Please use this identifier to cite or link to this item: https://hdl.handle.net/11000/38428

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

Title:
Cell-specific effects of the sole C. elegans Daughterless/E protein homolog, HLH-2, on nervous system development
Authors:
Masoudi, Neda  
Schanabel, Ralf
Yemini, Eviatar  
Leyva-Díaz, Eduardo  
Hobert, Oliver  
Editor:
The Company of Biologists Ltd
Issue Date:
2023-01
URI:
https://hdl.handle.net/11000/38428
Abstract:
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.
Keywords/Subjects:
caenorhabditis elegans
daughterless
E protein
HLH-2
neurogenesis
Type of document:
info:eu-repo/semantics/article
Access rights:
info:eu-repo/semantics/openAccess
Attribution-NonCommercial-NoDerivatives 4.0 Internacional
DOI:
10.1242/dev.201366
Published in:
Development . 2023 Jan 1;150(1):dev201366
Appears in Collections:
Instituto de Neurociencias



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