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Lateral Plate Mesoderm (lateral + plate_mesoderm)
Selected AbstractsUnderstanding heart development and congenital heart defects through developmental biology: A segmental approachCONGENITAL ANOMALIES, Issue 4 2005Masahide Sakabe ABSTRACT The heart is the first organ to form and function during development. In the pregastrula chick embryo, cells contributing to the heart are found in the postero-lateral epiblast. During the pregastrula stages, interaction between the posterior epiblast and hypoblast is required for the anterior lateral plate mesoderm (ALM) to form, from which the heart will later develop. This tissue interaction is replaced by an Activin-like signal in culture. During gastrulation, the ALM is committed to the heart lineage by endoderm-secreted BMP and subsequently differentiates into cardiomyocyte. The right and left precardiac mesoderms migrate toward the ventral midline to form the beating primitive heart tube. Then, the heart tube generates a right-side bend, and the d-loop and presumptive heart segments begin to appear segmentally: outflow tract (OT), right ventricle, left ventricle, atrioventricular (AV) canal, atrium and sinus venosus. T-box transcription factors are involved in the formation of the heart segments: Tbx5 identifies the left ventricle and Tbx20 the right ventricle. After the formation of the heart segments, endothelial cells in the OT and AV regions transform into mesenchyme and generate valvuloseptal endocardial cushion tissue. This phenomenon is called endocardial EMT (epithelial-mesenchymal transformation) and is regulated mainly by BMP and TGF,. Finally, heart septa that have developed in the OT, ventricle, AV canal and atrium come into alignment and fuse, resulting in the completion of the four-chambered heart. Altered development seen in the cardiogenetic process is involved in the pathogenesis of congenital heart defects. Therefore, understanding the molecular nature regulating the ,nodal point' during heart development is important in order to understand the etiology of congenital heart defects, as well as normal heart development. [source] Man1, an inner nuclear membrane protein, regulates left,right axis formation by controlling nodal signaling in a node-independent mannerDEVELOPMENTAL DYNAMICS, Issue 12 2008Akihiko Ishimura Abstract Man1, an inner nuclear membrane protein, regulates transforming growth factor , signaling by interacting with receptor-associated Smads. In Man1 -deficient (Man1,/,) embryos, vascular remodeling is perturbed by misregulation of Smad activity. Here, we show that Man1,/, embryos exhibit abnormal heart morphogenesis including the looping abnormality. We searched for the molecular basis underlying the heart abnormalities and found that the left side-specific genes responsible for left,right (LR) asymmetry, Nodal, Lefty2, and Pitx2, were expressed bilaterally in the lateral plate mesoderm and that their expression was enhanced significantly in mutants. Notably, Lefty1, a marker for the midline barrier, was maintained in Man1,/, mutants. Crossing Man1,/+ with Nodal hypomorphs (Nodalneo/+), in which Nodal signaling in the node is disrupted, to generate double homozygous embryos (Man1,/,; Nodalneo/neo) revealed that the bilateral Nodal was retained in Man1,/,; Nodalneo/neo embryos. These results suggest that Man1 regulates LR asymmetry by controlling Nodal signaling in a node-independent manner. Developmental Dynamics 237:3565,3576, 2008. © 2008 Wiley-Liss, Inc. [source] Developmental analysis of activin-like kinase receptor-4 (ALK4) expression in Xenopus laevisDEVELOPMENTAL DYNAMICS, Issue 2 2005Yumei Chen Abstract The type I transforming growth factor-beta (TGF,) receptor, activin-like kinase-4 (ALK4), is an important regulator of vertebrate development, with roles in mesoderm induction, primitive streak formation, gastrulation, dorsoanterior patterning, and left,right axis determination. To complement previous ALK4 functional studies, we have analyzed ALK4 expression in embryos of the frog, Xenopus laevis. Results obtained with reverse transcriptase-polymerase chain reaction indicate that ALK4 is present in both the animal and vegetal poles of blastula stage embryos and that expression levels are relatively constant amongst embryos examined at blastula, gastrula, neurula, and early tail bud stages. However, the tissue distribution of ALK4 mRNA, as assessed by whole-mount in situ hybridization, was found to change over this range of developmental stages. In the blastula stage embryo, ALK4 is detected in cells of the animal pole and the marginal zone. During gastrulation, ALK4 is detected in the outer ectoderm, involuting mesoderm, blastocoele roof, dorsal lip, and to a lesser extent, in the endoderm. At the onset of neurulation, ALK4 expression is prominent in the dorsoanterior region of the developing head, the paraxial mesoderm, and midline structures, including the prechordal plate and neural folds. Expression in older neurula stage embryos resolves to the developing brain, somites, notochord, and neural crest; thereafter, additional sites of ALK4 expression in tail bud stage embryos include the spinal cord, otic placode, developing eye, lateral plate mesoderm, branchial arches, and the bilateral heart fields. Together, these results not only reflect the multiple developmental roles that have been proposed for this TGF, receptor but also define spatiotemporal windows in which ALK4 may function to modulate fundamental embryological events. Developmental Dynamics 232:393,398, 2005. © 2004 Wiley-Liss, Inc. [source] Effects of cadmium on formation of the ventral body wall in chick embryos and their prevention by zinc pretreatmentBIRTH DEFECTS RESEARCH, Issue 2 2001Jennifer Thompson Background Cadmium (Cd) is an established experimental teratogen whose effects can be reversed by pretreatment with zinc. Mesodermal development is a frequently reported target for Cd teratogenicity. The aim of this study was to examine the mechanisms of Cd induced body wall defects in chick embryos. Methods Chick embryos in shell-less culture were treated with 50 ,l of cadmium acetate (8.9 × 10,5 M Cd2+) at 60-hr incubation (H.-H. stages 16,17). Controls received equimolar sodium acetate. Other embryos were treated with various concentrations of zinc acetate and then with Cd or NaAc 1 hrs later. Development was evaluated 48 hrs later. Resin-embedded 1-,m sections were examined at earlier stages. Results Cd caused embryolethality (35%), ventral body wall defect with malpositioned lower limbs (40%), and weight reduction in survivors. After 4-hr treatment with Cd, breakdown of junctions between peridermal cells with rounding up and desquamation occurred. Shape changes were also seen in the basal layer of the ectoderm. At 4 hr, cell death was evident in lateral plate mesoderm, somites, and neuroepithelium; the lateral plate mesoderm began to grow dorsally, carrying the attached limb buds with it. Zn pretreatment protected against the lethal, teratogenic, and growth-retarding effects of Cd, as well as ectodermal changes and cell death. Conclusions Cd disrupts peridermal cell adhesion and induces cell death in the mesoderm. This may result in abnormal growth of lateral plate mesoderm and in a body wall defect. Zn pretreatment prevents both the gross teratogenic effects and the cellular changes, most likely by competition with Cd. Teratology 64:87,97, 2001. © 2001 Wiley-Liss, Inc. [source] | ||||||||||