Two papers in this issue report that ZAG-1, the C. eleganshomologue of the vertebrate Zn-finger homeodomain protein δEF1, acts as a transcriptional repressor that regulates many crucial aspects of neuron terminal differentiation. Both groups discovered zag-1 in screens for mutant worms with defective neuronal development. These studies revealed that zag-1 mutations cause axon guidance, fasciculation and branching errors, and the misexpression of neuronal differentiation markers. The null mutant, as reported by Wacker et al. on , also highlights the involvement of zag-1 in pharynx development as mutant larvae die from starvation, being unable to swallow food. On , Clark and Chiu show that zag-1 is expressed in neurons and specific muscles,and directly represses its own expression, while also downregulating genes involved in neurotransmitter synthesis or reuptake. The authors expect future work on ZAG-1 targets to uncover novel and key regulators of axon guidance.
