Notch signaling is required in many invertebrate and vertebrate cells to promote proper cell fate determination. Mutations in sanpodo cause many different neuronal peripheral nervous system precursor cells to generate two identical daughter neurons, instead of a neuron and sibling cell. This phenotype is similar to that observed when Notch function is lost late in embryonic development and opposite to the numb loss-of-function phenotype. Genetic interaction studies show that sanpodo is epistatic to numb. sanpodo encodes a homolog of tropomodulin, an actin/tropomyosin-associated protein. Loss of sanpodo leads to an aberrant F-actin distribution and causes differentiation defects of actin-containing sensory structures. Our data suggest that an actin-based process is involved in Notch signaling.
|Number of pages||12|
|State||Published - 1998|