Syndecan contributes to heart cell specification and lumen formation during Drosophila cardiogenesis

The transmembrane proteoglycan Syndecan contributes to cell surface signaling of diverse ligands in mammals, yet in Drosophila, genetic evidence links Syndecan only to the Slit receptor Roundabout and to the receptor tyrosine phosphatase LAR. Here we characterize the requirement for syndecan in the determination and morphogenesis of the Drosophila heart, and reveal two phases of activity, indicating that Syndecan is a co-factor in at least two signaling events in this tissue. There is a stochastic failure to determine heart cell progenitors in a subset of abdominal hemisegments in embryos mutant for syndecan, and subsequent to Syndecan depletion by RNA interference. This phenotype is sensitive to gene dosage in the FGF receptor (Heartless), its ligand, Pyramus, as well as BMP-ligand Decapentaplegic (Dpp) and co-factor Sara. Syndecan is also required for lumen formation during assembly of the heart vessel, a phenotype shared with mutations in the Slit and Integrin signaling pathways. Phenotypic interactions of syndecan with slit and Integrin mutants suggest intersecting function, consistent with Syndecan acting as a co-receptor for Slit in the Drosophila heart.

Research highlights
► During early heart development, Syndecan contributes to the induction of heart cell fates in the dorsal mesoderm.
► Genetic evidence implicates the FGF receptor Htl, but involvement of receptors to the BMP homolog Dpp cannot be excluded.
► Vertebrate BMP and FGF pathways have contributions by Syndecan, but this report is the first in an invertebrate.
► Syndecan is required for the cell polarization signals that culminate in the formation of a lumen in the heart tube.
► Genetic evidence indicates participation in the Integrin and Slit/Robo signaling pathways.