scholarly journals A distinct set of founders and fusion-competent myoblasts make visceral muscles in the Drosophila embryo

Development ◽  
2001 ◽  
Vol 128 (17) ◽  
pp. 3331-3338 ◽  
Author(s):  
Beatriz San Martin ◽  
Mar Ruiz-Gómez ◽  
Matthias Landgraf ◽  
Michael Bate
Keyword(s):  
Myoblast Fusion ◽  
Drosophila Embryo ◽  
Visceral Muscle ◽  
Visceral Muscles ◽  
Fusion Competent Myoblasts ◽  
Longitudinal Muscles ◽  
Two Populations ◽  
Somatic Muscles

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.

Control of cell fates and segmentation in the Drosophila mesoderm

Development ◽  
1997 ◽  
Vol 124 (15) ◽  
pp. 2915-2922 ◽  
Author(s):  
V. Riechmann ◽  
U. Irion ◽  
R. Wilson ◽  
R. Grosskortenhaus ◽  
M. Leptin
Keyword(s):  
Fat Body ◽  
Cell Fates ◽  
Somatic Muscle ◽  
Visceral Muscle ◽  
Twist Expression ◽  
Visceral Muscles ◽  
Somatic Muscles

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.

Anterior-posterior subdivision and the diversification of the mesoderm in Drosophila

Development ◽  
1995 ◽  
Vol 121 (12) ◽  
pp. 4183-4193 ◽  
Author(s):  
O.M. Borkowski ◽  
N.H. Brown ◽  
M. Bate
Keyword(s):  
Progenitor Cell ◽  
Essential Element ◽  
Surface Protein ◽  
Drosophila Embryo ◽  
Visceral Mesoderm ◽  
Internal Cell ◽  
Visceral Muscles ◽  
Low Levels ◽  
Anterior Posterior ◽  
Somatic Muscles

We have used a novel cell marker, in which the twist promoter directs the synthesis of the cell surface protein CD2 (twi-CD2) to examine the development of the mesoderm in the Drosophila embryo after gastrulation and to locate the progenitor cell populations for different mesodermal derivatives. We find that the early mesoderm in each segment is divided into a more anterior region with relatively low levels of twist and twi-CD2 expression and a more posterior region where twist and twi-CD2 expression are high. This subdivision coincides with regional assignments of cells to form different progenitors: dorsal anterior cells invaginate to form an internal layer from which the visceral mesoderm is derived. Ventral anterior cells form progenitors of mesodermal glial cells. Dorsal posterior cells form heart. Ventral and dorsal posterior cells form somatic muscles. We conclude that the metamerically repeated anterior-posterior subdivision of the mesoderm is an essential element in laying out the pattern of mesodermal progenitor cells and in distinguishing between an internal cell layer which will give rise to the progenitors of visceral muscles and an external layer which will generate the somatic muscles and the heart.

The genetic control of the distinction between fat body and gonadal mesoderm in Drosophila

Development ◽  
1998 ◽  
Vol 125 (4) ◽  
pp. 713-723 ◽  
Author(s):  
V. Riechmann ◽  
K.P. Rehorn ◽  
R. Reuter ◽  
M. Leptin
Keyword(s):  
Genetic Control ◽  
Early Development ◽  
Fat Body ◽  
Homeotic Gene ◽  
Dorsoventral Patterning ◽  
Genetic Pathways ◽  
The Third ◽  
Body Development ◽  
Visceral Muscles ◽  
Somatic Muscles

The somatic muscles, the heart, the fat body, the somatic part of the gonad and most of the visceral muscles are derived from a series of segmentally repeated primordia in the Drosophila mesoderm. This work describes the early development of the fat body and its relationship to the gonadal mesoderm, as well as the genetic control of the development of these tissues. Segmentation and dorsoventral patterning genes define three regions in each parasegment in which fat body precursors can develop. Fat body progenitors in these regions are specified by different genetic pathways. Two regions require engrailed and hedgehog for their development while the third is controlled by wingless. decapentaplegic and one or more unknown genes determine the dorsoventral extent of these regions. In each of parasegments 10–12 one of these regions generates somatic gonadal precursors instead of fat body. The balance between fat body and somatic gonadal fate in these serially homologous cell clusters is controlled by at least five genes. We suggest a model in which tinman, engrailed and wingless are necessary to permit somatic gonadal develoment, while serpent counteracts the effects of these genes and promotes fat body development. The homeotic gene abdominalA limits the region of serpent activity by interfering in a mutually repressive feed back loop between gonadal and fat body development.

The gene tinman is required for specification of the heart and visceral muscles in Drosophila

Development ◽  
1993 ◽  
Vol 118 (3) ◽  
pp. 719-729 ◽  
Author(s):  
R. Bodmer
Keyword(s):  
Heart Development ◽  
Body Wall ◽  
Heart Cells ◽  
Visceral Muscle ◽  
Visceral Mesoderm ◽  
Body Wall Muscles ◽  
Visceral Muscles

The homeobox-containing gene tinman (msh-2, Bodmer et al., 1990 Development 110, 661–669) is expressed in the mesoderm primordium, and this expression requires the function of the mesoderm determinant twist. Later in development, as the first mesodermal subdivisions are occurring, expression becomes limited to the visceral mesoderm and the heart. Here, I show that the function of tinman is required for visceral muscle and heart development. Embryos that are mutant for the tinman gene lack the appearance of visceral mesoderm and of heart primordia, and the fusion of the anterior and posterior endoderm is impaired. Even though tinman mutant embryos do not have a heart or visceral muscles, many of the somatic body wall muscles appear to develop although abnormally. When the tinman cDNA is ubiquitously expressed in tinman mutant embryos, via a heatshock promoter, formation of heart cells and visceral mesoderm is partially restored, tinman seems to be one of the earliest genes required for heart development and the first gene reported for which a crucial function in the early mesodermal subdivisions has been implicated.

scholarly journals Intracellular signals direct integrin localization to sites of function in embryonic muscles.

1996 ◽  
Vol 134 (1) ◽  
pp. 217-226 ◽  
Author(s):  
M D Martin-Bermudo ◽  
N H Brown
Keyword(s):  
Subcellular Localization ◽  
Transmembrane Protein ◽  
Drosophila Embryo ◽  
Cellular Polarity ◽  
Intracellular Signals ◽  
Tendon Cells ◽  
Segment Polarity ◽  
Set Up ◽  
Longitudinal Muscles

In the Drosophila embryo, the alphaPS2betaPS integrin heterodimer is localized tightly at the termini of the multinucleate muscles where they attach to the alphaPS1betaPS-containing epidermal tendon cells. Here we examine the basis for alphaPS2betaPS integrin subcellular localization. We show that the betaPS cytoplasmic tail is sufficient to direct the localization of a heterologous transmembrane protein, CD2, to the muscle termini in vivo. This localization does not occur via an association with structures set up by the endogenous betaPS integrins, since it can occur even in the absence of the betaPS protein. Furthermore, the subcellular localization of the alphaPS2betaPS integrin is not dependent on any other interactions between the muscles and the tendon cells. In embryos that lack the segmental tendon cells, due to a mutation removing the related segment polarity genes engrailed and invected, alphaPS2betaPS is still localized to the muscle termini even though the ventral longitudinal muscles are not attached to the epidermis, but instead are attached end to end. Thus the alphaPS2betaPS integrin can be localized by an intracellular mechanism within the muscles. Our results challenge the view that the transmission of signals from the extracellular environment via integrins is required for the organization of the cytoskeleton and the resultant cellular polarity.

Blown fuse regulates stretching and outgrowth but not myoblast fusion of the circular visceral muscles in Drosophila

2006 ◽  
Vol 74 (9-10) ◽  
pp. 608-621 ◽  
Author(s):  
Roxane H. Schröter ◽  
Detlev Buttgereit ◽  
Lothar Beck ◽  
Anne Holz ◽  
Renate Renkawitz-Pohl
Keyword(s):  
Myoblast Fusion ◽  
Visceral Muscles

scholarly journals The control of chick myoblast fusion by ion channels operated by prostaglandins and acetylcholine.

1988 ◽  
Vol 106 (5) ◽  
pp. 1693-1702 ◽  
Author(s):  
A Entwistle ◽  
R J Zalin ◽  
S Bevan ◽  
A E Warner
Keyword(s):  
Acetylcholine Receptor ◽  
Myoblast Fusion ◽  
Chloride Ions ◽  
Calcium Flux ◽  
Extracellular Potassium ◽  
Ca Channel ◽  
High Potassium ◽  
Calcium Permeability ◽  
Fusion Competent Myoblasts ◽  
Alpha Bungarotoxin

Chick myoblast fusion in culture was investigated using prostanoid synthesis inhibitors to delay spontaneous fusion. During this delay myoblast fusion could be induced by prostaglandin E1 (PGE1), by raising extracellular potassium and by addition of carbachol. Carbachol-induced fusion, but not PGE-induced fusion, was prevented by the acetylcholine receptor blocker alpha-bungarotoxin. Fusion induced by any of these agents was prevented by the Ca channel blockers lanthanum and D600. The threshold for potassium-induced fusion was 7-8 mM; maximal fusion occurred at 16-20 mM. Low extracellular potassium inhibited spontaneous fusion. Intracellular potassium in fusion competent myoblasts was 101 m-moles/l cell. Calcium flux measurements demonstrated that high potassium increased calcium permeability in fusion-competent myoblasts. A 30-s exposure to high potassium or PGE1 was sufficient to initiate myoblast fusion. Anion-exchange inhibitors (SITS and DIDS) delayed spontaneous myoblast fusion and blocked fusion induced by PGE1 but not carbachol. Blocking the acetylcholine receptor shifted the dose-response relation for PGE-induced fusion to higher concentrations. PGE1-induced fusion required chloride ions; carbachol-induced fusion required sodium ions. Provided calcium channels were available, potassium always induced fusion. We conclude that myoblasts possess at least three, independent pathways, each of which can initiate myoblast fusion and that the PGE-activated pathway and the acetylcholine receptor-activated pathway act synergistically. We suggest that fusion competent myoblasts have a high resting membrane potential and that fusion is controlled by depolarization initiated directly (potassium), by an increase in permeability to chloride ions (PGE), or by activation of the acetylcholine receptor (carbachol); depolarization triggers a rise in calcium permeability. The consequent increase in intracellular calcium initiates myoblast fusion.

scholarly journals Drosophila mind bomb2 is required for maintaining muscle integrity and survival

2007 ◽  
Vol 179 (2) ◽  
pp. 219-227 ◽  
Author(s):  
Hanh T. Nguyen ◽  
Francesca Voza ◽  
Nader Ezzeddine ◽  
Manfred Frasch
Keyword(s):  
Muscle Development ◽  
Ubiquitin Ligases ◽  
Significant Degree ◽  
Mutant Phenotype ◽  
E3 Ubiquitin Ligases ◽  
Visceral Muscle ◽  
Apoptosis Markers ◽  
Somatic Muscles

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.

scholarly journals Asymmetric Mbc, active Rac1 and F-actin foci in the fusion-competent myoblasts during myoblast fusion in Drosophila

Development ◽  
2011 ◽  
Vol 138 (8) ◽  
pp. 1551-1562 ◽  
Author(s):  
S. Haralalka ◽  
C. Shelton ◽  
H. N. Cartwright ◽  
E. Katzfey ◽  
E. Janzen ◽  
...  
Keyword(s):  
Myoblast Fusion ◽  
Fusion Competent Myoblasts
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