473, Lechtreck and Witman locate this protein to the buried central pair (CP) of flagellar microtubules. The paralysis of cilia lacking hydin might be a basis for hydrocephalus-inducing brain fluid accumulation.
Flagella contain lots of hydin, but no one had yet localized the protein in any system. Lechtreck and Witman have now spotted the protein on the CP of flagellar microtubules in Chlamydomonas.
This alga's two flagella execute a sort of breaststroke that provides motility. The downward stroke that moves the cell forward requires active dynein on one side of the outer ring of microtubule doublets. But to return the arms to their starting position, dynein on the opposite side must be activated.
This dynein switch appears to be defective in algae lacking hydin, whose flagella were stuck at the end of either the power or recovery stroke. Based on hydin's position on the CP, the authors speculate that its conformational changes might transmit a signal across the flagellum that activates or inactivates dynein. Hydin's structural changes might be driven by another CP protein, KLP1, which is a kinesin-like motor that the authors found interacts with hydin.
Mouse hydin mutants accumulate fluids within brain cavities, which are lined with ciliated cells that express hydin. The resemblance of this mouse defect to human hydrocephalus suggests that paralyzed cilia might be one cause of the inadequate brain fluid transport in these patients.