THE WINGLESS SIGNALING PATHWAY IS DIRECTLY INVOLVED IN DROSOPHILA HEART DEVELOPMENT

Citation
My. Park et al., THE WINGLESS SIGNALING PATHWAY IS DIRECTLY INVOLVED IN DROSOPHILA HEART DEVELOPMENT, Developmental biology, 177(1), 1996, pp. 104-116
Citations number
61
Categorie Soggetti
Developmental Biology
Journal title
ISSN journal
00121606
Volume
177
Issue
1
Year of publication
1996
Pages
104 - 116
Database
ISI
SICI code
0012-1606(1996)177:1<104:TWSPID>2.0.ZU;2-U
Abstract
Heart development in both vertebrates and Drosophila is initiated by b ilaterally symmetrical primordia that may be of equivalent embryologic al origin: the anterior lateral plate mesoderm in vertebrates and the dorsal-most mesoderm in arthropods. These mesodermal progenitors then merge into a heart tube at the ventral midline (vertebrates) or the do rsal midline (Drosophila). These observations suggest that there may b e similarities between vertebrate and invertebrate heart development. The homeobox gene, tinman, is required for heart as well as visceral m esoderm formation in Drosophila, and at least one of several vertebrat e genes with similarities in protein sequence and cardiac expression t o tinman is crucial for heart development in vertebrates. Inductive si gnals are also required for Drosophila heart development: The secreted gene product of wingless (wg) is critical for heart development durin g a time period distinct from its function in segmentation and neuroge nesis. Here, we show that wg is epistatic to hedgehog (hh), another se creted segmentation gene product, in its requirement for heart formati on. We also provide evidence show that downstream of wg in the signal transduction cascade, dishevelled (dsh, a pioneer protein) and armadil lo (arm, beta-catenin homolog) are mediating the cardiogenic Wg signal . In particular, overexpression of dsh can restore heart formation in the absence of wg function. We discuss the possibility that Wg signali ng is part of a combinatorial mechanism to specify the cardiac mesoder m. (C) 1996 Academic Press, Inc.