Twist and Notch negatively regulate adult muscle differentiation in Drosophila

Development ◽  
1998 ◽  
Vol 125 (8) ◽  
pp. 1361-1369 ◽  
Author(s):  
S. Anant ◽  
S. Roy ◽  
K. Vijay Raghavan
Keyword(s):  
Cell Fate ◽  
Muscle Development ◽  
Flight Muscle ◽  
Mutant Phenotype ◽  
Indirect Flight Muscle ◽  
Adult Muscle ◽  
Drosophila Embryogenesis ◽  
Twist Expression ◽  
Somatic Muscles

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.

scholarly journals Muscle Organizers inDrosophila:The Role of Persistent Larval Fibers in Adult Flight Muscle Development

1996 ◽  
Vol 176 (2) ◽  
pp. 220-229 ◽  
Author(s):  
Elizabeth R. Farrell ◽  
Joyce Fernandes ◽  
Haig Keshishian
Keyword(s):  
Muscle Development ◽  
Flight Muscle

scholarly journals Epigenetic Regulation of Myogenesis: Focus on the Histone Variants

2021 ◽  
Vol 22 (23) ◽  
pp. 12727
Author(s):  
Joana Esteves de Lima ◽  
Frédéric Relaix
Keyword(s):  
Gene Expression ◽  
Cell Fate ◽  
Epigenetic Regulation ◽  
Muscle Development ◽  
Regulation Of Gene Expression ◽  
Histone Variants ◽  
Myoblast Differentiation ◽  
Post Translational Modifications ◽  
Differentiation Status

Skeletal muscle development and regeneration rely on the successive activation of specific transcription factors that engage cellular fate, promote commitment, and drive differentiation. Emerging evidence demonstrates that epigenetic regulation of gene expression is crucial for the maintenance of the cell differentiation status upon division and, therefore, to preserve a specific cellular identity. This depends in part on the regulation of chromatin structure and its level of condensation. Chromatin architecture undergoes remodeling through changes in nucleosome composition, such as alterations in histone post-translational modifications or exchange in the type of histone variants. The mechanisms that link histone post-translational modifications and transcriptional regulation have been extensively evaluated in the context of cell fate and differentiation, whereas histone variants have attracted less attention in the field. In this review, we discuss the studies that have provided insights into the role of histone variants in the regulation of myogenic gene expression, myoblast differentiation, and maintenance of muscle cell identity.

RyR1-mediated moderate endoplasmic reticulum stress is required for myogenic differentiation of myoblasts

2021 ◽  
Author(s):  
Kai Qiu ◽  
Yubo Wang ◽  
Doudou Xu ◽  
Linjuan He ◽  
Xin Zhang ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Cell Fate ◽  
Muscle Development ◽  
Myogenic Differentiation ◽  
C2c12 Cells ◽  
Stress Signaling ◽  
Congenital Myopathies ◽  
Myotube Formation

Abstract BackgroundCytosolic Ca2+ plays vital roles in myogenesis and muscle development. Key mutations of ryanodine receptor 1 (RyR1), a major Ca2+ release channel of endoplasmic reticulum (ER), are main causes of severe congenital myopathies. The role of RyR1 in myogenic differentiation has attracted intense research interest, however, it remains unclear. MethodsThis study employed RyR1-knockdown myoblasts and CRISPR/Cas9-based RyR1-knockout myoblasts cells to explore the role of RyR1 in myogenic differentiation, myotube formation as well as the potential mechanism of RyR1-related myopathies.ResultsCytoplasmic Ca2+ concentration was significantly elevated during myogenic differentiation of both primary myogenic cells and myoblasts C2C12 cells, accompanied with a dramatic increase in RyR1 expression and resultant ER stress. Inhibition of RyR1 by siRNA-mediated silence or chemical inhibitor, dantrolene, significantly reduced cytosolic Ca2+, alleviated ER stress, and blocked multinucleated myotube formation. Moderate activation of ER stress effectively relieved myogenic differentiation stagnation induced by RyR1 suppression and demonstrated that RyR1 modulates myogenic differentiation via activation of Ca2+ -induced ER stress signaling. RyR1 knockout-induced Ca2+ leakage led to severe ER stress and excessive unfolded protein response, and drove cell fate from differentiation into apoptosis. ConclusionsTherefore, we concluded that dramatic increase in RyR1 expression is required for myogenic differentiation, and RyR1-mediated Ca2+ release leading to the activation of ER stress signaling serves a double-edged sword role during myogenic differentiation. This study contributes to a novel understanding of the role of RyR1 in muscle development and related congenital myopathies, and provides a potential target for regulation of muscle regeneration and tissue engineering.

The development of indirect flight muscle innervation in Drosophila melanogaster

Development ◽  
1993 ◽  
Vol 118 (1) ◽  
pp. 215-227 ◽  
Author(s):  
J. Fernandes ◽  
K. VijayRaghavan
Keyword(s):  
Muscle Development ◽  
Flight Muscle ◽  
Neuromuscular Junctions ◽  
Indirect Flight Muscle ◽  
Larval Life ◽  
Spatial And Temporal Patterns ◽  
Muscle Innervation ◽  
Flight Muscles ◽  
Nerve Muscle ◽  
Longitudinal Muscles

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.

scholarly journals Roles of the troponin isoforms during indirect flight muscle development in Drosophila

2014 ◽  
Vol 93 (2) ◽  
pp. 379-388 ◽  
Author(s):  
SALAM HEROJEET SINGH ◽  
PRABODH KUMAR ◽  
NALLUR B. RAMACHANDRA ◽  
UPENDRA NONGTHOMBA
Keyword(s):  
Muscle Development ◽  
Flight Muscle ◽  
Indirect Flight Muscle

The structural role of high molecular weight tropomyosins in dipteran indirect flight muscle and the effect of phosphorylation

2006 ◽  
Vol 27 (3-4) ◽  
pp. 189-201 ◽  
Author(s):  
JESÚS MATEOS ◽  
RAÚL HERRANZ ◽  
ALBERTO DOMINGO ◽  
JOHN SPARROW ◽  
ROBERTO MARCO
Keyword(s):  
Molecular Weight ◽  
High Molecular Weight ◽  
Flight Muscle ◽  
Indirect Flight Muscle ◽  
Structural Role

Dual role of delta-like 1 homolog (DLK1) in skeletal muscle development and adult muscle regeneration

Development ◽  
2013 ◽  
Vol 140 (18) ◽  
pp. 3743-3753 ◽  
Author(s):  
D. C. Andersen ◽  
J. Laborda ◽  
V. Baladron ◽  
M. Kassem ◽  
S. P. Sheikh ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Regeneration ◽  
Muscle Development ◽  
Dual Role ◽  
Skeletal Muscle Development ◽  
Adult Muscle

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 Thin filaments elongate from their pointed ends during myofibril assembly in Drosophila indirect flight muscle

2001 ◽  
Vol 155 (6) ◽  
pp. 1043-1054 ◽  
Author(s):  
Michelle Mardahl-Dumesnil ◽  
Velia M. Fowler
Keyword(s):  
Thin Filament ◽  
Muscle Development ◽  
Striated Muscle ◽  
Flight Muscle ◽  
De Novo ◽  
Indirect Flight Muscle ◽  
Actin Dynamics ◽  
Thin Filaments ◽  
End Capping ◽  
Pointed End

Tropomodulin (Tmod) is an actin pointed-end capping protein that regulates actin dynamics at thin filament pointed ends in striated muscle. Although pointed-end capping by Tmod controls thin filament lengths in assembled myofibrils, its role in length specification during de novo myofibril assembly is not established. We used the Drosophila Tmod homologue, sanpodo (spdo), to investigate Tmod's function during muscle development in the indirect flight muscle. SPDO was associated with the pointed ends of elongating thin filaments throughout myofibril assembly. Transient overexpression of SPDO during myofibril assembly irreversibly arrested elongation of preexisting thin filaments. However, the lengths of thin filaments assembled after SPDO levels had declined were normal. Flies with a preponderance of abnormally short thin filaments were unable to fly. We conclude that: (a) thin filaments elongate from their pointed ends during myofibril assembly; (b) pointed ends are dynamically capped at endogenous levels of SPDO so as to allow elongation; (c) a transient increase in SPDO levels during myofibril assembly converts SPDO from a dynamic to a permanent cap; and (d) developmental regulation of pointed-end capping during myofibril assembly is crucial for specification of final thin filament lengths, myofibril structure, and muscle function.

scholarly journals Correction to: Roles of the troponin isoforms during indirect flight muscle development in Drosophila

2019 ◽  
Vol 98 (5) ◽  
Author(s):  
Salam Herojeet Singh ◽  
Prabodh Kumar ◽  
Nallur B. Ramachandra ◽  
Upendra Nongthomba
Keyword(s):  
Muscle Development ◽  
Flight Muscle ◽  
Indirect Flight Muscle
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