Yotam Levy

TL;DR: DNM2 knockdown via two different strategies can efficiently correct the myopathy due to DNM2 mutations, and it provides a common therapeutic strategy for several forms of centronuclear myopathy.

TL;DR: Results demonstrate that SIRT1 is a key regulator of MND sizes, although the underlying molecular mechanisms and the cause‐effect relationship between MND and muscle function remain to be fully defined.

TL;DR: Results indicate that, in the presence of prelamin A, the abundance of nuclei and myosin content is markedly reduced within muscle fibers, which leads to a concept by which the remaining myonuclei are very distant from each other and are pushed to function beyond their maximum cytoplasmic capacity, ultimately inducing muscle fiber weakness.

TL;DR: The hypotheses that the compromised functional and morphological attributes of skeletal muscles bearing ACTA1 mutations would be directly due to the inefficient actomyosin complex and could be restored by manipulating myosin expression are tested.

TL;DR: PGC‐1α and the related mitochondrial biogenesis programme are determinants of MND size and may facilitate the addition of new myonuclei in order to reach MND volumes that can support an increased mitochondrial density, according to Cell.