The fabulous destiny of the Drosophila heart

Medioni, Caroline; Senatore, Sébastien; Salmand, Pierre-Adrien; Lalevée, Nathalie; Perrin, Laurent; Sémériva, Michel

doi:10.1016/j.gde.2009.07.004

Cited by 53 publications

(39 citation statements)

References 47 publications

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“…The fly heart, which constitutes the entire cardiovascular system, is a simple muscular pump, working in an open circulation. Flies are even viable without their heart, supporting a role for the heart as a facilitator of nutrient circulation (Medioni et al, 2009). Lung asymmetries, too, seem not to be functionally relevant but might reflect space constraints in the thorax resulting from asymmetric heart placement.…”

Section: Why Did Organ Asymmetry Evolve?mentioning

confidence: 99%

The evolution and conservation of left-right patterning mechanisms

et al. 2014

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Morphological asymmetry is a common feature of animal body plans, from shell coiling in snails to organ placement in humans. The signaling protein Nodal is key for determining this laterality. Many vertebrates, including humans, use cilia for breaking symmetry during embryonic development: rotating cilia produce a leftward flow of extracellular fluids that induces the asymmetric expression of Nodal. By contrast, Nodal asymmetry can be induced flow-independently in invertebrates. Here, we ask when and why flow evolved. We propose that flow was present at the base of the deuterostomes and that it is required to maintain organ asymmetry in otherwise perfectly bilaterally symmetrical vertebrates.

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Section: Why Did Organ Asymmetry Evolve?mentioning

confidence: 99%

The evolution and conservation of left-right patterning mechanisms

et al. 2014

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“…The adhesion proteins b-catenin and E-cadherin accumulate at this initial adhesion site and trigger actin-mediated cell-shape changes that allow the cardioblasts to adopt a crescent-like shape to form a second, ventral adhesion site. Simultaneous with heart-cell-shape changes, cell-autonomous, repellant Slit/Robo signaling at the luminal surface of the cardioblasts ensures proper lumen formation (Helenius and Beitel 2008;Medioni et al 2008Medioni et al , 2009Santiago-Martínez et al 2008).…”

Section: Spg Likely Acts Upstream Of Rap1 In DV and Cns Developmentmentioning

confidence: 99%

Fine-Tuning of the Actin Cytoskeleton and Cell Adhesion During Drosophila Development by the Unconventional Guanine Nucleotide Exchange Factors Myoblast City and Sponge

2015

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The evolutionarily conserved Dock proteins function as unconventional guanine nucleotide exchange factors (GEFs). Upon binding to engulfment and cell motility (ELMO) proteins, Dock-ELMO complexes activate the Rho family of small GTPases to mediate a diverse array of biological processes, including cell motility, apoptotic cell clearance, and axon guidance. Overlapping expression patterns and functional redundancy among the 11 vertebrate Dock family members, which are subdivided into four families (Dock A, B, C, and D), complicate genetic analysis. In both vertebrate and invertebrate systems, the actin dynamics regulator, Rac, is the target GTPase of the Dock-A subfamily. However, it remains unclear whether Rac or Rap1 are the in vivo downstream GTPases of the Dock-B subfamily. Drosophila melanogaster is an excellent genetic model organism for understanding Dock protein function as its genome encodes one ortholog per subfamily: Myoblast city (Mbc; Dock A) and Sponge (Spg; Dock B). Here we show that the roles of Spg and Mbc are not redundant in the Drosophila somatic muscle or the dorsal vessel. Moreover, we confirm the in vivo role of Mbc upstream of Rac and provide evidence that Spg functions in concert with Rap1, possibly to regulate aspects of cell adhesion. Together these data show that Mbc and Spg can have different downstream GTPase targets. Our findings predict that the ability to regulate downstream GTPases is dependent on cellular context and allows for the fine-tuning of actin cytoskeletal or cell adhesion events in biological processes that undergo cell morphogenesis.

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“…Heart cells, which comprise the leading edge of migrating mesodermal cells, maintain contact with the dorsally migrating ectodermal leading edge from stages 13 through 16 (reviewed by Medioni et al, 2009;Tao and Schulz, 2007). We track the dorsal and medial progress of the cardial cells with the B2-3-20 enhancer trap, revealing an ordered and continuous row of cardial cell nuclei at all stages ( Fig.…”

Section: Syndecan Mutants Develop Early and Late Heart Morphogenesis mentioning

confidence: 99%

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

Knox¹,

Moyer²,

Yacoub³

et al. 2011

Developmental Biology

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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.

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The fabulous destiny of the Drosophila heart

Cited by 53 publications

References 47 publications

The evolution and conservation of left-right patterning mechanisms

The evolution and conservation of left-right patterning mechanisms

Fine-Tuning of the Actin Cytoskeleton and Cell Adhesion During Drosophila Development by the Unconventional Guanine Nucleotide Exchange Factors Myoblast City and Sponge

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

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