Abstract
The development of the dorsal vessel in Drosophila is one of the first systems in which key mechanisms regulating cardiogenesis have been defined in great detail at the genetic and molecular level. Due to evolutionary conservation, these findings have also provided major inputs into studies of cardiogenesis in vertebrates. Many of the major components that control Drosophila cardiogenesis were discovered based on candidate gene approaches and their functions were defined by employing the outstanding genetic tools and molecular techniques available in this system. More recently, approaches have been taken that aim to interrogate the entire genome in order to identify novel components and describe genomic features that are pertinent to the regulation of heart development. Apart from classical forward genetic screens, the availability of the thoroughly annotated Drosophila genome sequence made new genome-wide approaches possible, which include the generation of massive numbers of RNA interference (RNAi) reagents that were used in forward genetic screens, as well as studies of the transcriptomes and proteomes of the developing heart under normal and experimentally manipulated conditions. Moreover, genome-wide chromatin immunoprecipitation experiments have been performed with the aim to define the full set of genomic binding sites of the major cardiogenic transcription factors, their relevant target genes, and a more complete picture of the regulatory network that drives cardiogenesis. This review will give an overview on these genome-wide approaches to Drosophila heart development and on computational analyses of the obtained information that ultimately aim to provide a description of this process at the systems level.
Highlights
Studies on the specification and early development of the Drosophila heart have provided one of the first examples for the regulatory circuits guiding cardiogenesis
Similar approaches have shed light on later processes of heart morphogenesis and differentiation [1]. These studies in Drosophila have been highly successful, they have relied heavily on candidate approaches and fortuitous discoveries, often combined with reverse genetics, which led to the identification of signaling processes and of new members of transcription factor families that play key roles during Drosophila cardiogenesis
The similarities of the LanB1 and Cg25C phenotypes with those of the “broken hearted” class of mutants further support a functional connection between septate junction proteins and the correct assembly of the cardiac extracellular matrix (ECM), and underline the key role of the cardiac ECM for the integrity of the heart tube
Summary
Studies on the specification and early development of the Drosophila heart (more accurately known as dorsal vessel; Figure 1) have provided one of the first examples for the regulatory circuits guiding cardiogenesis. The insights from Drosophila have produced key inputs into studies on the molecular control of vertebrate heart development and resulted in important advances in this field. The findings from these studies provided a basic framework of the intersecting signaling and transcriptional networks and their temporal and spatial integration that control early heart development. Similar approaches have shed light on later processes of heart morphogenesis and differentiation [1] These studies in Drosophila have been highly successful, they have relied heavily on candidate approaches and fortuitous discoveries, often combined with reverse genetics, which led to the identification of signaling processes and of new members of transcription factor families that play key roles during Drosophila cardiogenesis. A6 and A7, transdifferentiation of the three anterior pairs of alary muscles into ventral longitudinal A6maunsdclAes7,(VtrLaMnssd),iffdeirfefenrteinattiiaotnioonf othfeptrherseuemapnttievreioorsptiaalirsceollfsaflarormy mthuescllaersvianltoaovretantirnatlolofunngcittuiodnianlal muossctilae,s f(oVrLmMatsi)o,ndiofffetrherneteiavtiaolnveosf, pforermsuamtiopntivoef othsteiaclocneilclsalfrhoemartthcehlaamrvbaelra, oarntda iantroedfuuncctitoionnianl othsteia, fornmumatbioenr ooff ptherriecearvdailavlecse,llfso.rmation of the conical heart chamber, and a reduction in the number of pericardial cells
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