Society of
General physiologists

Paul F. Cranefield Award

Farid Moussavi-Harami for “Machine learning meets Monte Carlo methods for models of muscle’s molecular machinery to classify mutations”; J Gen Physiol (2023) 155 (5): e202213291
doi.org/10.1085/jgp.202213291

Genetic cardiomyopathies result in changes in the temporal features of cardiac twitch contractions, but connecting these changes to underlying molecular mechanisms has been challenging. Utilizing spatially explicit models of the sarcomere and machine learning methods, Moussavi-Harami and colleagues show that machine learning holds great promise as a novel method for classifying the mechanistic changes that reshape twitch forces in cardiac diseases.

Cranefield Postdoctoral Fellow Award

Shuya Ishii for “Myosin and tropomyosin–troponin complementarily regulate thermal activation of muscles”; J Gen Physiol (2023) 155 (12): e202313414
doi.org/10.1085/jgp.202313414

Through studies of muscle contractile regulation in the physiological temperature range, Ishii and colleagues show that the lower thermal activation of thin filaments is compensated by the higher thermal activity of myosin, and that the inverse relationship holds for thin filaments and myosin in cardiac muscle. The higher temperature dependence of skeletal vs cardiac muscle may enable fast skeletal muscle contraction as the body temperature increases with exercise while maintaining efficient cardiac contraction.

Cranefield Student Award

Teresa Crespo for “A Cantú syndrome mutation produces dual effects on KATP channels by disrupting ankyrin B regulation”; J Gen Physiol (2023) 155 (1): e202112995
doi.org/10.1085/jgp.202112995

Inhibition of the K_ATP channel complex by physiological ATP links cellular electrical activity and metabolism. Mutations relieving this block cause Cantù syndrome, with larger reliefs correlating with more severe disease phenotypes. Crespo and colleagues reveal that mutations can also impair surface protein expression and interactions with ankyrin B, thus identifying a novel partner of the K_ATP complex. These results explain why a mutation with a predicted severe phenotype causes a mild form of the disease.

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