Ror2 pathway represents an alternative, distinct branch of noncanonical Wnt signaling that controls gene expression and is required in the regulation of convergent extension movements in Xenopus

Author Keywords: ;

Hello world!

Ce blog est dédié à Vincent Fleury, et à sa théorie. Il pourra trouver en un seul lieu des données qui ne sont pas tout à fait en accord avec ce qu’il pense :

vincentfleury 04-01-2007 à 22:36

S’agissant du Darwinisme, je suis arrivé à la conclusion, par le truchement d’équations très mathématiques, et d’une analyse très poussée du problème, qu’il est très très insuffisant pour expliquer l’évolution. Une grande partie de ce qui est observé (animaux, plantes etc) survient quasi automatiquement. Un tétrapode, c’est très facile à faire, je veux bine même enlever le « quasi ».La biologie du développement et l’évolution sont fondées sur un présupposé faux, qui est que les animaux sont des choses très compliquées. Ce n’est pas le cas. Les animaux résultent d’un écoulement tourbillonaire à 2D croisé avec un flambage dans la direction perpendiculaire. C’est tout. Ce , n’est pas plus compliqué qu’une canette de soda écrasée.

Comme toute théorie, le Darwinisme peut être remplacé par une théorie plus vaste, plus prédictive. Si la mienne l’emporte, j’en serai très fier, évidemment, mais je peux me tromper, et je demande bien pardon si ma théorie s’avère fausse un jour. Mais pour l’instant, je trouve qu’elle fait bonne figure.

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