Abstract
For coordinated circulation, vertebrate and invertebrate hearts require stereotyped arrangements of diverse cell populations. This study explores the process of cardiac cell diversification in the Drosophila heart, focusing on the two major cardioblast subpopulations: generic working myocardial cells and inflow valve-forming ostial cardioblasts. By screening a large collection of randomly induced mutants, we identified several genes involved in cardiac patterning. Further analysis revealed an unexpected, specific requirement of EGF signaling for the specification of generic cardioblasts and a subset of pericardial cells. We demonstrate that the Tbx20 ortholog Midline acts as a direct target of the EGFR effector Pointed to repress ostial fates. Furthermore, we identified Edl/Mae, an antagonist of the ETS factor Pointed, as a novel cardiac regulator crucial for ostial cardioblast specification. Combining these findings, we propose a regulatory model in which the balance between activation of Pointed and its inhibition by Edl controls cardioblast subtype-specific gene expression.
Highlights
The heart consists of a variety of cells with distinct molecular and physiological properties in both vertebrates and invertebrates
We mainly focus on the development of the two major cardioblast subpopulations: generic cardioblasts, which build the main portion of the contractile tube (‘working myocardium’), and ostial cardioblasts, which form bi-cellular valves for hemolymph inflow
No specific role for the specification of a particular cardioblast subtype or diversification of generic cardioblasts (gCBs) versus ostial cardioblasts (oCBs) progenitors had been previously attributed to RTK/Ras/MAPK signaling
Summary
The heart consists of a variety of cells with distinct molecular and physiological properties in both vertebrates and invertebrates. We have performed an unbiased large-scale mutagenesis screen to identify genes that regulate cardiac development in Drosophila embryos and found several mutants that show CB subtype-specific defects On this basis, we discovered a novel and rather unexpected function of the EGF pathway in specifying the gCBs of the working myocardium, revealing an intimate link between cardioblast specification and diversification. Our data provide the basis for an elaborated model of cardiac cell fate diversification that links MAPK signaling, Pnt activity and the cell-type-specific expression patterns of key cardiac transcription factors
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