Significance We show that interfering with insect chitin deacetylation by down-regulation of specific chitin deacetylase (CDA) isoforms, belonging to subfamily group I, causes breakage of the chitinous internal tendon cuticle… Click to show full abstract
Significance We show that interfering with insect chitin deacetylation by down-regulation of specific chitin deacetylase (CDA) isoforms, belonging to subfamily group I, causes breakage of the chitinous internal tendon cuticle at the femur–tibia joint, muscle detachment from both internal and external tendon cells, and defective locomotion. Our studies reveal a previously unrecognized role of CDA-like proteins in cooperation with zona pellucida domain-containing proteins in musculoskeletal connectivity, maintenance of tendon cell microtubule integrity, muscle force transmission, limb movement, and locomotion. We propose an essential function for group I CDAs, which are highly conserved among insect and other arthropod species, in invertebrate musculoskeletal connectivity involving partially deacetylated chitin in the extracellular matrix overlying the tendon cells.
               
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