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The actin-binding protein DBN-1 stabilizes actin in muscle cells and reversibly changes location between actin filaments and myosin-rich regions during muscle contraction in C. elegans.
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The actin-binding protein DBN-1 plays a crucial role in stabilizing actin and organizing other actin-binding proteins during muscle contraction in C. elegans.
Locomotion of C. elegans requires coordinated, efficient transmission of forces generated on the molecular scale by myosin and actin filaments in myocytes to dense bodies and the hypodermis and cuticle enveloping body wall muscles. The complex organization of the acto-myosin scaffold with its accessory proteins provides a fine-tuned machinery regulated by effectors that guarantees that sarcomere units undergo controlled, reversible cycles of contraction and relaxation. Actin filaments in sarcomeres dynamically undergo polymerization and depolymerization. In a recent study, the actin-binding protein DBN-1, the C. elegans ortholog of human drebrin and drebrin-like proteins, was discovered to stabilize actin in muscle cells. DBN-1 reversibly changes location between actin filaments and myosin-rich regions during muscle contraction. Mutations in DBN-1 result in mislocalization of other actin-binding proteins. Here we discuss implications of this finding for the regulation of sarcomere actin stability and the organization of other actin-binding proteins.
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Butkevich et al. (2016) conducted a review in Muscle contraction. DBN-1 (actin-binding protein) was evaluated. The actin-binding protein DBN-1 stabilizes actin in muscle cells and reversibly changes location between actin filaments and myosin-rich regions during muscle contraction in C. elegans.
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