Why the study?
Improper thin filament lengths associate with altered contractile activity and lethal myopathies, but the role of leiomodin in thin filament assembly and maintenance remains under dispute.
Leiomodin acts as a 'leaky cap' at the pointed end of actin-thin filaments, regulating their length by competing with tropomodulin for thin filament binding.
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Preclinical findings leave open leiomodin targeting in human cardiomyopathy; extends thin filament length control in model systems.
Tolkatchev et al. (2020) studied this question.
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