A cell without Par3 (bottom) sports a petite cilium (arrow).

Aprotein that induces cells to create tight junctions also helps the primary cilium grow, as Sfakianos et al. show. Although the details remain murky, the protein, Par3, helps lengthen the structures by connecting a molecular motor that travels along the cilium to proteins that are embedded in the cilia membrane.

Researchers know that Par3 teams up with three other proteins, but they don't know all of its effects. Some studies suggest that Par3 helps induce adhesive tight junctions between epithelial cells. Other work indicates it sets up cell polarity in neurons by defining the axon. Sfakianos et al. have identified yet another function for Par3.

The team used RNAi to quash the protein. Although cells lacking Par3 still established tight junctions, they took extra time to form. The cells seemed to polarize normally, suggesting that Par3 isn't necessary to complete this process. However, loss of Par3 fouled up construction of the cilium. Normal cells grew lengthy cilia, but cells lacking Par3 could only manage puny filaments.

Par3 hooks up with a molecular motor called Kif3a, which helps haul new cilium building blocks to the growing tip. Without this interaction, cilia were stumpy. But cilia were absent when cells were missing another protein called Crumbs3, which settles in the membrane along the cilium. The team showed that Par3 uses Crumbs3's PDZ-binding domain to maneuver Crumb3 into position. So Par3 might spur cilium elongation by tying the membrane protein to motor proteins that slide along the cilium. The next step for the researchers is to determine how these links guide fresh components to the end of the cilium.


Sfakianos, J., et al.
J. Cell Biol.