Key result
OGDH complex depletion disrupts amino acid homeostasis, causing severe myofibril and sarcomere defects.
Why the study?
It was not known how Zasp proteins effect myofibril growth to ensure sarcomere homogeneity and set myofibril diameter.
This preclinical study reveals a novel mechanism linking local Zasp-dependent myofibril growth control with a global metabolic growth control mechanism via amino acid availability.
Myofibrils are long intracellular cables specific to muscles, composed mainly of actin and myosin filaments. The actin and myosin filaments are organized into repeated units called sarcomeres, which form the myofibril cables. Muscle contraction is achieved by the simultaneous shortening of sarcomeres and for a highly coordinated contraction to occur all sarcomeres should have the same size. Muscles have evolved a variety of ways to ensure sarcomere homogeneity, one example being the controlled oligomerization of Zasp proteins that sets the diameter of the myofibril. To understand how Zasp proteins effect myofibril growth, we looked for Zasp-binding proteins at the Z-disc. We found that the E1 subunit of the oxoglutarate dehydrogenase complex is recruited to the Z-disc by Zasp52 and is required to sustain myofibril growth. By making specific mutants, we show that its enzymatic activity is important for myofibril growth, and that the other two subunits of the complex are also required for myofibril formation. Using super resolution microscopy, we revealed the overall organization of the complex at the Z-disc. Then, using metabolomic analysis, we uncovered an amino acid balance defect affecting protein synthesis, that we also confirmed by genetic tools. In summary, we show that Zasp controls the local amino acid pool responsible for myofibril growth by recruiting the OGDH complex to the Z-disc.
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González‐Morales et al. (2021) studied Myofibril growth and amino acid homeostasis. Genetic manipulation of the OGDH complex vs. Wild-type Drosophila was evaluated on Myofibril structure and sarcomere arrangement. Depletion of the oxoglutarate dehydrogenase complex caused severe myofibril growth defects and loss of sarcomere structure due to impaired amino acid homeostasis.
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