Cripto is required for correct orientation of the anterior–posterior axis in the mouse embryo

To assess the function of the distal visceral endoderm (DVE) of embryonic day 5.5 (E5.5) embryos, we established a system to directly ablate the DVE and observe the consequences after culture. When the DVE was successfully ablated, such embryos (DVE-ablated embryos) showed deregulated expression of Nodal and Wnt3 and ectopically formed the primitive streak at the proximal portion of the embryo. The DVE and anterior visceral endoderm (AVE) are implicated in the development of neurectoderm. We found that the distal epiblast of E5.

Section: Expression Of Endodermal Genes In the Distal Epiblast In Dvementioning

confidence: 81%

Section: Whole Mount In Situ Hybridizationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

The DVE changes distal epiblast fate from definitive endoderm to neurectoderm by antagonizing nodal signaling

Miura¹,

Mishina²

2007

“…First, polarity and, therefore, pattern appears to already exist in the epiblastal ectoderm before gastrulation as evinced by asymmetric patterns of gene expression typically encountered within epiblast (e.g., Bmp4,Otx2,Fgf8,T [Brachury],Cripto,Wnt3,Nodal,Hesx1,Hex,, VE-1, Lim1 [Lhx1], GATA, Dlx, and Dkk1; Lawson et al, 1991;Lawson and Pedersen, 1992;Dono et al, 1993;Simeone et al, 1993;Ang and Rossant, 1994;Crossley and Martin, 1995;Belo et al, 1997;Varlet et al, 1997;Eyal-Giladi, 1997;Beddington and Robertson, 1998;Biben et al, 1998;Ding et al, 1998;Shawlot et al, 1998;Thomas et al, 1998;Liu et al, 1999;Pera et al, 1999;Crossley et al, 2001;Tian et al, 2002;Chapman et al, 2002). This asymmetry is mirrored by the underlying hypoblast (visceral endoderm;e.g., Otx2, Lim1, Hesx1, Hex, HNF3␤, Lefty1, Nodal (Acampora et al, 1995;Thomas and Beddington, 1996;Belo et al, 1997;Filosa et al, 1997;Varlet et al, 1997;Thomas et al, 1998;Meno et al, 1999;Shimono and Berhinger, 1999;Kim...…”

Section: First Perambulations: Polarity and Pattern In The Pregastrulmentioning

confidence: 99%

21^st Century neontology and the comparative development of the vertebrate skull

Depew

Simpson

2006

Classic neontology (comparative embryology and anatomy), through the application of the concept of homology, has demonstrated that the development of the gnathostome (jawed vertebrate) skull is characterized both by a fidelity to the gnathostome bauplan and the exquisite elaboration of final structural design. Just as homology is an old concept amended for modern purposes, so are many of the questions regarding the development of the skull. With due deference to Geoffroy-St. Hilaire, Cuvier, Owen, Lankester et al., we are still asking: How are bauplan fidelity and elaboration of design maintained, coordinated, and modified to generate the amazing diversity seen in cranial morphologies? What establishes and maintains pattern in the skull? Are there universal developmental mechanisms underlying gnathostome autapomorphic structural traits? Can we detect and identify the etiologies of heterotopic (change in the topology of a developmental event), heterochronic (change in the timing of a developmental event), and heterofacient (change in the active capacetence, or the elaboration of capacity, of a developmental event) changes in craniofacial development within and between taxa? To address whether jaws are all made in a like manner (and if not, then how not), one needs a starting point for the sake of comparison. To this end, we present here a "hinge and caps" model that places the articulation, and subsequently the polarity and modularity, of the upper and lower jaws in the context of cranial neural crest competence to respond to positionally located epithelial signals. This model expands on an evolving model of polarity within the mandibular arch and seeks to explain a developmental patterning system that apparently keeps gnathostome jaws in functional registration yet tractable to potential changes in functional demands over time. It relies upon a system for the establishment of positional information where pattern and placement of the "hinge" is driven by factors common to the junction of the maxillary and mandibular branches of the first arch and of the "caps" by the signals emanating from the distal-most first arch midline and the lamboidal junction (where the maxillary branch meets the frontonasal processes). In this particular model, the functional registration of jaws is achieved by the integration of "hinge" and "caps" signaling, with the "caps" sharing at some critical level a developmental history that potentiates their own coordination. We examine the evidential foundation for this model in mice, examine the robustness with which it can be applied to other taxa, and examine potential proximate sources of the signaling centers. Lastly, as developmental biologists have long held that the anterior-most mesendoderm (anterior archenteron roof or prechordal plate) is in some way integral to the normal formation of the head, including the cranial skeletal midlines, we review evidence that the seminal patterning influences on the early anterior ectoderm extend well beyond the neural plate and are just as importan...

“…The Nodal ligand binds a receptor complex that includes Activin type 1 and type 2 receptors (Whitman, 2001), together with an EGF-CFC-type coreceptor (Shen et al, 1997;Ding et al, 1998;Zhang et al, 1998;Dorey and Hill, 2006;Onuma et al, 2006). Lefty, a divergent member of the TGF␤ family whose transcription is directly regulated by Nodal signaling, is one of the principal extracellular feedback inhibitors of Nodal signaling (Meno et al, 1996(Meno et al, , 1999Thisse and Thisse, 1999;Cheng et al, 2000;Tanegashima et al, 2000;Branford and Yost, 2002;Cha et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Xenopus Lefty requires proprotein cleavage but not N‐linked glycosylation to inhibit nodal signaling

Westmoreland

Takahashi

Wright

2007

The Nodal and Nodal-related morphogens are utilized for the specification of distinct cellular identity throughout development by activating discrete target genes in a concentration-dependant manner. Lefty is a principal extracellular antagonist involved in the spatiotemporal regulation of the Nodal morphogen gradient during mesendoderm induction. The Xenopus Lefty proprotein contains a single N-linked glycosylation motif in the mature domain and two potential cleavage sites that would be expected to produce long (Xlefty L ) and short (Xlefty S ) isoforms. Here we demonstrate that both isoforms were secreted from Xenopus oocytes, but that Xlefty L is the only isoform detected when embryonic tissue was analyzed. In mesoderm induction assays, Xlefty L is the functional blocker of Xnr signaling. When secreted from oocytes, vertebrate Lefty molecules were N-linked glycosylated. However, glycan addition was not required to inhibit Xnr signaling and did not influence its movement through the extracellular space. These findings demonstrate that Lefty molecules undergo post-translational modifications and that some of these modifications are required for the Nodal inhibitory function.