THE CAENORHABDITIS-ELEGANS LIN-26 PROTEIN IS REQUIRED TO SPECIFY AND OR MAINTAIN ALL NONNEURONAL ECTODERMAL CELL FATES/

The C. elegans gene lin-26, which encodes a presumptive zinc-finger tr anscription factor, is required for hypodermal cells to acquire their proper fates. Here we show that lin-26 is expressed not only in all hy podermal cells but also in all glial-like cells, During asymmetric cel l divisions that generate a neuronal cell and a non-neuronal cell, LIN -26 protein is symmetrically segregated and then lost from the neurona l cell. Expression in glial-like cells (socket and sheath cells) is bi ologically important, as some of these neuronal support cells die or s eem sometimes to be transformed to neuron-like cells in embryos homozy gous for strong loss-of-function mutations. In addition, most of these glial-like cells are structurally and functionally defective in anima ls carrying the weak loss-of-function mutation lin-26(n156). lin-26 mu tant phenotypes and expression patterns together suggest that lin-26 i s required to specify and/or maintain the fates not only of hypodermal cells but also of all other non-neuronal ectodermal cells in C. elega ns. We speculate that lin-26 acts by repressing the expression of neur onal-specific genes in non-neuronal cells.