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• W2010671145 abstract "The earliest steps in tooth development depend on signaling interactions that result in the condensation of mandibular mesenchyme into the tooth bud. Reporting in this issue of Developmental Cell,Mammoto et al., 2011Mammoto T. Mammoto A. Torisawa Y.S. Tat T. Gibbs A. Derda R. Mannix R. de Bruijn M. Yung C.W. Huh D. et al.Dev. Cell. 2011; 21 (this issue): 758-769Abstract Full Text Full Text PDF PubMed Scopus (122) Google Scholar find that chemotactic signals coordinate condensation and that the compressive force generated is sufficient to induce tooth bud gene expression. The earliest steps in tooth development depend on signaling interactions that result in the condensation of mandibular mesenchyme into the tooth bud. Reporting in this issue of Developmental Cell,Mammoto et al., 2011Mammoto T. Mammoto A. Torisawa Y.S. Tat T. Gibbs A. Derda R. Mannix R. de Bruijn M. Yung C.W. Huh D. et al.Dev. Cell. 2011; 21 (this issue): 758-769Abstract Full Text Full Text PDF PubMed Scopus (122) Google Scholar find that chemotactic signals coordinate condensation and that the compressive force generated is sufficient to induce tooth bud gene expression. The starting point for the differentiation of mesenchymal derivatives is the formation of aggregations of highly packed cells. These knots of cells or condensations presage the differentiation of structures that include skeletal elements, feathers and hair, teeth, somites, and the kidney (Hall and Miyake, 2000Hall B.K. Miyake T. Bioessays. 2000; 22: 138-147Crossref PubMed Scopus (640) Google Scholar, Thorogood and Hinchliffe, 1975Thorogood P.V. Hinchliffe J.R. J. Embryol. Exp. Morphol. 1975; 33: 581-606PubMed Google Scholar). In all cases, the formation of condensations is thought to result from upstream molecular cues that impart a genetic identity onto the precondensed mesenchyme. In this view, it is the genetic program that causes the specialization of the mesenchyme that then in turn brings about changes in cellular properties important for aggregation. Looking at the formation of the tooth bud, Mammoto and et al. (2011) suggest in this issue an alternative view: it is the force generated in the process of condensation that results in the activation of a genetic cascade specific for tooth induction. That is to say, the specialization of mesenchyme is a consequence of condensation, rather than the cause. Teeth are formed from the epithelium and the mesenchyme of the first branchial arch, with the epithelium giving rise to the enamel and the mesenchyme the dentine and pulp (Pispa and Thesleff, 2003Pispa J. Thesleff I. Dev. Biol. 2003; 262: 195-205Crossref PubMed Scopus (351) Google Scholar). Their formation is controlled by an ongoing conversation between these two tissue layers, where the opening phrase is a signal from the epithelium to the mesenchyme that includes Fgf8, a member of the fibroblast growth factor family. The local action of these signals induces the expression of Pax9 in the mesenchyme (Neubüser et al., 1997Neubüser A. Peters H. Balling R. Martin G.R. Cell. 1997; 90: 247-255Abstract Full Text Full Text PDF PubMed Scopus (484) Google Scholar). The patch of Pax9-positive mesenchymal cells is also characterized by increased cellular density and at this point is called the tooth bud. Here it acts as a signaling center and engages in the instructive dialog that leads to tooth formation. How do signals from the epithelium induce the tooth bud? In a beautiful series of experiments, Mammoto and colleagues from the Ingber group use an ex vivo approach to grapple with this problem. They find that one function of Fgf8 is as a chemo-attractant, drawing mesenchymal cells closer to the epithelium. This causes cells to aggregate but does not induce Pax9 expression, the other feature of the tooth bud. The attractant gradient therefore needs a counterpoint, a short-range repulsive signal provided by a member of the semaphorin family, Sema3f. Together with Fgf8, both signals squeeze mesenchyme cells into a condensation. The very act of squeezing causes mandibular mesenchymal cells to become smaller and rounder and induces the expression of Pax9. Both effects can be recreated ex vivo. Compression of mandibular mesenchyme between steady pressures initiates the condensation process and, more importantly, induces the expression of Pax9. Similarly, culturing mandibular mesenchymal cells at a high density (with plating density serving as a proxy for compressive force) also leads to Pax9 expression. Compression causes the cells to adopt a smaller, rounder profile. To explore whether this shape change was sufficient to divert cell fate, the authors plated individual mesenchymal cells on photolithograph-printed fibronectin dots, which constrain each cell to approximately the size it would adopt in a condensation. Mammoto et al., 2011Mammoto T. Mammoto A. Torisawa Y.S. Tat T. Gibbs A. Derda R. Mannix R. de Bruijn M. Yung C.W. Huh D. et al.Dev. Cell. 2011; 21 (this issue): 758-769Abstract Full Text Full Text PDF PubMed Scopus (122) Google Scholar found that this size constraint led to the expression of Pax9, suggesting that the physical forces that cause an individual cell to adopt a smaller, rounded shape are sufficient to enact cell fate choice. Condensations do occur throughout the embryo during development. One of the clearest examples of this is the formation of skeletal elements (Fell, 1925Fell H.B. J. Morphol. 1925; 40: 417-459Crossref Scopus (217) Google Scholar). The size and shape of the precartilage condensation is predictive for the size and shape of the skeletal element it will form. Several lines of evidence suggest that chondrogenic mechanisms may be similar to the ones that initiate tooth bud aggregation (Hall and Miyake, 2000Hall B.K. Miyake T. Bioessays. 2000; 22: 138-147Crossref PubMed Scopus (640) Google Scholar). For example, mechanical force in known to induce a type of cartilage, known as secondary cartilage, at muscle attachment sites or articulations of membrane bones (the clavicle or some of the bones of the face) (Hall and Miyake, 2000Hall B.K. Miyake T. Bioessays. 2000; 22: 138-147Crossref PubMed Scopus (640) Google Scholar). In vitro models of chondrogenesis (called micromass cultures and consisting of dispersed limb-bud mesenchyme taken from embryos prior to cartilage formation) have also provided evidence that cell packing density and the resulting compression lead to cartilage formation (Archer et al., 1985Archer C.W. Rooney P. Cottrill C.P. J. Embryol. Exp. Morphol. 1985; 90: 33-48PubMed Google Scholar). In this system, cartilage is only generated when the cells are plated at high density, which (similar to the case with tooth bud cells) changes the size and shape of the cells. Interestingly, cartilage formation does not occur uniformly throughout the culture, but instead the cells organize into nodules with forms that depend on the initial plating density. The pattern of the nodules, which range from sparse dots, spots, and/or stripes to a sheet-like configuration, can be predicted by a Turing reaction-diffusion mechanism (Kondo and Miura, 2010Kondo S. Miura T. Science. 2010; 329: 1616-1620Crossref PubMed Scopus (861) Google Scholar), and a number of groups have provided well-resolved mathematical models that describe the interplay of chemical or physical activators and inhibitors during the process of in vitro cartilage condensation (Christley et al., 2007Christley S. Alber M.S. Newman S.A. PLoS Comput. Biol. 2007; 3: e76Crossref PubMed Scopus (55) Google Scholar, Oster et al., 1983Oster G.F. Murray J.D. Harris A.K. J. Embryol. Exp. Morphol. 1983; 78: 83-125PubMed Google Scholar). Returning to tooth bud formation, it seems likely that mechanisms mirroring this self-organizing activation-inhibition network, predicted by models of chondrogenesis, are also active in the tooth. Indeed, actual tooth bud condensations form in only a subset of the mesenchyme that is in contact with epithelial Fgf8 and Sema3f, suggesting that there are mechanisms that refine and stabilize the condensation after the initial compressive activity. The understanding of how these mechanisms work and what their molecular identities are will have significant bearings on how the morphology of the tooth, and by analogy the skeletal element, is established. As with all signaling systems, we encounter the problem of specificity in the mechanochemical model for cell differentiation. This is especially evident in the neural crest-derived mesenchyme of the mandibular arch, which can give rise to both tooth buds and cartilage. If the differentiation of either cell type depends on condensation-generated force, how do the cells know that they are in an odontogenic condensation and should therefore not be chondrogenic? One can postulate the presence of other signals that collaborate and conspire with condensation-generating factors to determine cell fate, but it is clear that more work is needed to investigate the integration of other signals into the mechanotransduction pathway triggered by condensation to shed more light on how it steers cell lineage. Mechanochemical Control of Mesenchymal Condensation and Embryonic Tooth Organ FormationMammoto et al.Developmental CellSeptember 15, 2011In BriefMesenchymal condensation is critical for organogenesis, yet little is known about how this process is controlled. Here we show that Fgf8 and Sema3f, produced by early dental epithelium, respectively, attract and repulse mesenchymal cells, which cause them to pack tightly together during mouse tooth development. Resulting mechanical compaction-induced changes in cell shape induce odontogenic transcription factors (Pax9, Msx1) and a chemical cue (BMP4), and mechanical compression of mesenchyme is sufficient to induce tooth-specific cell fate switching. Full-Text PDF Open Archive" @default.
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• W2010671145 title "Squeezing into Differentiation" @default.
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