Splicing transitions of the anchoring protein ENH during striated muscle development

2012 ◽  
Vol 421 (2) ◽  
pp. 232-238 ◽  
Author(s):  
Jumpei Ito ◽  
Taiki Hashimoto ◽  
Sho Nakamura ◽  
Yusuke Aita ◽  
Tomoko Yamazaki ◽  
...  
Animals ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 1443
Author(s):  
Susana A. Teixeira ◽  
Daniele B. D. Marques ◽  
Thaís C. Costa ◽  
Haniel C. Oliveira ◽  
Karine A. Costa ◽  
...  

Since pre- and postnatal development are programmed during early prenatal life, studies addressing the complete transcriptional landscape during organogenesis are needed. Therefore, we aimed to disentangle differentially expressed (DE) genes between fetuses (at 35 days old) and embryos (at 25 days old) through RNA-sequencing analysis using the pig as model. In total, 1705 genes were DE, including the top DE IBSP, COL6A6, HBE1, HBZ, HBB, and NEUROD6 genes, which are associated with developmental transition from embryos to fetuses, such as ossification, skeletal muscle development, extracellular matrix organization, cardiovascular system, erythrocyte differentiation, and neuronal system. In pathway analysis, embryonic development highlighted those mainly related to morphogenic signaling and cell interactions, which are crucial for transcriptional control during the establishment of the main organs in early prenatal development, while pathways related to myogenesis, neuronal development, and cardiac and striated muscle contraction were enriched for fetal development, according to the greater complexity of organs and body structures at this developmental stage. Our findings provide an exploratory and informative transcriptional landscape of pig organogenesis, which might contribute to further studies addressing specific developmental events in pigs and in other mammals.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Osvaldo Contreras ◽  
Fabio M. V. Rossi ◽  
Marine Theret

AbstractStriated muscle is a highly plastic and regenerative organ that regulates body movement, temperature, and metabolism—all the functions needed for an individual’s health and well-being. The muscle connective tissue’s main components are the extracellular matrix and its resident stromal cells, which continuously reshape it in embryonic development, homeostasis, and regeneration. Fibro-adipogenic progenitors are enigmatic and transformative muscle-resident interstitial cells with mesenchymal stem/stromal cell properties. They act as cellular sentinels and physiological hubs for adult muscle homeostasis and regeneration by shaping the microenvironment by secreting a complex cocktail of extracellular matrix components, diffusible cytokines, ligands, and immune-modulatory factors. Fibro-adipogenic progenitors are the lineage precursors of specialized cells, including activated fibroblasts, adipocytes, and osteogenic cells after injury. Here, we discuss current research gaps, potential druggable developments, and outstanding questions about fibro-adipogenic progenitor origins, potency, and heterogeneity. Finally, we took advantage of recent advances in single-cell technologies combined with lineage tracing to unify the diversity of stromal fibro-adipogenic progenitors. Thus, this compelling review provides new cellular and molecular insights in comprehending the origins, definitions, markers, fate, and plasticity of murine and human fibro-adipogenic progenitors in muscle development, homeostasis, regeneration, and repair.


Development ◽  
1997 ◽  
Vol 124 (11) ◽  
pp. 2179-2189 ◽  
Author(s):  
M. Krause ◽  
M. Park ◽  
J.M. Zhang ◽  
J. Yuan ◽  
B. Harfe ◽  
...  

The E proteins of mammals, and the related Daughterless (DA) protein of Drosophila, are ubiquitously expressed helix-loop-helix (HLH) transcription factors that play a role in many developmental processes. We report here the characterization of a related C. elegans protein, CeE/DA, which has a dynamic and restricted distribution during development. CeE/DA is present embryonically in neuronal precursors, some of which are marked by promoter activity of a newly described Achaete-scute-like gene hlh-3. In contrast, we have been unable to detect CeE/DA in CeMyoD-positive striated muscle cells. In vitro gel mobility shift analysis detects dimerization of CeE/DA with HLH-3 while efficient interaction of CeE/DA with CeMyoD is not seen. These studies suggest multiple roles for CeE/DA in C. elegans development and provide evidence that both common and alternative strategies have evolved for the use of related HLH proteins in controlling cell fates in different species.


Development ◽  
2000 ◽  
Vol 127 (10) ◽  
pp. 2041-2051 ◽  
Author(s):  
A.K. Corsi ◽  
S.A. Kostas ◽  
A. Fire ◽  
M. Krause

The basic helix-loop-helix (bHLH) transcription factor Twist plays a role in mesodermal development in both invertebrates and vertebrates. In an effort to understand the role of the unique Caenorhabditis elegans Twist homolog, hlh-8, we analyzed mesodermal development in animals with a deletion in the hlh-8 locus. This deletion was predicted to represent a null allele because the HLH domain is missing and the reading frame for the protein is disrupted. Animals lacking CeTwist function were constipated and egg-laying defective. Both of these defects were rescued in transgenic mutant animals expressing wild-type hlh-8. Observing a series of mesoderm-specific markers allowed us to characterize the loss of hlh-8 function more thoroughly. Our results demonstrate that CeTwist performs an essential role in the proper development of a subset of mesodermal tissues in C. elegans. We found that CeTwist was required for the formation of three out of the four non-striated enteric muscles born in the embryo. In contrast, CeTwist was not required for the formation of the embryonically derived striated muscles. Most of the post-embryonic mesoderm develops from a single lineage. CeTwist was necessary for appropriate patterning in this lineage and was required for expression of two downstream target genes, but was not required for the expression of myosin, a marker of differentiation. Our results suggest that mesodermal patterning by Twist is an evolutionarily conserved function.


1989 ◽  
Vol 108 (6) ◽  
pp. 2459-2466 ◽  
Author(s):  
J Joseph-Silverstein ◽  
S A Consigli ◽  
K M Lyser ◽  
C Ver Pault

The identification of acidic and basic fibroblast growth factors (FGFs) in a number of embryonic tissue extracts has implicated these growth factors in the regulation of a variety of embryonic events including angiogenesis, eye development, and muscle differentiation. Lack of information concerning the cellular distribution of the growth factor within these tissues has made it extremely difficult to assign developmental roles to FGF. We have localized bFGF in the developing chick embryo using immunohistochemical techniques and our monospecific polyclonal rabbit anti-human bFGF IgG. The spatial pattern for bFGF localization was highly specific. The anti-human bFGF antibodies recognized striated muscle cells and their precursors in 2-6-d chick embryos. Myocardium, somite myotome, and limb bud muscle all stain positively for bFGF. In addition, the anti-human bFGF antibodies localized specifically to the cell, rather than to the extracellular matrix or nucleus of myotubes. The localization of bFGF demonstrated here provides further support for the hypothesis (Clegg et al., 1987; Seed et al., 1988) that this growth factor is involved in muscle development.


2008 ◽  
Vol 294 (5) ◽  
pp. C1175-C1182 ◽  
Author(s):  
Jianlin Zhang ◽  
Marie-Louise Bang ◽  
David S. Gokhin ◽  
Yingchun Lu ◽  
Li Cui ◽  
...  

Syncoilin is a striated muscle-specific intermediate filament-like protein, which is part of the dystrophin-associated protein complex (DPC) at the sarcolemma and provides a link between the extracellular matrix and the cytoskeleton through its interaction with α-dystrobrevin and desmin. Its upregulation in various neuromuscular diseases suggests that syncoilin may play a role in human myopathies. To study the functional role of syncoilin in cardiac and skeletal muscle in vivo, we generated syncoilin-deficient ( syncoilin−/−) mice. Our detailed analysis of these mice up to 2 yr of age revealed that syncoilin is entirely dispensable for cardiac and skeletal muscle development and maintenance of cellular structure but is required for efficient lateral force transmission during skeletal muscle contraction. Notably, syncoilin−/− skeletal muscle generates less maximal isometric stress than wild-type (WT) muscle but is as equally susceptible to eccentric contraction-induced injury as WT muscle. This suggests that syncoilin may play a supportive role for desmin in the efficient coupling of mechanical stress between the myofibril and fiber exterior. It is possible that the reduction in isometric stress production may predispose the syncoilin skeletal muscle to a dystrophic condition.


Author(s):  
Sumana Sundaramurthy ◽  
SarahBeth Votra ◽  
Arianna Laszlo ◽  
Tim Davies ◽  
David Pruyne

AbstractThe striated body wall muscles of Caenorhabditis elegans are a simple model system with well-characterized sarcomeres that have many vertebrate protein homologs. Previously, we observed deletion mutants for two formin genes, fhod-1 and cyk-1, developed thin muscles with abnormal dense bodies/sarcomere Z-lines. However, the nature of the cyk-1 mutation necessitated maternal CYK-1 expression for viability of the examined animals. Here, we tested the effects of complete loss of CYK-1 using a fast acting temperature-sensitive cyk-1(ts) mutant. Surprisingly, neither post-embryonic loss of CYK-1 nor acute loss of CYK-1 during embryonic sarcomerogenesis caused muscle defects, suggesting CYK-1 might not play a direct role in muscle development. Consistent with this, examination of cyk-1(Δ) mutants re-expressing CYK-1 in a mosaic pattern showed CYK-1 cannot rescue muscle defects in a muscle cell autonomous manner, suggesting muscle phenotypes caused by cyk-1 deletion are likely indirect. Conversely, mosaic re-expression of FHOD-1 in fhod-1(Δ) mutants promoted muscle cell growth, as well as proper Z-line organization, in a muscle cell autonomous manner. As we can observe no effect of loss of any other worm formin on muscle development, we conclude that FHOD-1 is the only formin that directly promotes striated muscle development in C. elegans.


2021 ◽  
Vol 35 (S1) ◽  
Author(s):  
Gabrielle Gentile ◽  
Jennifer Gamarra ◽  
Nichlas Engels ◽  
R. Blue ◽  
Hannah Wiedner ◽  
...  

2019 ◽  
Vol 30 (3) ◽  
pp. 293-301 ◽  
Author(s):  
Josephine A. Bonventre ◽  
Chelsea Holman ◽  
Aayushi Manchanda ◽  
Sara J. Codding ◽  
Trisha Chau ◽  
...  

The precise spatial and temporal expression of genes is essential for proper organismal development. Despite their importance, however, many developmental genes have yet to be identified. We have determined that Fer1l6, a member of the ferlin family of genes, is a novel factor in zebrafish development. We find that Fer1l6 is expressed broadly in the trunk and head of zebrafish larvae and is more restricted to gills and female gonads in adult zebrafish. Using both genetic mutant and morpholino knockdown models, we found that loss of Fer1l6 led to deformation of striated muscle tissues, delayed development of the heart, and high morbidity. Further, expression of genes associated with muscle cell proliferation and differentiation were affected. Fer1l6 was also detected in the C2C12 cell line, and unlike other ferlin homologues, we found Fer1l6 expression was independent of the myoblast-to-myotube transition. Finally, analysis of cell and recombinant protein–based assays indicate that Fer1l6 colocalizes with syntaxin 4 and vinculin, and that the putative C2 domains interact with lipid membranes. We conclude that Fer1l6 has diverged from other vertebrate ferlins to play an essential role in zebrafish skeletal and cardiac muscle development.


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