Cell-specific effects of the sole C. elegans Daughterless/E protein homolog, HLH-2, on nervous system development

Are there common mechanisms of neurogenesis used throughout an entire nervous system? We explored to what extent canonical proneural class I/II bHLH complexes are responsible for neurogenesis throughout the entire Caenorhabditis elegans nervous system. Distinct, lineage-specific proneural class II bHLH factors are generally thought to operate via interaction with a common, class I bHLH subunit, encoded by Daughterless in flies, the E proteins in vertebrates and HLH-2 in C. elegans. To eliminate function of all proneuronal class I/II bHLH complexes, we therefore genetically removed maternal and zygotic hlh-2 gene activity. We observed broad effects on neurogenesis, but still detected normal neurogenesis in many distinct neuron-producing lineages of the central and peripheral nervous system. Moreover, we found that hlh-2 selectively affects some aspects of neuron differentiation while leaving others unaffected. Although our studies confirm the function of proneuronal class I/II bHLH complexes in many different lineages throughout a nervous system, we conclude that their function is not universal, but rather restricted by lineage, cell type and components of differentiation programs affected.

Automated summary

We investigated whether there are common mechanisms of neurogenesis throughout the entire nervous system of C. elegans. Our findings suggest that while distinct proneural class II bHLH factors play a role in neurogenesis, their function is not universal and is instead limited by lineage, cell type, and differentiation programs affected. Genetic removal of the hlh-2 gene activity showed broad effects on neurogenesis but still allowed for normal neurogenesis in many neuron-producing lineages.