Mésoderme | EPFL Graph Search

vignette|Schéma en coupe transversale juste après la mise en place du mésoderme. vignette|Schéma en coupe transversale juste après la différenciation du mésoderme Le mésoderme (ou mésoblaste), par opposition à l'endoderme et à l'ectoderme, est le feuillet cellulaire intermédiaire de l'embryon des métazoaires triploblastiques qui se met en place au moment de la gastrulation. Seuls les Bilatériens le possèdent, les porifères (éponges) et cnidaires (méduses, coraux, hydres, anémones de mer) en sont dépourvus. Ils possèdent en revanche une mésoglée, qui n'est pas un feuillet embryonnaire mais un tissu pauvre en cellules avec une matrice extracellulaire importante. Les cellules qui dérivent du mésoderme forment en tout ou partie les organes internes à l'exception du système nerveux (dérivant de l'ectoderme) et des organes des systèmes digestif et respiratoire (issus de l'endoderme). Ainsi, chez les Cordés, le mésoderme donne naissance :

à la notochorde (ou chorde, ou mésoderme axial), ré

Role of Bicaudal-C in Left-Right Axis Formation and Kidney Morphogenesis

Charlotte Maisonneuve

The KH domain RNA binding protein Bicaudal-C is known to play a role in anterior-posterior (AP) patterning in Drosophila by acting on oskar mRNA. In mammals, its expression is induced at late gastrulation in the mesodermal layer of the ventral node. Renal cysts arise in mice and frogs lacking Bicaudal-C. Polycystic diseases and left-right (LR) axis malformations are frequently linked to cilia defects. However, a role for BicC in cilia function has not been demonstrated. Here, I report that targeted inactivation of BicC confirms a role in inducing polycystic kidney disease (PKD). In addition, this targeted mutation was found to randomize left-right (LR) asymmetry by disrupting the planar alignment of motile cilia required for cilia-driven fluid flow. Furthermore, depending on its SAM domain, BicC can uncouple Dvl2 signaling from the canonical Wnt pathway, which has been implicated in antagonizing planar cell polarity (PCP). The SAM domain is shown to concentrate BicC in cytoplasmic structures harboring RNA-processing bodies (P-bodies) and Dvl2. P-bodies are implicated degrading target mRNAs that are silenced by microRNAs. These results suggest a model whereby BicC links the orientation of cilia to PCP, possibly by regulating RNA silencing in P-bodies. In the kidney, BicC is localized in proximal tubules. The cystic phenotype is accompanied by increased levels of cAMP and of Adcy6 protein. BicC is proposed to inhibit target mRNA at the translation-initiation stage by regulating the assembly of miRNP/P-bodies.

EPFL2010

A crucial interaction between embryonic red blood cell progenitors and paraxial mesoderm revealed in spadetail embryos

Andrew Charles Oates, Laurel Ann Rohde

Zebrafish embryonic red blood cells (RBCs) develop in trunk intermediate mesoderm (IM), and early macrophages develop in the head, suggesting that local microenvironmental cues regulate differentiation of these two blood lineages. s padetail (spt) mutant embryos, which lack trunk paraxial mesoderm (PM) due to a cell-autonomous defect in tbx16, fail to produce embryonic RBCs but retain head macrophage development. In spt mutants, initial hematopoietic gene expression is absent in trunk IM, although endothelial and pronephric expression is retained, suggesting that early blood progenitor development is specifically disrupted. Using cell transplantation, we reveal that spt is required cell autonomously for early hematopoietic gene expression in trunk IM. Further, we uncover an interaction between embryonic trunk PM and blood progenitors that is essential for RBC development. Importantly, our data identify a hematopoietic microenvironment that allows embryonic RBC production in the zebrafish. © 2004 by Cell Press.

2004

Generation of segment polarity in the paraxial mesoderm of the zebrafish through a T-box-dependent inductive event

Andrew Charles Oates, Laurel Ann Rohde

The first morphological sign of vertebrate postcranial body segmentation is the sequential production from posterior paraxial mesoderm of blocks of cells termed somites. Each of these embryonic structures is polarized along the anterior/posterior axis, a subdivision first distinguished by marker gene expression restricted to rostral or caudal territories of forming somites. To better understand the generation of segment polarity in vertebrates, we have studied the zebrafish mutant fused somites (fss), because its paraxial mesoderm lacks segment polarity. Previously examined markers of caudal half-segment identity are widely expressed, whereas markers of rostral identity are either missing or dramatically down-regulated, suggesting that the paraxial mesoderm of the fss mutant embryo is profoundly caudalized. These findings gave rise to a model for the formation of segment polarity in the zebrafish in which caudal is the default identity for paraxial mesoderm, upon which is patterned rostral identity in an fss-dependent manner. In contrast to this scheme, the caudal marker gene ephrinA1 was recently shown to be down-regulated in fss embryos. We now show that notch5, another caudal identity marker and a component of the Delta/Notch signaling system, is not expressed in the paraxial mesoderm of early segmentation stage fss embryos. We use cell transplantation to create genetic mosaics between fss and wild-type embryos in order to assay the requirement for fss function in notch5 expression. In contrast to the expression of rostral markers, which have a cell-autonomous requirement for fss, expression of notch5 is induced in fss cells at short range by nearby wild-type cells, indicating a cell-non-autonomous requirement for fss function in this process. These new data suggest that segment polarity is created in a three-step process in which cells that have assumed a rostral identity must subsequently communicate with their partially caudalized neighbors in order to induce the fully caudalized state. © 2005 Elsevier Inc. All rights reserved.

2005

Generation of segment polarity in the paraxial mesoderm of the zebrafish through a T-box-dependent inductive event

Andrew Charles Oates, Laurel Ann Rohde

2005