The muscle-specific UNC-45b assists in the folding of sarcomeric myosin. Analysis of the zebrafish unc-45b upstream region revealed that unc-45b promoter fragments reliably drive GFP expression after germline transmission. The muscle-specific 503-bp minimal promoter 503unc was identified to drive gene expression in the zebrafish musculature. In transgenic Tg(-503unc:GFP) zebrafish, GFP fluorescence was detected in the adaxial cells, their slow fiber descendants, and the fast muscle. At later stages, robust GFP fluorescence is eminent in the cardiac, cranial, fin, and trunk muscle, thereby recapitulating the unc-45b expression pattern. We propose that the 503unc promoter is a small and muscle-specific promoter that drives robust gene expression throughout the zebrafish musculature, making it a valuable tool for the exploration of zebrafish muscle.
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http://dx.doi.org/10.1002/dvg.22385 | DOI Listing |
Physiol Rep
January 2025
Department of Nutrition and Health Sciences, University of Nebraska-Lincoln, Lincoln, Nebraska, USA.
MicroRNAs (miRNAs) are small, noncoding RNAs that play a critical role in regulating gene expression post-transcriptionally. They are involved in various developmental and physiological processes, and their dysregulation is linked to various diseases. Skeletal muscle-specific miRNAs, including miR-1, play a crucial role in the development and maintenance of skeletal muscle.
View Article and Find Full Text PDFGeroscience
December 2024
Department of Internal Medicine-Gerontology and Geriatric Medicine, Wake Forest University School of Medicine, Winston-Salem, NC, USA.
Free Radic Biol Med
January 2025
Department of Radiology, University of Washington School of Medicine, Seattle, WA, USA; Department of Laboratory Medicine and Pathology, University of Washington School of Medicine, Seattle, WA, USA.
Introduction: Skeletal muscle mitochondrial dysfunction is a key characteristic of aging muscle and contributes to age related diseases such as sarcopenia, frailty, and type 2 diabetes. Mitochondrial oxidative stress has been implicated as a driving factor in these age-related diseases, however whether it is a cause, or a consequence of mitochondrial dysfunction remains to be determined. The development of flexible genetic models is an important tool to test the mechanistic role of mitochondrial oxidative stress on skeletal muscle metabolic dysfunction.
View Article and Find Full Text PDFbioRxiv
September 2024
Department of Radiology, University of Washington School of Medicine, Seattle, WA, USA.
Introduction: Skeletal muscle mitochondrial dysfunction is a key characteristic of aging muscle and contributes to age related diseases such as sarcopenia, frailty, and type 2 diabetes. Mitochondrial oxidative distress has been implicated as a driving factor in these age-related diseases, however whether it is a cause, or a consequence of mitochondrial dysfunction remains to be determined. The development of more flexible genetic models is an important tool to test the mechanistic role of mitochondrial oxidative stress on skeletal muscle metabolic dysfunction.
View Article and Find Full Text PDFJ Cachexia Sarcopenia Muscle
December 2024
Graduate Institute of Microbiology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Background: Nuclear receptor interaction protein (NRIP) is versatile and engages with various proteins to execute its diverse biological function. NRIP deficiency was reported to cause small myofibre size in adult muscle regeneration, indicating a crucial role of NRIP in myoblast fusion.
Methods: The colocalization and interaction of NRIP with actin were investigated by immunofluorescence and immunoprecipitation assay, respectively.
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