ArticleBiophysical journal2025
A Drosophila cardiac myosin increases jump muscle stretch activation and shortening deactivation.
Article in Biophysical journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Fine-tuning striated muscle performance: conserved sarcomere-level mechanisms across insect and vertebrate systems.Frontiers in physiology · 2026Review
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11 authors.
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Abstract
Stretch activation (SA), a delayed increase in force production after rapid muscle lengthening, is critical to the function of vertebrate cardiac muscle and insect asynchronous indirect flight muscle. SA enables or increases power generation in muscle types used in a cyclical manner. Recently, myosin isoform expression has been implicated as a mechanism for varying the amplitude of SA in some muscle types. For instance, we found that expressing a larval Drosophila myosin isoform in a muscle type with minimal SA, the Drosophila jump muscle, substantially increased SA amplitude and enabled positive cyclical power generation. To test whether other myosin isoforms could increase SA amplitude and whether the Drosophila heart benefits from SA, we identified two Drosophila cardiac myosin isoforms, CardM1 and CardM2, and expressed them in Drosophila jump muscle. CardM1, CardM2, and control jump muscle fibers all displayed the characteristic phase 3 of SA, with CardM2 SA amplitude ∼60% greater than that of CardM1 and control fibers. Increasing [P
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