In holometabolous insects, metamorphosis involves restructuring the musculature to accommodate adult-specific anatomy and behaviors. Evidence from experiments on remodeled muscles, as well as those that develop de novo, suggests that signals from the nervous system support adult muscle development by controlling myoblast proliferation rate. However, the dorsolongitudinal flight muscles (DLMs) of Manduca sexta undergo a mixed developmental program involving larval muscle fibers, and it is not known if neurons play the same role in the formation of these muscles. To address this question, we have blocked the most promising candidate pathways for neural input and examined the DLMs for changes in proliferation. Our results show that DLM development does not depend on neural activity, Hedgehog signaling, or EGF signaling. It remains to be determined how DLM growth is controlled and why neurally mediated proliferation differs between individual muscles.
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http://dx.doi.org/10.1016/j.asd.2022.101232 | DOI Listing |
Biochim Biophys Acta Mol Cell Res
January 2025
Designing Future Health Initiative, Center for Promotion of Innovation Strategy, Head Office of Enterprise Partnerships, Tohoku University, Miyagi 980-8579, Japan.
Proteasome-dependent protein degradation and the digestion of peptides by aminopeptidases are essential for myogenesis. Methionine aminopeptidases (MetAPs) are uniquely involved in, both, the proteasomal degradation of proteins and in the regulation of translation (via involvement in post-translational modification). Suppressing MetAP1 and MetAP2 expression inhibits the myogenic differentiation of C2C12 myoblasts.
View Article and Find Full Text PDFFASEB J
January 2025
Shirley Ryan AbilityLab, Chicago, Illinois, USA.
Following injury, skeletal muscle undergoes repair via satellite cell (SC)-mediated myogenic progression. In SCs, the circadian molecular clock gene, Bmal1, is necessary for appropriate myogenic progression and repair with evidence that muscle molecular clocks can also affect force production. Utilizing a mouse model allowing for inducible depletion of Bmal1 within SCs, we determined contractile function, SC myogenic progression and muscle damage and repair following eccentric contractile-induced injury.
View Article and Find Full Text PDFCell Struct Funct
January 2025
College of Animal Sciences and Technology and College of Veterinary Medicine, Huazhong Agricultural University.
The process of mammalian myogenesis is fundamental to understanding muscle development and holds broad relevance across multiple fields, from developmental biology to regenerative medicine. This review highlights two key aspects: myoblast proliferation and the role of cilia in this process. Myoblasts, as muscle precursor cells, must undergo tightly regulated cycles of proliferation and differentiation to ensure proper muscle growth and function.
View Article and Find Full Text PDFInt J Biol Macromol
January 2025
College of Animal Science, Xinjiang Agricultural University, Urumqi 830052, China. Electronic address:
N6-methyladenosine (mA), a well-known post-transcriptional modification, is implicated in diverse cellular and physiological processes. However, much remains unknown regarding the precise role and mechanism of mA modification on muscle development. In this study, we make observation that the levels of mA and METTL3 are markedly elevated during the differentiation phase (DM) compared to the growth phase (GM) in both C2C12 and bovine myoblasts.
View Article and Find Full Text PDFCancer Lett
January 2025
Peggy and Charles Stephenson Cancer Center, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA; Department of Pathology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA. Electronic address:
Anorexia is a major cause of cancer cachexia and is induced by growth differentiation factor-15 (GDF15), which activates the rearranged during transfection (RET) protein tyrosine kinase in the hindbrain through GDF family receptor α-like (GFRAL), raising the possibility of targeting RET for cancer cachexia treatment. RET-altered cancer patients treated with RET-selective kinase inhibitors gain weight, however, it is unclear whether this results from tumor regression that improves the overall health of patients. Thus, the potential of using a RET inhibitor to address cancer cachexia remains unknown.
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