Regulation of the evolutionarily conserved muscle myofibrillar matrix by cell type dependent and independent mechanisms

Peter T. Ajayi, Prasanna Katti, Yingfan Zhang, T. Bradley Willingham, Ye Sun, Christopher K. E. Bleck and Brian Glancy ()
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Peter T. Ajayi: NHLBI, NIH
Prasanna Katti: NHLBI, NIH
Yingfan Zhang: NHLBI, NIH
T. Bradley Willingham: NHLBI, NIH
Ye Sun: NHLBI, NIH
Christopher K. E. Bleck: NHLBI, NIH
Brian Glancy: NHLBI, NIH

Nature Communications, 2022, vol. 13, issue 1, 1-12

Abstract: Abstract Skeletal muscles play a central role in human movement through forces transmitted by contraction of the sarcomere. We recently showed that mammalian sarcomeres are connected through frequent branches forming a singular, mesh-like myofibrillar matrix. However, the extent to which myofibrillar connectivity is evolutionarily conserved as well as mechanisms which regulate the specific architecture of sarcomere branching remain unclear. Here, we demonstrate the presence of a myofibrillar matrix in the tubular, but not indirect flight (IF) muscles within Drosophila melanogaster. Moreover, we find that loss of transcription factor H15 increases sarcomere branching frequency in the tubular jump muscles, and we show that sarcomere branching can be turned on in IF muscles by salm-mediated conversion to tubular muscles. Finally, we demonstrate that neurochondrin misexpression results in myofibrillar connectivity in IF muscles without conversion to tubular muscles. These data indicate an evolutionarily conserved myofibrillar matrix regulated by both cell-type dependent and independent mechanisms.

Date: 2022
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DOI: 10.1038/s41467-022-30401-9

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