Myoblast fusion in Drosophila

Dworak, Heather A.; Sink, Helen

doi:10.1002/bies.10115

Cited by 78 publications

(51 citation statements)

References 51 publications

(65 reference statements)

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“…This arrangement underlies the amazingly similar patterns of immunoreactivity in the eye disc, wing disc and somatic muscle as well as in the pupal optic lobe (Bao and Cagan, 2005;Dworak and Sink, 2002;Fischbach et al, 2009). We also found that these proteins are located in opposing cell membranes in the lamina.…”

Section: Possible Conserved Roles Of the Restricted Domains Of Nephrimentioning

confidence: 70%

Recognition of pre- and postsynaptic neurons via nephrin/NEPH1 homologs is a basis for the formation of theDrosophilaretinotopic map

et al. 2010

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SUMMARYTopographic maps, which maintain the spatial order of neurons in the order of their axonal connections, are found in many parts of the nervous system. Here, we focus on the communication between retinal axons and their postsynaptic partners, lamina neurons, in the first ganglion of the Drosophila visual system, as a model for the formation of topographic maps. Post-mitotic lamina precursor cells differentiate upon receiving Hedgehog signals delivered through newly arriving retinal axons and, before maturing to extend neurites, extend short processes toward retinal axons to create the lamina column. The lamina column provides the cellular basis for establishing stereotypic synapses between retinal axons and lamina neurons. In this study, we identified two cell-adhesion molecules: Hibris, which is expressed in post-mitotic lamina precursor cells; and Roughest, which is expressed on retinal axons. Both proteins belong to the nephrin/NEPH1 family. We provide evidence that recognition between post-mitotic lamina precursor cells and retinal axons is mediated by interactions between Hibris and Roughest. These findings revealed mechanisms by which axons of presynaptic neurons deliver signals to induce the development of postsynaptic partners at the target area. Postsynaptic partners then recognize the presynaptic axons to make ensembles, thus establishing a topographic map along the anterior/posterior axis.

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Section: Possible Conserved Roles Of the Restricted Domains Of Nephrimentioning

confidence: 70%

Recognition of pre- and postsynaptic neurons via nephrin/NEPH1 homologs is a basis for the formation of theDrosophilaretinotopic map

et al. 2010

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“…Myoblast fusion has been studied in mammalian myoblastic cell lines, mice, and Drosophila, and some of the molecules involved have been identified. Genetic screens and biochemical analyses have identified many proteins involved in muscle cell fusion located at the cell surface, in the cytoplasm, and in the nucleus (reviewed in Dworak and Sink, 2002;Taylor, 2002). The membrane proteins implicated in myotube formation in vertebrates include ␤1 integrin, ADAM12 (a member of a disintegrin and metalloproteinase family), NCAM, and M-cadherin (Rosen et al, 1992;Zeschnigk et al, 1995;Fazeli et al, 1996;Huovila et al, 1996;Charlton et al, 2000;Schwander et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

RhoA GTPase Regulates M-Cadherin Activity and Myoblast Fusion

Charrasse

Comunale

Grumbach

et al. 2006

MBoC

120

131

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The Rho family of GTP-binding proteins plays critical roles during myogenesis induction. To elucidate their role later during myogenesis, we have analyzed RhoA function during myoblast fusion into myotubes. We find that RhoA activity is rapidly and transiently increased when cells are shifted into differentiation medium and then is decreased until myoblast fusion. RhoA activity must be down-regulated to allow fusion, because expression of a constitutively active form of RhoA (RhoAV14) inhibits this process. RhoAV14 perturbs the expression and localization of M-cadherin, a member of the Ca 2؉ -dependent cell-cell adhesion molecule family that has an essential role in skeletal muscle cell differentiation. This mutant does not affect N-cadherin and other proteins involved in myoblast fusion, ␤1-integrin and ADAM12. Active RhoA induces the entry of M-cadherin into a degradative pathway and thus decreases its stability in correlation with the monoubiquitination of M-cadherin. Moreover, p120 catenin association with M-cadherin is decreased in RhoAV14-expressing cells, which is partially reverted by the inhibition of the RhoA effector Rho-associated kinase ROCK. ROCK inhibition also restores M-cadherin accumulation at the cell-cell contact sites. We propose that the sustained activation of the RhoA pathway inhibits myoblast fusion through the regulation of p120 activity, which controls cadherin internalization and degradation.

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“…After establishment of myoblast diversity, the fusion process starts, leading in a first fusion step to muscle precursor cells and in a second fusion step to formation of mature myotubes (Doberstein et al, 1997;Rau et al, 2001). This process can be disturbed at distinct levels (reviewed by Dworak and Sink, 2002;Taylor, 2002). Besides lateral inhibition and determination through distinct transcription factors cell-cell signalling is an important mechanism in myogenesis.…”

Section: Introductionmentioning

confidence: 99%

Myoblast determination in the somatic and visceral mesoderm depends on Notch signalling as well as onmilliways(miliAlk) as receptor for Jeb signalling

et al. 2004

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The visceral muscles of the Drosophila midgut consist of syncytia and arise by fusion of founder and fusion-competent myoblasts, as described for the somatic muscles. A single-step fusion results in the formation of binucleate circular midgut muscles, whereas a multiple-step fusion process produces the longitudinal muscles. A prerequisite for muscle fusion is the establishment of myoblast diversity in the mesoderm prior to the fusion process itself. We provide evidence for a role of Notch signalling during establishment of the different cell types in the visceral mesoderm,demonstrating that the basic mechanism underlying the segregation of somatic muscle founder cells is also conserved during visceral founder cell determination.Searching for genes involved in the determination and differentiation of the different visceral cell types, we identified two independent mutations causing loss of visceral midgut muscles. In both of these mutants visceral muscle founder cells are missing and the visceral mesoderm consists of fusion-competent myoblasts only. Thus, no fusion occurs resulting in a complete disruption of visceral myogenesis. Subsequent characterisation of the mutations revealed that they are novel alleles of jelly belly(jeb) and the Drosophila Alk homologue named milliways (miliAlk). We show that the process of founder cell determination in the visceral mesoderm depends on Jeb signalling via the Milliways/Alk receptor.Moreover, we demonstrate that in the somatic mesoderm determination of the opposite cell type, the fusion-competent myoblasts, also depends on Jeb and Alk, revealing different roles for Jeb signalling in specifying myoblast diversity. This novel mechanism uncovers a crosstalk between somatic and visceral mesoderm leading not only to the determination of different cell types but also maintains the separation of mesodermal tissues, the somatic and splanchnic mesoderm.

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Myoblast fusion in Drosophila

Cited by 78 publications

References 51 publications

Recognition of pre- and postsynaptic neurons via nephrin/NEPH1 homologs is a basis for the formation of theDrosophilaretinotopic map

Recognition of pre- and postsynaptic neurons via nephrin/NEPH1 homologs is a basis for the formation of theDrosophilaretinotopic map

RhoA GTPase Regulates M-Cadherin Activity and Myoblast Fusion

Myoblast determination in the somatic and visceral mesoderm depends on Notch signalling as well as onmilliways(miliAlk) as receptor for Jeb signalling

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