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Annals of Neurology: Volume 87, Number 4, April 2020
Publication year - 2020
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.25713
Subject(s) - skeletal muscle , anatomy , troponin , biology , troponin t , actin , myopathy , zebrafish , fish <actinopterygii> , pathology , medicine , gene , microbiology and biotechnology , genetics , myocardial infarction , fishery
A fluorescence photomicrograph of skeletal muscle from a zebrafish larva in which the slow skeletal muscle troponin T protein was knocked down resulting in a myopathic phenotype characterized by reduced muscle mass and curvature of the body. A novel mutation in the slow skeletal muscle troponin T (TNNT1) gene causes a type of congenital core‐rod myopathy in humans. Actin is immunostained green and nuclei are stained blue. The muscle fibers in the affected fish model are disrupted and irregular in appearance compared to normal control fish (see Pellerin et al., pp. 568–583). Injecting the wild type human TNNT1 mRNA corrected both the morphological abnormalities and the body curvature.

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