ZMYND10 (zinc finger MYND-type containing 10) is a cytoplasmic protein essential for axonemal dynein arm assembly and cilia motility. Primary function: ZMYND10 regulates the cytoplasmic pre-assembly of both inner dynein arms (IDA) and outer dynein arms (ODA) required for proper axoneme structure 1. Mechanism: ZMYND10 acts as a co-chaperone that confers specificity for the FKBP8-HSP90 chaperone complex toward axonemal dynein clients 2. It stabilizes intermediate chain proteins including DNAI1, which subsequently stabilizes other dynein components 3. ZMYND10 interacts with ODA assembly factors such as LRRC6, DYX1C1, and C21ORF59 4. Disease relevance: Biallelic ZMYND10 mutations cause primary ciliary dyskinesia (PCD) characterized by absent or severely reduced dynein arms, complete cilia immotility, hydrocephalus, laterality defects, and male infertility 1. Clinical significance: ZMYND10 mutations account for approximately 16% of PCD cases with combined IDA and ODA defects 1. Disease-causing variants disrupt the FKBP8-HSP90 co-chaperone function, suggesting PCD represents a cell-type specific protein-misfolding disease 2. Beyond ciliary function, ZMYND10 exhibits tumor-suppressive properties in breast cancer through miR145-5p/NEDD9 regulation 5.