cnd-1 encodes a basic helix-loop-helix protein that is most closely related to the vertebrate NeuroD transcription factors; during development, CND-1 is predicted to function as a transcriptional regulator whose activity is required for several aspects of motor neuron fate specification, including cell division patterns, proper spatiotemporal expression of fate-specific markers, and normal axonal morphology and pathfinding; CND-1::GFP expression begins in early embryogenesis (<20 cells) in four AB descendants and then continues in mitotically active AB-derived neuronal precursors, unidentified nuclei during gastrulation and enclosure, and postmitotic neurons in the head and ventral cord; at hatching CND-1::GFP expression is visible in ventral cord neurons, but this expression disappears completely by the end of the first larval stage; CND-1::GFP does not appear to be expressed in any non-neuronal ectodermal cells, as its expression does not overlap with that of LIN-26.
Predicted to enable DNA-binding transcription factor activity, RNA polymerase II-specific and E-box binding activity. Involved in axonal fasciculation and negative regulation of gliogenesis. Located in nucleus. Expressed in several structures, including ABalpapaa; ABalppapa; motor neurons; neuroblasts; and somatic nervous system. Human ortholog(s) of this gene implicated in developmental and epileptic encephalopathy 72; glucose metabolism disease (multiple); and obesity. Is an ortholog of several human genes including NEUROD1 (neuronal differentiation 1); NEUROD2 (neuronal differentiation 2); and NEUROD4 (neuronal differentiation 4).
Inferred by orthology to human genes with DO annotation (HGNC:7763)
Disease_relevance
In humans, mutations in Neurogenic Differentiation 1 (NeuroD1) have been implicated in Diabetes Mellitus, Type II and Maturity-onset diabetes of the young, type VI; in elegans, cnd-1, seems to have combined the function of several vertebrate neurogenic bHLH proteins, and is required for the proper fate specification and terminal differentiation of motor neurons.