We report on the formation and early differentiation of the somites in the avian embryo. The somites are derived from the avian embryo. The somites are derived from the mesoderm which, in the body (excluding the head), is subdivided into four compartments: the axial, paraxial, intermediate and lateral plate mesoderm. Somites develop from the paraxial mesoderm and constitute the segmental pattern of the body. They are formed in pairs by epithelialization, first at the cranial end of the paraxial mesoderm, proceeding caudally, while new mesenchyme cells enter the paraxial mesoderm as a consequence of gastrulation. After their formation, which depends upon cell-cell and cell-matrix interactions, the somites impose segmental pattern upon peripheral nerves and vascular primordia. The newly formed somite consists of an epithelial ball of columnar cells enveloping mesenchymal cells within a central cavity, the somitocoel. Each somite is surrounded by extracellular matrix material connecting the somite with adjacent structures. The competence to form skeletal muscle is a unique property of the somites and becomes realized during compartmentalization, under control of signals emanating from surrounding tissues. Compartmentalization is accompanied by altered patterns of expression of Pax genes within the somite. These are believed to be involved in the specification of somite cell lineages. Somites are also regionally specified, giving rise to particular skeletal structures at different axial levels. This axial specification appears to be reflected in Hox gene expression. MyoD is first expressed in the dorsomedial quadrant of the still epithelial somite whose cells are not yet definitely committed. During early maturation, the ventral wall of the somite undergoes an epithelio-mesenchymal transition forming the sclerotome. The sclerotome later becomes subdivided into rostral and caudal halves which are separated laterally by von Ebner's fissure. The lateral part of the caudal half of the sclerotome mainly forms the ribs, neural arches and pedicles of vertebrae, whereas within the lateral part of the rostral half the spinal nerve develops. The medially migrating sclerotomal cells form the peri-notochordal sheath, and later give rise to the vertebral bodies and intervertebral discs. The somitocoel cells also contribute to the sclerotome. The dorsal half of the somite remains epithelial and is referred to as the dermomyotome because it gives rise to the dermis of the back and the skeletal musculature. the cells located within the lateral half of the dermomyotome are the precursors of the muscles of the hypaxial domain of the body, whereas those in the medial half are precursors of the epaxial (back) muscles.(ABSTRACT TRUNCATED AT 400 WORDS)

Previous studies have shown that during avian heart development, epicardial and coronary vascular smooth muscle precursors are derived from the proepicardium, a derivative of the developing liver. This finding led to a model of coronary vascular development in which epicardial cells migrate over the postlooped heart, followed by migration of committed endothelial and smooth muscle precursors from the proepicardium through the subepicardial matrix where the coronary arteries develop. Here we show that epicardial cells undergo epithelial-mesenchymal transformation to become coronary vascular smooth muscle, perivascular fibroblasts, and intermyocardial fibroblasts. We began by establishing primary cultures of quail epicardial cells that retain morphologic and antigenic identity to epicardial cells in vivo. Quail epicardial monolayers stimulated with serum or vascular growth factors produced invasive mesenchyme in collagen gels. Chick epicardial cells labeled in ovo with DiI invaded the subepicardial extracellular matrix, demonstrating that mesenchymal transformation of epicardium occurs in vivo. To determine the fates of epicardially derived mesenchymal cells, quail epicardial cells labeled in vitro with LacZ were grafted into the pericardial space of E2 chicks. These cells attached to the heart, formed a chimeric epicardium, invaded the subepicardial matrix and myocardial wall, and became coronary vascular smooth muscle, perivascular fibroblasts, and intermyocardial fibroblasts, demonstrating the common epicardial origin of these cell types. A general model of coronary vascular development should now include epicardial-mesenchymal transformation and direct participation of mesenchyme derived from the epicardium in coronary morphogenesis.

Multicellular organisms express many genes in a cell-typespecific fashion. The mechanisms governing cell-specific gene expression are becoming increasingly understood at two levels. First, there are numerous examples in which the binding of nuclear transcription factors to cis elements within gene regulatory regions has been shown to govern cell-specific activation of gene transcription. A second level of regulation has been proposed to be mediated by the remodeling of chromatin organization both globally and at individual gene loci. Chromatin remodeling itself encompasses many types of changes, including nucleosome phasing, alterations of chromosomal protein content (histone and nonhistone), and posttranslational modification of chromosomal proteins by acetylation, phosphorylation, poly(ADP-ribosyl)ation, methylation, and ubiquitination (6). Although it is widely acknowledged that both levels must govern the cell-specific expression of individual genes, there has been little information as to mechanisms that might integrate these two levels of regulation. Recently, however, histone acetyltransferases have been shown to bind to specific trans-acting factors (recently reviewed in references 22, 29, and 55). Such protein-protein binding suggests a mechanism by which chromatin histones can be modified locally (as opposed to globally) through binding of histone acetyltransferases to transcription factors that are in turn bound to DNA cis elements within the regulatory regions of specific genes. We report here a new mechanism by which these two levels of gene regulation can be integrated; through direct binding of the chromatin-modifying protein, poly(ADP-ribose) polymerase (PARP), to DNA sequences within MCAT1 regulatory elements.

We have examined the effect of implantation of a supernumerary notochord or floor plate on dorsoventral somitic organization. We show that notochord and floor plate are able to inhibit the differentiation of the dorsal somitic derivatives-i.e., axial muscles and dermis-thus converting the entire somite into cartilage, which normally arises only from its ventral part. We infer from these results that the dorsoventral patterning of somitic derivatives is controlled by sigals provided by ventral axial structures.

We have studied the angiogenic potential of the unsegmented paraxial mesoderm and epithelial somites of the trunk with homotopical grafts between quail and chick embryos. Quail endothelial cells of the grafts were stained with the QH-1 antibody after 1-6 days of reincubation. The unsegmented paraxial mesoderm and all parts of the epithelial somite were found to contain angioblasts which develop into QH-1 positive endothelial cells. These cells are incorporated into the lining of the host's blood vessels such as the perineural vascular plexus and the dorsal branches of the aorta. There is a certain preference as concerns the location of endothelial cells derived from different parts of the somites. Angioblasts from ventral somite halves are mainly found in ventrolateral blood vessels. Those from dorsomedial quadrants form vessels in the dermis of the back, and those from dorsolateral quadrants can be found in the ventrolateral body wall and the wing. With the exception of the dorsal perineural vascular plexus, angioblasts do not cross the median plane of the body. This shows that, although angioblasts migrate extensively, there is bilaterality of the vascular system in the trunk. It remains to be studied whether the notochord plays a role in the establishment of this bilaterality. 0 1995 Wiley-Liss, Inc.

The cardiac troponin T (cTNT) promoter contains a highly muscle specific distal promoter element capable of conferring muscle-specific transcription from a heterologous TATA box-transcription initiation site.

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protein and iso-mRNA levels in cultured cardiac myocytes were quantified during hypertrophy stimulated by the a,-adrenergic agonist, norepinephrine (NE). fl-MHC iso-protein content was increased 3.2-fold vs. control (P < 0.001), whereas a-MHC isoprotein content was not changed significantly (1.4-fold vs. control, P = NS). MHC iso-mRNA levels were quantified by nuclease Si analysis, using a single oligonucleotide probe. NE increased fl-MHC iso-mRNA content by 3.9-fold