page 549), but on controlling the extension of microvilli.Microvilli are actin-filled apical protrusions on epithelial cells. Actin bundling and polymerizing proteins are the usual suspects regulating microvilli length. But the new results reveal that a plasma membrane protein, a cadherin family member called Cad99C, is also necessary.
Female flies lacking Cad99C had short, misshapen microvilli on their follicle cells, which secrete the material used to make egg shells. Overexpression of Cad99C, by contrast, resulted in abnormally long microvilli.
Mutations in a related vertebrate cadherin, called protocadherin 15 (PCDH15), cause deafness associated with abnormal cochlear microvilli. Scientists have generally guessed that PCDH15 links and aligns microvilli similar to the classical cadherin involvement in adherens junctions. But this might not be the case, based on the new findings. Follicle cell microvilli were too far apart for Cad99C to link them, and Cad99C overexpression created large microvilli that fanned out rather than clumping together.
The transmembrane and extracellular domains of Cad99C were sufficient to control its microvilli function. The authors hypothesize that several Cad99C molecules might interact in cis to stiffen the membrane of a growing microvillus. As another possibility, Cad99C might sense extracellular molecules and transmit their signals to nearby membrane proteins that control actin reorganization.