The role of cell adhesion molecules in Drosophila heart morphogenesis: Faint sausage, shotgun/DE-cadherin, and laminin A are required for discrete stages in heart development

Citation
Ta. Haag et al., The role of cell adhesion molecules in Drosophila heart morphogenesis: Faint sausage, shotgun/DE-cadherin, and laminin A are required for discrete stages in heart development, DEVELOP BIO, 208(1), 1999, pp. 56-69
Citations number
34
Categorie Soggetti
Cell & Developmental Biology
Journal title
DEVELOPMENTAL BIOLOGY
ISSN journal
00121606 → ACNP
Volume
208
Issue
1
Year of publication
1999
Pages
56 - 69
Database
ISI
SICI code
0012-1606(19990401)208:1<56:TROCAM>2.0.ZU;2-U
Abstract
Heart development in the Drosophila embryo starts with the specification of cardiac precursors from the dorsal edge of the mesoderm through signaling from the epidermis. Cardioblasts then become aligned in a single row of cel ls that migrate dorsally. After contacting their contralateral counterparts , cardioblasts undergo a cytoskeletal rearrangement and form a lumen. Its s imple architecture and cellular composition makes the heart a good system t o study mesodermal patterning, intergerm layer signaling, and the function of cell adhesion molecules (CAMs) during morphogenesis. In this paper we fo cus on three adhesion molecules, faint sausage (fas) shotgun/DE-cadherin (s hg/DE-Cad), and laminin A (lam A), that are essential for heart development , fas encodes an Ig-like CAM and is required for the correct number of card ioblasts to become specified, as well as proper alignment of cardioblasts. shg/DE-Cad is expressed and required at a later stage than fas; in embryos lacking this gene, cardioblasts are specified normally and become aligned, but do not form a lumen. Additionally, cardioblasts of shg mutant embryos s how a redistribution of phosphotyrosine as well as a loss of Armadillo from the membrane, indicating defects in cell polarity. The shg phenotype could be phenocopied by applying EGTA or cytochalasin D, supporting the view tha t Ca2+-dependent adhesion and the actin cytoskeleton are instrumental for h eart lumen formation. As opposed to cell-cell adhesion, cell-substrate adhe sion mechanisms are not required for heart morphogenesis, but only for main tenance of the differentiated heart. Embryos lacking the lam A gene initial ly developed a normal heart, but showed twists and breaks of cardioblasts a t late embryonic stages. We discuss our findings in light of recent results that elucidate the function of different adhesion systems in vertebrate he art development, (C) 1999 Academic Press.