Journal articles on the topic 'Drosophila muscles'
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1
Haines, Nicola, Sara Seabrooke, and Bryan A. Stewart. "Dystroglycan and Protein O-Mannosyltransferases 1 and 2 Are Required to Maintain Integrity of Drosophila Larval Muscles." Molecular Biology of the Cell 18, no. 12 (December 2007): 4721–30. http://dx.doi.org/10.1091/mbc.e07-01-0047.
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In vertebrates, mutations in Protein O-mannosyltransferase1 (POMT1) or POMT2 are associated with muscular dystrophy due to a requirement for O-linked mannose glycans on the Dystroglycan (Dg) protein. In this study we examine larval body wall muscles of Drosophila mutant for Dg, or RNA interference knockdown for Dg and find defects in muscle attachment, altered muscle contraction, and a change in muscle membrane resistance. To determine if POMTs are required for Dg function in Drosophila, we examine larvae mutant for genes encoding POMT1 or POMT2. Larvae mutant for either POMT, or doubly mutant for both, show muscle attachment and muscle contraction phenotypes identical to those associated with reduced Dg function, consistent with a requirement for O-linked mannose on Drosophila Dg. Together these data establish a central role for Dg in maintaining integrity in Drosophila larval muscles and demonstrate the importance of glycosylation to Dg function in Drosophila. This study opens the possibility of using Drosophila to investigate muscular dystrophy.
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Tracy, Claire B., Janet Nguyen, Rayna Abraham, and Troy R. Shirangi. "Evolution of sexual size dimorphism in the wing musculature of Drosophila." PeerJ 8 (January 17, 2020): e8360. http://dx.doi.org/10.7717/peerj.8360.
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Male courtship songs in Drosophila are exceedingly diverse across species. While much of this variation is understood to have evolved from changes in the central nervous system, evolutionary transitions in the wing muscles that control the song may have also contributed to song diversity. Here, focusing on a group of four wing muscles that are known to influence courtship song in Drosophila melanogaster, we investigate the evolutionary history of wing muscle anatomy of males and females from 19 Drosophila species. We find that three of the wing muscles have evolved sexual dimorphisms in size multiple independent times, whereas one has remained monomorphic in the phylogeny. These data suggest that evolutionary changes in wing muscle anatomy may have contributed to species variation in sexually dimorphic wing-based behaviors, such as courtship song. Moreover, wing muscles appear to differ in their propensity to evolve size dimorphisms, which may reflect variation in the functional constraints acting upon different wing muscles.
3
Fernandes, J., and K. VijayRaghavan. "The development of indirect flight muscle innervation in Drosophila melanogaster." Development 118, no. 1 (May 1, 1993): 215–27. http://dx.doi.org/10.1242/dev.118.1.215.
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We have examined the development of innervation to the indirect flight muscles of Drosophila. During metamorphosis, the larval intersegmental nerve of the mesothorax is remodelled to innervate the dorsal longitudinal muscles and two of the dorsoventral muscles. Another modified larval nerve innervates the remaining dorsoventral muscle. The dorsal longitudinal muscles develop using modified larval muscles as templates while dorsoventral muscles develop without the use of such templates. The development of innervation to the two groups of indirect flight muscles differs in spatial and temporal patterns, which may reflect the different ways in which these muscles develop. The identification of myoblasts associated with thoracic nerves during larval life and the association of migrating myoblasts with nerves during metamorphosis indicate the existence of nerve-muscle interactions during indirect flight muscle development. In addition, the developing pattern of axonal branching suggests a role for the target muscles in respecifying neuromuscular junctions during metamorphosis.
4
Gomez Ruiz, M., and M. Bate. "Segregation of myogenic lineages in Drosophila requires numb." Development 124, no. 23 (December 1, 1997): 4857–66. http://dx.doi.org/10.1242/dev.124.23.4857.
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Terminal divisions of myogenic lineages in the Drosophila embryo generate sibling myoblasts that found larval muscles or form precursors of adult muscles. Alternative fates adopted by sibling myoblasts are associated with distinct patterns of gene expression. Genes expressed in the progenitor cell are maintained in one sibling and repressed in the other. These differences depend on an asymmetric segregation of Numb between sibling cells. In numb mutants, muscle fates associated with repression are duplicated and alternative muscles are lost. If numb is overexpressed the reverse transformation occurs. Numb acts to block Notch-mediated repression of genes expressed in muscle progenitor cells. Thus asymmetric cell divisions are essential determinants of muscle fates during myogenesis in Drosophila
5
Fernandes, J. J., and H. Keshishian. "Nerve-muscle interactions during flight muscle development in Drosophila." Development 125, no. 9 (May 1, 1998): 1769–79. http://dx.doi.org/10.1242/dev.125.9.1769.
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During Drosophila pupal metamorphosis, the motoneurons and muscles differentiate synchronously, providing an opportunity for extensive intercellular regulation during synapse formation. We examined the existence of such interactions by developmentally delaying or permanently eliminating synaptic partners during the formation of indirect flight muscles. When we experimentally delayed muscle development, we found that although adult-specific primary motoneuron branching still occurred, the higher order (synaptic) branching was suspended until the delayed muscle fibers reached a favourable developmental state. In reciprocal experiments we found that denervation caused a decrease in the myoblast pool. Furthermore, the formation of certain muscle fibers (dorsoventral muscles) was specifically blocked. Exceptions were the adult muscles that use larval muscle fibers as myoblast fusion targets (dorsal longitudinal muscles). However, when these muscles were experimentally compelled to develop without their larval precursors, they showed an absolute dependence on the motoneurons for their formation. These data show that the size of the myoblast pool and early events in fiber formation depend on the presence of the nerve, and that, conversely, peripheral arbor development and synaptogenesis is closely synchronized with the developmental state of the muscle.
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Poovathumkadavil, Preethi, and Krzysztof Jagla. "Genetic Control of Muscle Diversification and Homeostasis: Insights from Drosophila." Cells 9, no. 6 (June 25, 2020): 1543. http://dx.doi.org/10.3390/cells9061543.
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In the fruit fly, Drosophila melanogaster, the larval somatic muscles or the adult thoracic flight and leg muscles are the major voluntary locomotory organs. They share several developmental and structural similarities with vertebrate skeletal muscles. To ensure appropriate activity levels for their functions such as hatching in the embryo, crawling in the larva, and jumping and flying in adult flies all muscle components need to be maintained in a functionally stable or homeostatic state despite constant strain. This requires that the muscles develop in a coordinated manner with appropriate connections to other cell types they communicate with. Various signaling pathways as well as extrinsic and intrinsic factors are known to play a role during Drosophila muscle development, diversification, and homeostasis. In this review, we discuss genetic control mechanisms of muscle contraction, development, and homeostasis with particular emphasis on the contractile unit of the muscle, the sarcomere.
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Rout, Pratiti, Mathieu Preußner, and Susanne Filiz Önel. "Drosophila melanogaster: A Model System to Study Distinct Genetic Programs in Myoblast Fusion." Cells 11, no. 3 (January 19, 2022): 321. http://dx.doi.org/10.3390/cells11030321.
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Muscle fibers are multinucleated cells that arise during embryogenesis through the fusion of mononucleated myoblasts. Myoblast fusion is a lifelong process that is crucial for the growth and regeneration of muscles. Understanding the molecular mechanism of myoblast fusion may open the way for novel therapies in muscle wasting and weakness. Recent reports in Drosophila and mammals have provided new mechanistic insights into myoblast fusion. In Drosophila, muscle formation occurs twice: during embryogenesis and metamorphosis. A fundamental feature is the formation of a cell–cell communication structure that brings the apposing membranes into close proximity and recruits possible fusogenic proteins. However, genetic studies suggest that myoblast fusion in Drosophila is not a uniform process. The complexity of the players involved in myoblast fusion can be modulated depending on the type of muscle that is formed. In this review, we introduce the different types of multinucleated muscles that form during Drosophila development and provide an overview in advances that have been made to understand the mechanism of myoblast fusion. Finally, we will discuss conceptual frameworks in cell–cell fusion in Drosophila and mammals.
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Lin, S. C., M. H. Lin, P. Horvath, K. L. Reddy, and R. V. Storti. "PDP1, a novel Drosophila PAR domain bZIP transcription factor expressed in developing mesoderm, endoderm and ectoderm, is a transcriptional regulator of somatic muscle genes." Development 124, no. 22 (November 15, 1997): 4685–96. http://dx.doi.org/10.1242/dev.124.22.4685.
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In vertebrates, transcriptional control of skeletal muscle genes during differentiation is regulated by enhancers that direct the combinatorial binding and/or interaction of MEF2 and the bHLH MyoD family of myogenic factors. We have shown that Drosophila MEF2 plays a role similar to its vertebrate counterpart in the regulation of the Tropomyosin I gene in the development of Drosophila somatic muscles, however, unlike vertebrates, Drosophila MEF2 interacts with a muscle activator region that does not have binding sites for myogenic bHLH-like factors or any other known Drosophila transcription factors. We describe here the isolation and characterization of a component of the muscle activator region that we have named PDP1 (PAR domain protein 1). PDP1 is a novel transcription factor that is highly homologous to the PAR subfamily of mammalian bZIP transcription factors HLF, DBP and VBP/TEF. This is the first member of the PAR subfamily of bZIP transcription factors to be identified in Drosophila. We show that PDP1 is involved in regulating expression of the Tropomyosin I gene in somatic body-wall and pharyngeal muscles by binding to DNA sequences within the muscle activator that are required for activator function. Mutations that eliminate PDP1 binding eliminate muscle activator function and severely reduce expression of a muscle activator plus MEF2 mini-enhancer. These and previous results suggest that PDP1 may function as part of a larger protein/DNA complex that interacts with MEF2 to regulate transcription of Drosophila muscle genes. Furthermore, in addition to being expressed in the mesoderm that gives rise to the somatic muscles, PDP1 is also expressed in the mesodermal fat body, the developing midgut endoderm, the hindgut and Malpighian tubules, and the epidermis and central nervous system, suggesting that PDP1 is also involved in the terminal differentiation of these tissues.
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Callahan, C. A., J. L. Bonkovsky, A. L. Scully, and J. B. Thomas. "derailed is required for muscle attachment site selection in Drosophila." Development 122, no. 9 (September 1, 1996): 2761–67. http://dx.doi.org/10.1242/dev.122.9.2761.
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During development, muscles must form and attach at highly stereotyped positions to allow for coordinated movements. In Drosophila, muscles grow towards and attach to specifically positioned cells within the epidermis. At the molecular level, very little is known about how muscles recognize these attachment sites. The derailed gene encodes a receptor tyrosine kinase family member that is essential for the pathfinding ability of expressing neurons. Here we show that the Drl RTK is also expressed by a small subset of developing embryonic muscles and neighboring epidermal cells during muscle attachment site selection. In drl mutants, these muscles often fail to attach at appropriate locations although their epidermal attachment cells appear unaffected. These results show that, similar to its role in neuronal pathway recognition, the Drl RTK participates in a mechanism required for muscle attachment site selection. The data suggest that both neurons and muscles use common mechanisms to recognize their paths or targets, and that Drl plays an analogous role in both developing systems.
10
Chaturvedi, Dhananjay, Sunil Prabhakar, Aman Aggarwal, Krishan B. Atreya, and K. VijayRaghavan. "Adult Drosophila muscle morphometry through microCT reveals dynamics during ageing." Open Biology 9, no. 6 (June 2019): 190087. http://dx.doi.org/10.1098/rsob.190087.
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Indirect flight muscles (IFMs) in adult Drosophila provide the key power stroke for wing beating. They also serve as a valuable model for studying muscle development. An age-dependent decline in Drosophila free flight has been documented, but its relation to gross muscle structure has not yet been explored satisfactorily. Such analyses are impeded by conventional histological preparations and imaging techniques that limit exact morphometry of flight muscles. In this study, we employ microCT scanning on a tissue preparation that retains muscle morphology under homeostatic conditions. Focusing on a subset of IFMs called the dorsal longitudinal muscles (DLMs), we find that DLM volumes increase with age, partially due to the increased separation between myofibrillar fascicles, in a sex-dependent manner. We have uncovered and quantified asymmetry in the size of these muscles on either side of the longitudinal midline. Measurements of this resolution and scale make substantive studies that test the connection between form and function possible. We also demonstrate the application of this method to other insect species making it a valuable tool for histological analysis of insect biodiversity.
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Nguyen, Hanh T., Francesca Voza, Nader Ezzeddine, and Manfred Frasch. "Drosophila mind bomb2 is required for maintaining muscle integrity and survival." Journal of Cell Biology 179, no. 2 (October 22, 2007): 219–27. http://dx.doi.org/10.1083/jcb.200708135.
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We report that the Drosophila mind bomb2 (mib2) gene is a novel regulator of muscle development. Unlike its paralogue, mib1, zygotic expression of mib2 is restricted to somatic and visceral muscle progenitors, and their respective differentiated musculatures. We demonstrate that in embryos that lack functional Mib2, muscle detachment is observed beginning in mid stage 15 and progresses rapidly, culminating in catastrophic degeneration and loss of most somatic muscles by stage 17. Notably, the degenerating muscles are positive for apoptosis markers, and inhibition of apoptosis in muscles prevents to a significant degree the muscle defects. Rescue experiments with Mib1 and Neuralized show further that these E3 ubiquitin ligases are not capable of ameliorating the muscle mutant phenotype of mib2. Our data suggest strongly that mib2 is involved in a novel Notch- and integrin-independent pathway that maintains the integrity of fully differentiated muscles and prevents their apoptotic degeneration.
12
Deng, Hua, John B. Bell, and Andrew J. Simmonds. "Vestigial Is Required during Late-Stage Muscle Differentiation in Drosophila melanogaster Embryos." Molecular Biology of the Cell 21, no. 19 (October 2010): 3304–16. http://dx.doi.org/10.1091/mbc.e10-04-0364.
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The somatic muscles of Drosophila develop in a complex pattern that is repeated in each embryonic hemi-segment. During early development, progenitor cells fuse to form a syncytial muscle, which further differentiates via expression of muscle-specific factors that induce specific responses to external signals to regulate late-stage processes such as migration and attachment. Initial communication between somatic muscles and the epidermal tendon cells is critical for both of these processes. However, later establishment of attachments between longitudinal muscles at the segmental borders is largely independent of the muscle–epidermal attachment signals, and relatively little is known about how this event is regulated. Using a combination of null mutations and a truncated version of Sd that binds Vg but not DNA, we show that Vestigial (Vg) is required in ventral longitudinal muscles to induce formation of stable intermuscular attachments. In several muscles, this activity may be independent of Sd. Furthermore, the cell-specific differentiation events induced by Vg in two cells fated to form attachments are coordinated by Drosophila epidermal growth factor signaling. Thus, Vg is a key factor to induce specific changes in ventral longitudinal muscles 1–4 identity and is required for these cells to be competent to form stable intermuscular attachments with each other.
13
Ruiz-Gomez, M., S. Romani, C. Hartmann, H. Jackle, and M. Bate. "Specific muscle identities are regulated by Kruppel during Drosophila embryogenesis." Development 124, no. 17 (September 1, 1997): 3407–14. http://dx.doi.org/10.1242/dev.124.17.3407.
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During Drosophila embryogenesis, mesodermal cells are recruited to form a complex pattern of larval muscles. The formation of the pattern is initiated by the segregation of a special class of founder myoblasts. Single founders fuse with neighbouring nonfounder myoblasts to form the precursors of individual muscles. Founders and the muscles that they give rise to have specific patterns of gene expression and it has been suggested that it is the expression of these founder cell genes that determines individual muscle attributes such as size, shape, insertion sites and innervation. We find that the segmentation gene Kruppel is expressed in a subset of founders and muscles, regulates specific patterns of gene expression in these cells and is required for the acquisition of proper muscle identity. We show that gain and loss of Kruppel expression in sibling founder cells is sufficient to switch these cells, and the muscles that they give rise to, between alternative cell fates.
14
Jagla, T., F. Bellard, Y. Lutz, G. Dretzen, M. Bellard, and K. Jagla. "ladybird determines cell fate decisions during diversification of Drosophila somatic muscles." Development 125, no. 18 (September 15, 1998): 3699–708. http://dx.doi.org/10.1242/dev.125.18.3699.
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In the mesoderm of Drosophila embryos, a defined number of cells segregate as progenitors of individual body wall muscles. Progenitors and their progeny founder cells display lineage-specific expression of transcription factors but the mechanisms that regulate their unique identities are poorly understood. Here we show that the homeobox genes ladybird early and ladybird late are expressed in only one muscle progenitor and its progeny: the segmental border muscle founder cell and two precursors of adult muscles. The segregation of the ladybird-positive progenitor requires coordinate action of neurogenic genes and an interplay of inductive Hedgehog and Wingless signals from the overlying ectoderm. Unlike so far described progenitors but similar to the neuroblasts, the ladybird-positive progenitor undergoes morphologically asymmetric division. We demonstrate that the ectopic ladybird expression is sufficient to change the identity of a subset of progenitor/founder cells and to generate an altered pattern of muscle precursors. When ectopically expressed, ladybird transforms the identity of neighbouring, Kruppel-positive progenitors leading to the formation of giant segmental border muscles and supernumerary precursors of lateral adult muscles. In embryos lacking ladybird gene function, specification of two ladybird-expressing myoblast lineages is affected. The segmental border muscles do not form or have abnormal shapes and insertion sites while the number of lateral precursors of adult muscles is dramatically reduced. Altogether our results provide new insights into the genetic control of diversification of muscle precursors and indicate a further similarity between the myogenic and neurogenic pathways.
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Bate, M. "The embryonic development of larval muscles in Drosophila." Development 110, no. 3 (November 1, 1990): 791–804. http://dx.doi.org/10.1242/dev.110.3.791.
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Each of the abdominal hemisegments A2-A7 in the Drosophila larva has a stereotyped pattern of 30 muscles. The pattern is complete by 13 h after egg laying, but the development of individual muscles has begun with the definition of precursors at least by the onset of germ band shortening, some 5.5 h earlier. The earliest signs of muscle differentiation are cell fusions, which occur in the ventralmost mesoderm overlying the CNS and at stereotyped positions in the rest of the mesoderm as the germ band shortens. At the end of shortening, the pattern of muscle precursors produced by these fusions is complete. Precursors filled with dye reveal extensive fine processes probably involved initially in cell fusion and, subsequently, in navigation over the epidermis to form attachment points. The muscle pattern is formed before innervation and without cell death. Thus, neither of these processes is involved in determining the distribution of precursors. Evidence is presented for the view that the development of the larval muscle pattern in Drosophila depends on a prior segregation of founder cells at appropriate locations in the mesoderm with which other cells fuse to form the precursors.
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Sink, H., and P. M. Whitington. "Early ablation of target muscles modulates the arborisation pattern of an identified embryonic Drosophila motor axon." Development 113, no. 2 (October 1, 1991): 701–7. http://dx.doi.org/10.1242/dev.113.2.701.
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The Drosophila RP3 motor axon establishes a stereotypic arborisation along the adjoining edges of muscles 6 and 7 by the end of embryogenesis. The present study has examined the role of the target muscles in determining this axonal arborisation pattern. Target muscles were surgically ablated prior to the arrival of the RP3 axon. Following further development of the embryo in culture medium, the morphology of target-deprived RP3 motor axons was assayed by intracellular injection with the dye Lucifer Yellow. Axonal arborisations were formed on a variety of non-target muscles when muscles 6 and 7 were removed and these contacts were maintained into stage 16. The pattern of axonal arborisations over non-target muscles varied between preparations in terms of the number of muscles contacted, and the distribution of arborisations on individual muscles. Following removal of muscle 6, the RP3 motor axon frequently contacted muscle 7, and axonal arborisations were present along the distal edge of the muscle. In the absence of muscle 7, the RP3 axon often did not contact muscle 6 and when muscle 6 was contacted, the arborisation of RP3 was poorly developed. Axonal processes were retained on non-target muscles when only one target muscle was present. Therefore, the establishment of a stereotypic arborisation by the RP3 motor axon is apparently dependent on growth cone contact with both target muscles.
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DeSimone, S., C. Coelho, S. Roy, K. VijayRaghavan, and K. White. "ERECT WING, the Drosophila member of a family of DNA binding proteins is required in imaginal myoblasts for flight muscle development." Development 122, no. 1 (January 1, 1996): 31–39. http://dx.doi.org/10.1242/dev.122.1.31.
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The erect wing locus of the fruit fly Drosophila melanogaster encodes a protein, EWG, that shares extensive homology with the P3A2 DNA binding protein of sea urchin and a recently identified mammalian transcription factor. Loss-of-function erect wing alleles result in embryonic lethality. Viable alleles of erect wing cause severe abnormalities of the indirect flight muscles. We have analyzed the spatial pattern of erect wing expression in the developing indirect flight muscles during postembryonic development. EWG is detected, 10 hours after puparium formation, in myoblasts that will form the indirect flight muscles. The early events of muscle development are normal in ewg mutants. However, a few hours after the onset of erect wing expression in myoblasts, defects are seen in the developing indirect flight muscles which subsequently degenerate. We present results that show that the normal development of the indirect flight muscles requires erect wing expression in the progenitor myoblasts themselves. Finally, we examine the role of target muscles in the arborization of motor axons by studying the developing innervation to the flight muscle in erect wing mutants. Our study demonstrates, for the first time, a role for a regulatory gene expressed in imaginal myoblasts in Drosophila.
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Oas, Sandy T., Anton L. Bryantsev, and Richard M. Cripps. "Arrest is a regulator of fiber-specific alternative splicing in the indirect flight muscles of Drosophila." Journal of Cell Biology 206, no. 7 (September 22, 2014): 895–908. http://dx.doi.org/10.1083/jcb.201405058.
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Drosophila melanogaster flight muscles are distinct from other skeletal muscles, such as jump muscles, and express several uniquely spliced muscle-associated transcripts. We sought to identify factors mediating splicing differences between the flight and jump muscle fiber types. We found that the ribonucleic acid–binding protein Arrest (Aret) is expressed in flight muscles: in founder cells, Aret accumulates in a novel intranuclear compartment that we termed the Bruno body, and after the onset of muscle differentiation, Aret disperses in the nucleus. Down-regulation of the aret gene led to ultrastructural changes and functional impairment of flight muscles, and transcripts of structural genes expressed in the flight muscles became spliced in a manner characteristic of jump muscles. Aret also potently promoted flight muscle splicing patterns when ectopically expressed in jump muscles or tissue culture cells. Genetically, aret is located downstream of exd (extradenticle), hth (homothorax), and salm (spalt major), transcription factors that control fiber identity. Our observations provide insight into a transcriptional and splicing regulatory network for muscle fiber specification.
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Cooper, Robin L., and Rebecca M. Krall. "Hyperpolarization Induced by Lipopolysaccharides but Not by Chloroform Is Inhibited by Doxapram, an Inhibitor of Two-P-Domain K+ Channel (K2P)." International Journal of Molecular Sciences 23, no. 24 (December 13, 2022): 15787. http://dx.doi.org/10.3390/ijms232415787.
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Bacterial septicemia is commonly induced by Gram-negative bacteria. The immune response is triggered in part by the secretion of bacterial endotoxin lipopolysaccharide (LPS). LPS induces the subsequent release of inflammatory cytokines which can result in pathological conditions. There is no known blocker to the receptors of LPS. The Drosophila larval muscle is an amendable model to rapidly screen various compounds that affect membrane potential and synaptic transmission such as LPS. LPS induces a rapid hyperpolarization in the body wall muscles and depolarization of motor neurons. These actions are blocked by the compound doxapram (10 mM), which is known to inhibit a subtype of the two-P-domain K+ channel (K2P channels). However, the K2P channel blocker PK-THPP had no effect on the Drosophila larval muscle at 1 and 10 mM. These channels are activated by chloroform, which also induces a rapid hyperpolarization of these muscles, but the channels are not blocked by doxapram. Likewise, chloroform does not block the depolarization induced by doxapram. LPS blocks the postsynaptic glutamate receptors on Drosophila muscle. Pre-exposure to doxapram reduces the LPS block of these ionotropic glutamate receptors. Given that the larval Drosophila body wall muscles are depolarized by doxapram and hyperpolarized by chloroform, they offer a model to begin pharmacological profiling of the K2P subtype channels with the potential of identifying blockers for the receptors to mitigate the actions of the Gram-negative endotoxin LPS.
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Riechmann, V., U. Irion, R. Wilson, R. Grosskortenhaus, and M. Leptin. "Control of cell fates and segmentation in the Drosophila mesoderm." Development 124, no. 15 (August 1, 1997): 2915–22. http://dx.doi.org/10.1242/dev.124.15.2915.
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The primordia for heart, fat body, and visceral and somatic muscles arise in specific areas of each segment in the Drosophila mesoderm. We show that the primordium of the somatic muscles, which expresses high levels of twist, a crucial factor of somatic muscle determination, is lost in sloppy-paired mutants. Simultaneously, the primordium of the visceral muscles is expanded. The visceral muscle and fat body primordia require even-skipped for their development and the mesoderm is thought to be unsegmented in even-skipped mutants. However, we find that even-skipped mutants retain the segmental modulation of the expression of twist. Both the domain of even-skipped function and the level of twist expression are regulated by sloppy-paired. sloppy-paired thus controls segmental allocation of mesodermal cells to different fates.
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Dahl-Halvarsson, Martin, Montse Olive, Malgorzata Pokrzywa, Katarina Ejeskär, Ruth H. Palmer, Anne Elisabeth Uv, and Homa Tajsharghi. "Drosophila model of myosin myopathy rescued by overexpression of a TRIM-protein family member." Proceedings of the National Academy of Sciences 115, no. 28 (June 26, 2018): E6566—E6575. http://dx.doi.org/10.1073/pnas.1800727115.
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Myosin is a molecular motor indispensable for body movement and heart contractility. Apart from pure cardiomyopathy, mutations in MYH7 encoding slow/β-cardiac myosin heavy chain also cause skeletal muscle disease with or without cardiac involvement. Mutations within the α-helical rod domain of MYH7 are mainly associated with Laing distal myopathy. To investigate the mechanisms underlying the pathology of the recurrent causative MYH7 mutation (K1729del), we have developed a Drosophila melanogaster model of Laing distal myopathy by genomic engineering of the Drosophila Mhc locus. Homozygous MhcK1728del animals die during larval/pupal stages, and both homozygous and heterozygous larvae display reduced muscle function. Flies expressing only MhcK1728del in indirect flight and jump muscles, and heterozygous MhcK1728del animals, were flightless, with reduced movement and decreased lifespan. Sarcomeres of MhcK1728del mutant indirect flight muscles and larval body wall muscles were disrupted with clearly disorganized muscle filaments. Homozygous MhcK1728del larvae also demonstrated structural and functional impairments in heart muscle, which were not observed in heterozygous animals, indicating a dose-dependent effect of the mutated allele. The impaired jump and flight ability and the myopathy of indirect flight and leg muscles associated with MhcK1728del were fully suppressed by expression of Abba/Thin, an E3-ligase that is essential for maintaining sarcomere integrity. This model of Laing distal myopathy in Drosophila recapitulates certain morphological phenotypic features seen in Laing distal myopathy patients with the recurrent K1729del mutation. Our observations that Abba/Thin modulates these phenotypes suggest that manipulation of Abba/Thin activity levels may be beneficial in Laing distal myopathy.
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Fernandes, J. J., and H. Keshishian. "Patterning the dorsal longitudinal flight muscles (DLM) of Drosophila: insights from the ablation of larval scaffolds." Development 122, no. 12 (December 1, 1996): 3755–63. http://dx.doi.org/10.1242/dev.122.12.3755.
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The six Dorsal Longitudinal flight Muscles (DLMs) of Drosophila develop from three larval muscles that persist into metamorphosis and serve as scaffolds for the formation of the adult fibers. We have examined the effect of muscle scaffold ablation on the development of DLMs during metamorphosis. Using markers that are specific to muscle and myoblasts we show that in response to the ablation, myoblasts which would normally fuse with the larval muscle, fuse with each other instead, to generate the adult fibers in the appropriate regions of the thorax. The development of these de novo DLMs is delayed and is reflected in the delayed expression of erect wing, a transcription factor thought to control differentiation events associated with myoblast fusion. The newly arising muscles express the appropriate adult-specific Actin isoform (88F), indicating that they have the correct muscle identity. However, there are frequent errors in the number of muscle fibers generated. Ablation of the larval scaffolds for the DLMs has revealed an underlying potential of the DLM myoblasts to initiate de novo myogenesis in a manner that resembles the mode of formation of the Dorso-Ventral Muscles, DVMs, which are the other group of indirect flight muscles. Therefore, it appears that the use of larval scaffolds is a superimposition on a commonly used mechanism of myogenesis in Drosophila. Our results show that the role of the persistent larval muscles in muscle patterning involves the partitioning of DLM myoblasts, and in doing so, they regulate formation of the correct number of DLM fibers.
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Martin, Beatriz San, Mar Ruiz-Gómez, Matthias Landgraf, and Michael Bate. "A distinct set of founders and fusion-competent myoblasts make visceral muscles in the Drosophila embryo." Development 128, no. 17 (September 1, 2001): 3331–38. http://dx.doi.org/10.1242/dev.128.17.3331.
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The embryonic Drosophila midgut is enclosed by a latticework of longitudinal and circular visceral muscles. We find that these muscles are syncytial. Like the somatic muscles they are generated by the prior segregation of two populations of cells: fusion-competent myoblasts and founder myoblasts specialised to seed the formation of particular muscles. Visceral muscle founders are of two classes: those that seed circular muscles and those that seed longitudinal muscles. These specialisations are revealed in mutant embryos where myoblast fusion fails. In the absence of fusion, founders make mononucleate circular or longitudinal fibres, while their fusion-competent neighbours remain undifferentiated.
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Koppes, Ryan A., Douglas M. Swank, and David T. Corr. "A new experimental model for force enhancement: steady-state and transient observations of the Drosophila jump muscle." American Journal of Physiology-Cell Physiology 309, no. 8 (October 15, 2015): C551—C557. http://dx.doi.org/10.1152/ajpcell.00202.2015.
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The increase in steady-state force after active lengthening in skeletal muscle, termed force enhancement (FE), has been observed for nearly one century. Although demonstrated experimentally at various structural levels, the underlying mechanism(s) remain unknown. We recently showed that the Drosophila jump muscle is an ideal model for investigating mechanisms behind muscle physiological properties, because its mechanical characteristics, tested thus far, duplicate those of fast mammalian skeletal muscles, and Drosophila has the advantage that it can be more easily genetically modified. To determine if Drosophila would be appropriate to investigate FE, we performed classic FE experiments on this muscle. Steady-state FE (FESS), following active lengthening, increased by 3, 7, and 12% of maximum isometric force, with increasing stretch amplitudes of 5, 10, and 20% of optimal fiber length (FLOPT), yet was similar for stretches across increasing stretch velocities of 4, 20, and 200% FLOPT/s. These FESS characteristics of the Drosophila jump muscle closely mimic those observed previously. Jump muscles also displayed typical transient FE characteristics. The transient force relaxation following active stretch was fit with a double exponential, yielding two phases of force relaxation: a fast initial relaxation of force, followed by a slower recovery toward steady state. Our analyses identified a negative correlation between the slow relaxation rate and FESS, indicating that there is likely an active component contributing to FE, in addition to a passive component. Herein, we have established the Drosophila jump muscle as a new and genetically powerful experimental model to investigate the underlying mechanism(s) of FE.
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Raghavan, K. Vijay, and Ludwin Pinto. "The cell lineage of the muscles of the Drosophila head." Development 85, no. 1 (February 1, 1985): 285–94. http://dx.doi.org/10.1242/dev.85.1.285.
Full textAbstract:
Using a cell marker mutation the cell lineage of the muscles of the Drosophila head are traced out. Three sets of muscles separated by lineage restrictions are observed, even when cells are marked as early as the blastoderm stage. Each set underlies the derivatives of one of the three pairs of imaginal discs which differentiate to form the epidermis of the adult head. Clones of the homoeotic mutation engrailed (en10) were apparently normal in the muscles of the head. The muscle clone frequency, at the blastoderm stage, in each hemisegment of the fly is similar, indicating an equal partitioning of cells during segmentation.
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Becker, S., G. Pasca, D. Strumpf, L. Min, and T. Volk. "Reciprocal signaling between Drosophila epidermal muscle attachment cells and their corresponding muscles." Development 124, no. 13 (July 1, 1997): 2615–22. http://dx.doi.org/10.1242/dev.124.13.2615.
Full textAbstract:
Directed intercellular interactions between distinct cell types underlie the basis for organogenesis during embryonic development. This paper focuses on the establishment of the final somatic muscle pattern in Drosophila, and on the possible cross-talk between the myotubes and the epidermal muscle attachment cells, occurring while both cell types undergo distinct developmental programs. Our findings suggest that the stripe gene is necessary and sufficient to initiate the developmental program of epidermal muscle attachment cells. In stripe mutant embryos, these cells do not differentiate correctly. Ectopic expression of Stripe in various epidermal cells transforms these cells into muscle-attachment cells expressing an array of epidermal muscle attachment cell-specific markers. Moreover, these ectopic epidermal muscle attachment cells are capable of attracting somatic myotubes from a limited distance, providing that the myotube has not yet been attached to or been influenced by a closer wild-type attachment cell. Analysis of the relationships between muscle binding and differentiation of the epidermal muscle attachment cell was performed in mutant embryos in which loss of muscles, or ectopic muscles were induced. This analysis indicated that, although the initial expression of epidermal muscle-attachment cell-specific genes including stripe and groovin is muscle independent, their continuous expression is maintained only in epidermal muscle attachment cells that are connected to muscles. These results suggest that the binding of a somatic muscle to an epidermal muscle attachment cell triggers a signal affecting gene expression in the attachment cell. Taken together, our results suggest the presence of a reciprocal signaling mechanism between the approaching muscles and the epidermal muscle attachment cells. First the epidermal muscle attachment cells signal the myotubes and induce myotube attraction and adhesion to their target cells. Following this binding, the muscle cells send a reciprocal signal to the epidermal muscle attachment cells inducing their terminal differentiation into tendon-like cells.
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Fernandes, J., M. Bate, and K. Vijayraghavan. "Development of the indirect flight muscles of Drosophila." Development 113, no. 1 (September 1, 1991): 67–77. http://dx.doi.org/10.1242/dev.113.1.67.
Full textAbstract:
We have followed the pupal development of the indirect flight muscles (IFMs) of Drosophila melanogaster. At the onset of metamorphosis larval muscles start to histolyze, with the exception of a specific set of thoracic muscles. Myoblasts surround these persisting larval muscles and begin the formation of one group of adult indirect flight muscles, the dorsal longitudinal muscles. We show that the other group of indirect flight muscles, the dorsoventral muscles, develops simultaneously but without the use of larval templates. By morphological criteria and by patterns of specific gene expression, our experiments define events in IFM development.
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Hastings, G. A., and C. P. Emerson. "Myosin functional domains encoded by alternative exons are expressed in specific thoracic muscles of Drosophila." Journal of Cell Biology 114, no. 2 (July 15, 1991): 263–76. http://dx.doi.org/10.1083/jcb.114.2.263.
Full textAbstract:
The Drosophila 36B muscle myosin heavy chain (MHC) gene has five sets of alternatively spliced exons that encode functionally important domains of the MHC protein and provide a combinatorial potential for expression of as many as 480 MHC isoforms. In this study, in situ hybridization analysis has been used to examine the complexity and muscle specificity of MHC isoform expression in the fibrillar indirect flight muscle (IFM), the tubular direct flight muscles (DFM) and tubular tergal depressor of the trochanter muscle (TDT), and the visceral esophageal muscle in the adult thorax. Our results show that alternative splicing of the MHC gene transcripts is precisely regulated in these thoracic muscles, which express three MHC isoforms. Individual thoracic muscles each express transcripts of only one isoform, as detectable by in situ hybridization. An apparently novel fourth MHC isoform, with sequence homology to the rod but not to the head domain of the 36B MHC, is expressed in two direct flight muscles. These findings form a basis for transgenic experiments designed to analyze the muscle-specific functions of MHC domains encoded by alternative exons.
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Nose, A., T. Umeda, and M. Takeichi. "Neuromuscular target recognition by a homophilic interaction of connectin cell adhesion molecules in Drosophila." Development 124, no. 8 (April 15, 1997): 1433–41. http://dx.doi.org/10.1242/dev.124.8.1433.
Full textAbstract:
Drosophila Connectin (CON) is a cell surface protein of the leucine-rich repeat family. During the formation of neuromuscular connectivity, CON is expressed on the surface of a subset of embryonic muscles and on the growth cones and axons of the motoneurons that innervate these muscles, including primarily SNa motoneurons and their synaptic targets (lateral muscles). In vitro, CON can mediate homophilic cell adhesion. In this study, we generated transgenic lines that ectopically expressed CON on all muscles. In the transformant embryos and larvae, SNa motoneurons often inappropriately innervated a neighboring non-target muscle (muscle 12) that ectopically expressed CON. Furthermore, the ectopic synapse formation was dependent on the endogenous CON expression on the SNa motoneurons. These results show that CON can function as an attractive and homophilic target recognition molecule in vivo.
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Becker, K. D., P. T. O'Donnell, J. M. Heitz, M. Vito, and S. I. Bernstein. "Analysis of Drosophila paramyosin: identification of a novel isoform which is restricted to a subset of adult muscles." Journal of Cell Biology 116, no. 3 (February 1, 1992): 669–81. http://dx.doi.org/10.1083/jcb.116.3.669.
Full textAbstract:
In this report we show that Drosophila melanogaster muscles contain the standard form of the thick filament protein paramyosin, as well as a novel paramyosin isoform, which we call miniparamyosin. We have isolated Drosophila paramyosin using previously established methods. This protein is approximately 105 kD and cross-reacts with polyclonal antibodies made against Caenorhabditis elegans or Heliocopris dilloni paramyosin. The Heliocopris antibody also cross-reacts with a approximately 55-kD protein which may be miniparamyosin. We have cloned and sequenced cDNA's encoding both Drosophila isoforms. Standard paramyosin has short nonhelical regions at each terminus flanking the expected alpha-helical heptad repeat seen in other paramyosins and in myosin heavy chains. The COOH-terminal 363 amino acids are identical in standard and miniparamyosin. However, the smaller isoform has 114 residues at the NH2 terminus that are unique as compared to the current protein sequence data base. The paramyosin gene is located at chromosome position 66E1. It appears to use two promoters to generate mRNA's that have either of two different 5' coding sequences joined to common 3' exons. Each protein isoform is encoded by two transcripts that differ only in the usage of polyadenylation signals. This results in four size classes of paramyosin mRNA which are expressed in a developmentally regulated pattern consistent with that observed for other muscle-specific RNA's in Drosophila. In situ hybridization to Drosophila tissue sections shows that standard paramyosin is expressed in all larval and adult muscle tissues whereas miniparamyosin is restricted to a subset of the adult musculature. Thus miniparamyosin is a novel muscle-specific protein that likely plays a role in thick filament structure or function in some adult muscles of Drosophila.
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Wolf, B., M. A. Seeger, and A. Chiba. "Commissureless endocytosis is correlated with initiation of neuromuscular synaptogenesis." Development 125, no. 19 (October 1, 1998): 3853–63. http://dx.doi.org/10.1242/dev.125.19.3853.
Full textAbstract:
We show that the Commissureless (COMM) transmembrane protein is required at neuromuscular synaptogenesis. All muscles in the Drosophila embryo express COMM during the period of motoneuron-muscle interaction. It is endocytosed into muscles before synaptogenesis. In comm loss-of-function mutants, motoneuron growth cones fail to initiate synaptogenesis at target muscles. This stall phenotype is rescued by supplying wild-type COMM to the muscles. Cytoplasmically truncated COMM protein fails to internalize. Expressing this mutant protein in muscles phenocopies the synaptogenesis defects of comm mutants. Thus, synaptogenesis initiation is positively correlated with endocytosis of COMM in postsynaptic muscle cells. We propose that COMM is an essential part of the dynamic cell surface remodeling needed by postsynaptic cells in coordinating synaptogenesis initiation.
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Ghazi, A., S. Anant, and K. Vijay Raghavan. "Apterous mediates development of direct flight muscles autonomously and indirect flight muscles through epidermal cues." Development 127, no. 24 (December 15, 2000): 5309–18. http://dx.doi.org/10.1242/dev.127.24.5309.
Full textAbstract:
Two physiologically distinct types of muscles, the direct and indirect flight muscles, develop from myoblasts associated with the Drosophila wing disc. We show that the direct flight muscles are specified by the expression of Apterous, a Lim homeodomain protein, in groups of myoblasts. This suggests a mechanism of cell-fate specification by labelling groups of fusion competent myoblasts, in contrast to mechanisms in the embryo, where muscle cell fate is specified by single founder myoblasts. In addition, Apterous is expressed in the developing adult epidermal muscle attachment sites. Here, it functions to regulate the expression of stripe, a gene that is an important element of early patterning of muscle fibres, from the epidermis. Our results, which may have broad implications, suggest novel mechanisms of muscle patterning in the adult, in contrast to embryonic myogenesis.
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Johnston, J. Spencer, Mary E. Zapalac, and Carl E. Hjelmen. "Flying High—Muscle-Specific Underreplication in Drosophila." Genes 11, no. 3 (February 26, 2020): 246. http://dx.doi.org/10.3390/genes11030246.
Full textAbstract:
Drosophila underreplicate the DNA of thoracic nuclei, stalling during S phase at a point that is proportional to the total genome size in each species. In polytene tissues, such as the Drosophila salivary glands, all of the nuclei initiate multiple rounds of DNA synthesis and underreplicate. Yet, only half of the nuclei isolated from the thorax stall; the other half do not initiate S phase. Our question was, why half? To address this question, we use flow cytometry to compare underreplication phenotypes between thoracic tissues. When individual thoracic tissues are dissected and the proportion of stalled DNA synthesis is scored in each tissue type, we find that underreplication occurs in the indirect flight muscle, with the majority of underreplicated nuclei in the dorsal longitudinal muscles (DLM). Half of the DNA in the DLM nuclei stall at S phase between the unreplicated G0 and fully replicated G1. The dorsal ventral flight muscle provides the other source of underreplication, and yet, there, the replication stall point is earlier (less DNA replicated), and the endocycle is initiated. The differences in underreplication and ploidy in the indirect flight muscles provide a new tool to study heterochromatin, underreplication and endocycle control.
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Roy, S., and K. Vijay Raghavan. "Homeotic genes and the regulation of myoblast migration, fusion, and fibre-specific gene expression during adult myogenesis in Drosophila." Development 124, no. 17 (September 1, 1997): 3333–41. http://dx.doi.org/10.1242/dev.124.17.3333.
Full textAbstract:
We have investigated the roles of homeotic selector genes in the migration and fusion of myoblasts, and in the differentiation of adult muscle fibres of Drosophila. Altering intrinsic homeotic identities of myoblasts does not affect their segment-specific migration patterns. By transplanting meso - and metathoracic myoblasts into the abdomen, we demonstrate that the fusion abilities of myoblasts are independent of their segmental identities. However, transplanted thoracic myoblast nuclei are ‘entrained’ by those of the host abdominal muscles to which they fuse and are unable to ‘switch on’ a thoracic muscle-specific reporter gene. This process is likely to be mediated by homeotic repression because mis-expression of an abdominal muscle-specific homeotic gene, Ultrabithorax, in the thoracic muscles results in the repression of the thoracic muscle-specific reporter gene. Finally, we show that removal of Ultrabithorax function specifically from muscle cells of the first abdominal segment, results in the expression of thoracic muscle properties. Many of these functions of homeotic genes in muscle patterning in Drosophila could be conserved during myogenesis in other organisms.
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Anant, S., S. Roy, and K. Vijay Raghavan. "Twist and Notch negatively regulate adult muscle differentiation in Drosophila." Development 125, no. 8 (April 15, 1998): 1361–69. http://dx.doi.org/10.1242/dev.125.8.1361.
Full textAbstract:
Twist is required in Drosophila embryogenesis for mesodermal specification and cell-fate choice. We have examined the role of Twist and Notch during adult indirect flight muscle development. Reduction in levels of Twist leads to abnormal myogenesis. Notch reduction causes a similar mutant phenotype and reduces Twist levels. Conversely, persistent expression, in myoblasts, of activated Notch causes continued twist expression and failure of differentiation as assayed by myosin expression. The gain-of-function phenotype of Notch is very similar to that seen upon persistent twist expression. These results point to a relationship between Notch function and twist regulation during indirect flight muscle development and show that decline in Twist levels is a requirement for the differentiation of these muscles, unlike the somatic muscles of the embryo.
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Schaub, Christoph, Marcel Rose, and Manfred Frasch. "Yorkie and JNK revert syncytial muscles into myoblasts during Org-1–dependent lineage reprogramming." Journal of Cell Biology 218, no. 11 (October 7, 2019): 3572–82. http://dx.doi.org/10.1083/jcb.201905048.
Full textAbstract:
Lineage reprogramming has received increased research attention since it was demonstrated that lineage-restricted transcription factors can be used in vitro for direct reprogramming. Recently, we reported that the ventral longitudinal musculature of the adult Drosophila heart arises in vivo by direct lineage reprogramming from larval alary muscles, a process that starts with the dedifferentiation and fragmentation of syncytial muscle cells into mononucleate myoblasts and depends on Org-1 (Drosophila Tbx1). Here, we shed light on the events occurring downstream of Org-1 in this first step of transdifferentiation and show that alary muscle lineage-specific activation of Yorkie plays a key role in initiating the dedifferentiation and fragmentation of these muscles. An additional necessary input comes from active dJNK signaling, which contributes to the activation of Yorkie and furthermore activates dJun. The synergistic activities of the Yorkie/Scalloped and dJun/dFos transcriptional activators subsequently initiate alary muscle fragmentation as well as up-regulation of Myc and piwi, both crucial for lineage reprogramming.
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Jawkar, Saroj, and Upendra Nongthomba. "Indirect flight muscles in Drosophila melanogaster as a tractable model to study muscle development and disease." International Journal of Developmental Biology 64, no. 1-2-3 (2020): 167–73. http://dx.doi.org/10.1387/ijdb.190333un.
Full textAbstract:
Myogenesis is a complex multifactorial process leading to the formation of the adult muscle. An amalgamation of autonomous processes including myoblast fusion and myofibrillogenesis, as well as non-autonomous processes, such as innervations from neurons and precise connections with attachment sites, are responsible for successful development and function of muscles. In this review, we describe the development of the indirect flight muscles (IFMs) in Drosophila melanogaster, and highlight the use of the IFMs as a model for studying muscle development and disease, based on recent studies on the development and function of IFMs.
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Wojtas, K., N. Slepecky, L. von Kalm, and D. Sullivan. "Flight muscle function in Drosophila requires colocalization of glycolytic enzymes." Molecular Biology of the Cell 8, no. 9 (September 1997): 1665–75. http://dx.doi.org/10.1091/mbc.8.9.1665.
Full textAbstract:
Structural relationships between the myofibrillar contractile apparatus and the enzymes that generate ATP for muscle contraction are not well understood. We explored whether glycolytic enzymes are localized in Drosophila flight muscle and whether localization is required for function. We find that glycerol-3-phosphate dehydrogenase (GPDH) is localized at Z-discs and M-lines. The glycolytic enzymes aldolase and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) are also localized along the sarcomere with a periodic pattern that is indistinguishable from that of GPDH localization. Furthermore, localization of aldolase and GAPDH requires simultaneous localization of GPDH, because aldolase and GAPDH are not localized along the sarcomere in muscles of strains that carry Gpdh null alleles. In an attempt to understand the process of glycolytic enzyme colocalization, we have explored in more detail the mechanism of GPDH localization. In flight muscle, there is only one GPDH isoform, GPDH-1, which is distinguished from isoforms found in other tissues by having three C-terminal amino acids: glutamine, asparagine, and leucine. Transgenic flies that can produce only GPDH-1 display enzyme colocalization similar to wild-type flies. However, transgenic flies that synthesize only GPDH-3, lacking the C-terminal tripeptide, do not show the periodic banding pattern of localization at Z-discs and M-lines for GPDH. In addition, neither GAPDH nor aldolase colocalize at Z-discs and M-lines in the sarcomeres of muscles from GPDH-3 transgenic flies. Failure of the glycolytic enzymes to colocalize in the sarcomere results in the inability to fly, even though the full complement of active glycolytic enzymes is present in flight muscles. Therefore, the presence of active enzymes in the cell is not sufficient for muscle function; colocalization of the enzymes is required. These results indicate that the mechanisms by which ATP is supplied to the myosin ATPase, for muscle contraction, requires a highly organized cellular system.
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Rushton, E., R. Drysdale, S. M. Abmayr, A. M. Michelson, and M. Bate. "Mutations in a novel gene, myoblast city, provide evidence in support of the founder cell hypothesis for Drosophila muscle development." Development 121, no. 7 (July 1, 1995): 1979–88. http://dx.doi.org/10.1242/dev.121.7.1979.
Full textAbstract:
We have used mutations in the newly identified gene myoblast city to investigate the founder cell hypothesis of muscle development in Drosophila melanogaster. In embryos mutant for myoblast city the fusion of myoblasts into multinucleate muscles is virtually abolished. Nevertheless, a subset of the myoblasts develop specific muscle-like characteristics, including gene expression appropriate to particular muscles, migration to the appropriate part of the segment, correct position and orientation, and contact by motor neurons. We suggest that this subset of myoblasts represents the proposed muscle founder cells and we draw an analogy between these founder cells and the muscle pioneers described for grasshopper muscle development.
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Chechenova, Maria B., Sara Maes, Sandy T. Oas, Cloyce Nelson, Kaveh G. Kiani, Anton L. Bryantsev, and Richard M. Cripps. "Functional redundancy and nonredundancy between two Troponin C isoforms inDrosophilaadult muscles." Molecular Biology of the Cell 28, no. 6 (March 15, 2017): 760–70. http://dx.doi.org/10.1091/mbc.e16-07-0498.
Full textAbstract:
We investigated the functional overlap of two muscle Troponin C (TpnC) genes that are expressed in the adult fruit fly, Drosophila melanogaster: TpnC4 is predominantly expressed in the indirect flight muscles (IFMs), whereas TpnC41C is the main isoform in the tergal depressor of the trochanter muscle (TDT; jump muscle). Using CRISPR/Cas9, we created a transgenic line with a homozygous deletion of TpnC41C and compared its phenotype to a line lacking functional TpnC4. We found that the removal of either of these genes leads to expression of the other isoform in both muscle types. The switching between isoforms occurs at the transcriptional level and involves minimal enhancers located upstream of the transcription start points of each gene. Functionally, the two TpnC isoforms were not equal. Although ectopic TpnC4 in TDT muscles was able to maintain jumping ability, TpnC41C in IFMs could not effectively support flying. Simultaneous functional disruption of both TpnC genes resulted in jump-defective and flightless phenotypes of the survivors, as well as abnormal sarcomere organization. These results indicated that TpnC is required for myofibril assembly, and that there is functional specialization among TpnC isoforms in Drosophila.
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Volk, T., and K. VijayRaghavan. "A central role for epidermal segment border cells in the induction of muscle patterning in the Drosophila embryo." Development 120, no. 1 (January 1, 1994): 59–70. http://dx.doi.org/10.1242/dev.120.1.59.
Full textAbstract:
The correct patterning of muscles in the Drosophila embryo depends on the migration of developing muscles over the ectoderm and on the attachment of these muscles to specific attachment sites. We investigate the mechanisms that are involved in this process and describe experiments that allow a genetic dissection of the role of the ectoderm in muscle migration and attachment. We show that cells along the segmental border in the ectoderm are used by the developing muscles to reach their attachment sites. These segment border cells are recognized by dissociated myotubes in single suspensions in culture. Thus, developing muscles have properties that allow the specific recognition of the segment border cells and migrate to attach to these cells. The segment border cells are absent in the mutant wingless and naked. In these mutants, the muscles are severely disorganized. We show that this is not a mere consequence of disruption of the epidermis, since, in the mutant patched, where segmental patterning is affected, the segment border cells are present near their normal position; the muscles in this mutant are relatively organized. Similarly, in the mutant lines where ectopic segment border cells are present, the observed muscle derangement correlates well with the ectopic attachment sites that are present. Finally, we have analyzed mutants at the stripe locus and have shown that lethal alleles disrupt muscle organization during embryogenesis. Enhancer-trap alleles of stripe that we have analyzed show reporter gene expression in the segment border cells. Our results indicate a role for the segment border cells in guidance of migrating muscle fibers to their attachment sites.
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Chan, W. P., and M. H. Dickinson. "In vivo length oscillations of indirect flight muscles in the fruit fly Drosophila virilis." Journal of Experimental Biology 199, no. 12 (December 1, 1996): 2767–74. http://dx.doi.org/10.1242/jeb.199.12.2767.
Full textAbstract:
We have used high-speed video microscopy to measure in vivo length oscillations of the indirect flight muscles of the fruit fly Drosophila virilis during tethered flight. The changes in muscle strain were measured by tracking the deformation of the thoracic exoskeleton at the origin and insertion of both the dorsal longitudinal (DLM) and the dorsal ventral (DVM) muscles. The mean peak-to-peak strain amplitudes were found to be 3.5% for the DLMs and 3.3% for the DVMs, although the strain amplitude within individual cycles ranged from 2 to 5%. These values are consistent with the small number of previous measurements of indirect flight muscle strain in other insects, but almost an order of magnitude greater than the strain amplitudes used in most biophysical studies of skinned Drosophila fibers. The results suggest that serial compliance within this sarcomere would need to relieve approximately 70% of the total strain in order for individual crossbridges to remain attached throughout a complete contraction-extension cycle.
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Currie, D. A., and M. Bate. "Innervation is essential for the development and differentiation of a sex-specific adult muscle in Drosophila melanogaster." Development 121, no. 8 (August 1, 1995): 2549–57. http://dx.doi.org/10.1242/dev.121.8.2549.
Full textAbstract:
The adult abdominal muscles in Drosophila are generated de novo during metamorphosis and form a simple and characteristic pattern. Throughout adult abdominal development there is a close association between nerves and myoblasts. However, the role of innervation in adult myogenesis is unclear. In males there is an additional muscle, which is unique to abdominal segment 5 (A5). This male specific muscle forms from the same pool of myoblasts as other dorsal muscles in A5 but develops several distinctive characteristics. Previous work indicates the genotype of the innervation of this male specific muscle may play a crucial role in its proper development, although the part played by innervation in the development of other muscles is unknown. Here we test directly the function of innervation in adult myogenesis in general and for the development and differentiation of the male specific muscle in particular. After denervation at the onset of metamorphosis, muscle growth is impaired although the overall muscle pattern continues to develop. Uniquely, the male specific muscle fails to form. Our results indicate that there is an essential role for innervation during the period of metamorphosis for the formation of a full complement of abdominal muscles and for muscle growth. Furthermore, innervation is absolutely required for the formation of the male specific muscle and the development of its special characteristics.
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Gong, Henry, Weikang Ma, Shaoshuai Chen, Geng Wang, Ramzi Khairallah, and Thomas Irving. "Localization of the Elastic Proteins in the Flight Muscle of Manduca sexta." International Journal of Molecular Sciences 21, no. 15 (July 31, 2020): 5504. http://dx.doi.org/10.3390/ijms21155504.
Full textAbstract:
The flight muscle of Manduca sexta (DLM1) is an emerging model system for biophysical studies of muscle contraction. Unlike the well-studied indirect flight muscle of Lethocerus and Drosophila, the DLM1 of Manduca is a synchronous muscle, as are the vertebrate cardiac and skeletal muscles. Very little has been published regarding the ultrastructure and protein composition of this muscle. Previous studies have demonstrated that DLM1 express two projectin isoform, two kettin isoforms, and two large Salimus (Sls) isoforms. Such large Sls isoforms have not been observed in the asynchronous flight muscles of Lethocerus and Drosophila. The spatial localization of these proteins was unknown. Here, immuno-localization was used to show that the N-termini of projectin and Salimus are inserted into the Z-band. Projectin spans across the I-band, and the C-terminus is attached to the thick filament in the A-band. The C-terminus of Sls was also located in the A-band. Using confocal microscopy and experimental force-length curves, thin filament lengths were estimated as ~1.5 µm and thick filament lengths were measured as ~2.5 µm. This structural information may help provide an interpretive framework for future studies using this muscle system.
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Roy, Sudipto, and K. VijayRaghavan. "Patterning Muscles Using Organizers: Larval Muscle Templates and Adult Myoblasts Actively Interact to Pattern the Dorsal Longitudinal Flight Muscles of Drosophila." Journal of Cell Biology 141, no. 5 (June 1, 1998): 1135–45. http://dx.doi.org/10.1083/jcb.141.5.1135.
Full textAbstract:
Pattern formation in muscle development is often mediated by special cells called muscle organizers. During metamorphosis in Drosophila, a set of larval muscles function as organizers and provide scaffolding for the development of the dorsal longitudinal flight muscles. These organizers undergo defined morphological changes and dramatically split into templates as adult fibers differentiate during pupation. We have investigated the cellular mechanisms involved in the use of larval fibers as templates. Using molecular markers that label myoblasts and the larval muscles themselves, we show that splitting of the larval muscles is concomitant with invasion by imaginal myoblasts and the onset of differentiation. We show that the Erect wing protein, an early marker of muscle differentiation, is not only expressed in myoblasts just before and after fusion, but also in remnant larval nuclei during muscle differentiation. We also show that interaction between imaginal myoblasts and larval muscles is necessary for transformation of the larval fibers. In the absence of imaginal myoblasts, the earliest steps in metamorphosis, such as the escape of larval muscles from histolysis and changes in their innervation, are normal. However, subsequent events, such as the splitting of these muscles, fail to progress. Finally, we show that in a mutant combination, null for Erect wing function in the mesoderm, the splitting of the larval muscles is aborted. These studies provide a genetic and molecular handle for the understanding of mechanisms underlying the use of muscle organizers in muscle patterning. Since the use of such organizers is a common theme in myogenesis in several organisms, it is likely that many of the processes that we describe are conserved.
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Loya, Amy K., Sarah K. Van Houten, Bernadette M. Glasheen, and Douglas M. Swank. "Shortening deactivation: quantifying a critical component of cyclical muscle contraction." American Journal of Physiology-Cell Physiology 322, no. 4 (April 1, 2022): C653—C665. http://dx.doi.org/10.1152/ajpcell.00281.2021.
Full textAbstract:
A muscle undergoing cyclical contractions requires fast and efficient muscle activation and relaxation to generate high power with relatively low energetic cost. To enhance activation and increase force levels during shortening, some muscle types have evolved stretch activation (SA), a delayed increased in force following rapid muscle lengthening. SA’s complementary phenomenon is shortening deactivation (SD), a delayed decrease in force following muscle shortening. SD increases muscle relaxation, which decreases resistance to subsequent muscle lengthening. Although it might be just as important to cyclical power output, SD has received less investigation than SA. To enable mechanistic investigations into SD and quantitatively compare it to SA, we developed a protocol to elicit SA and SD from Drosophila and Lethocerus indirect flight muscles (IFM) and Drosophila jump muscle. When normalized to isometric tension, Drosophila IFM exhibited a 118% SD tension decrease, Lethocerus IFM dropped by 97%, and Drosophila jump muscle decreased by 37%. The same order was found for normalized SA tension: Drosophila IFM increased by 233%, Lethocerus IFM by 76%, and Drosophila jump muscle by only 11%. SD occurred slightly earlier than SA, relative to the respective length change, for both IFMs; but SD was exceedingly earlier than SA for jump muscle. Our results suggest SA and SD evolved to enable highly efficient IFM cyclical power generation and may be caused by the same mechanism. However, jump muscle SA and SD mechanisms are likely different, and may have evolved for a role other than to increase the power output of cyclical contractions.
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Lawrence, Peter A., and Paul Johnston. "Observations on cell lineage of internal organs of Drosophila." Development 91, no. 1 (February 1, 1986): 251–66. http://dx.doi.org/10.1242/dev.91.1.251.
Full textAbstract:
Adult Drosophila mosaics can be used to study cell lineage and to map relative positions of primordia at the blastoderm stage. This information can define which germ layer an organ comes from and can help build models of genetic regulation of development. Here we use the sdh cell marker to map internal organs in mosaics made by nuclear transplantation. We confirm that oenocytes arise from the same progenitors as the adult epidermis, but that muscles and fat body have a separate (mesodermal) origin and that the precursors of epidermis and central neurones are closely intermingled in the ventral, but not dorsal, epidermis. We find that the malpighian tubules are more closely related to the hindgut than the midgut and are therefore ectodermal in origin. We find that each intersegmental muscle in the thorax arises from one specific parasegment in the embryo, but that very small numbers of myoblasts wander and contribute to muscles of inappropriate segments. We present evidence indicating that the visceral muscles of the midgut have a widely dispersed origin (over much of the embryo) while the somatic mesoderm of the female gonad comes from a small number of abdominal segments. The visceral mesoderm of the hindgut develops from a localized posterior region of the embryo.
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Armand, P., A. C. Knapp, A. J. Hirsch, E. F. Wieschaus, and M. D. Cole. "A novel basic helix-loop-helix protein is expressed in muscle attachment sites of the Drosophila epidermis." Molecular and Cellular Biology 14, no. 6 (June 1994): 4145–54. http://dx.doi.org/10.1128/mcb.14.6.4145-4154.1994.
Full textAbstract:
We have found that a novel basic helix-loop-helix (bHLH) protein is expressed almost exclusively in the epidermal attachments sites for the somatic muscles of Drosophila melanogaster. A Drosophila cDNA library was screened with radioactively labeled E12 protein, which can dimerize with many HLH proteins. One clone that emerged from this screen encoded a previously unknown protein of 360 amino acids, named delilah, that contains both basic and HLH domains, similar to a group of cellular transcription factors implicated in cell type determination. Delilah protein formed heterodimers with E12 that bind to the muscle creatine kinase promoter. In situ hybridization with the delilah cDNA localized the expression of the gene to a subset of cells in the epidermis which form a distinct pattern involving both the segmental boundaries and intrasegmental clusters. This pattern was coincident with the known sites of attachment of the somatic muscles to tendon cells in the epidermis. delilah expression persists in snail mutant embryos which lack mesoderm, indicating that expression of the gene was not induced by attachment of the underlying muscles. The similarity of this gene to other bHLH genes suggests that it plays an important role in the differentiation of epidermal cells into muscle attachment sites.
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Armand, P., A. C. Knapp, A. J. Hirsch, E. F. Wieschaus, and M. D. Cole. "A novel basic helix-loop-helix protein is expressed in muscle attachment sites of the Drosophila epidermis." Molecular and Cellular Biology 14, no. 6 (June 1994): 4145–54. http://dx.doi.org/10.1128/mcb.14.6.4145.
Full textAbstract:
We have found that a novel basic helix-loop-helix (bHLH) protein is expressed almost exclusively in the epidermal attachments sites for the somatic muscles of Drosophila melanogaster. A Drosophila cDNA library was screened with radioactively labeled E12 protein, which can dimerize with many HLH proteins. One clone that emerged from this screen encoded a previously unknown protein of 360 amino acids, named delilah, that contains both basic and HLH domains, similar to a group of cellular transcription factors implicated in cell type determination. Delilah protein formed heterodimers with E12 that bind to the muscle creatine kinase promoter. In situ hybridization with the delilah cDNA localized the expression of the gene to a subset of cells in the epidermis which form a distinct pattern involving both the segmental boundaries and intrasegmental clusters. This pattern was coincident with the known sites of attachment of the somatic muscles to tendon cells in the epidermis. delilah expression persists in snail mutant embryos which lack mesoderm, indicating that expression of the gene was not induced by attachment of the underlying muscles. The similarity of this gene to other bHLH genes suggests that it plays an important role in the differentiation of epidermal cells into muscle attachment sites.
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Martin-Bermudo, M. D., and N. H. Brown. "The localized assembly of extracellular matrix integrin ligands requires cell-cell contact." Journal of Cell Science 113, no. 21 (November 1, 2000): 3715–23. http://dx.doi.org/10.1242/jcs.113.21.3715.
Full textAbstract:
The assembly of an organism requires the interaction between different layers of cells, in many cases via an extracellular matrix. In the developing Drosophila larva, muscles attach in an integrin-dependent manner to the epidermis, via a specialized extracellular matrix called tendon matrix. Tiggrin, a tendon matrix integrin ligand, is primarily synthesized by cells distant to the muscle attachment sites, yet it accumulates specifically at these sites. Previous work has shown that the PS integrins are not required for tiggrin localization, suggesting that there is redundancy among tiggrin receptors. We have examined this by testing whether the PS2 integrin can recruit tiggrin to ectopic locations within the Drosophila embryo. We found that neither the wild type nor modified forms of the PS2 integrin, which have higher affinity for tiggrin, can recruit tiggrin to new cellular contexts. Next, we genetically manipulated the fate of the muscles and the epidermal muscle attachment cells, which demonstrated that muscles have the primary role in recruiting tiggrin to the tendon matrix and that cell-cell contact is necessary for this recruitment. Thus we propose that the inherent polarity of the muscle cells leads to a molecular specialization of their ends, and interactions between the ends produces an integrin-independent tiggrin receptor. Thus, interaction between cells generates an extracellular environment capable of nucleating extracellular matrix assembly.