lin-32

One candidate, gene lin-32 (abnormal cell LINeage 32), which encodes an atonal homolog, is required for the neural fate determination of AIB interneurons and functions by regulating the expression of electrical and chemical synapse genes, namely, inx-1 (innexin 1) and AMPA-type ionotropic glutamate receptor glr-1.

The anterior-posterior patterning of LIN-32 expression and of differentiated ray neuroglial fates is brought about by the Wnt/β-catenin asymmetry pathway, including the Wnt ligand LIN-44, its receptor LIN-17, and downstream components LIT-1 (NLK), SYS-1 (β-catenin), and POP-1 (TCF).

Here we show that the distribution of LIN-32 during the ray sublineage is markedly asymmetric, localizing to anterior daughter cells in two successive cell divisions.

Similarity in the function and structure of the lin-32 protein (LIN-32) to transcription factors of the achaete-scute gene family in Drosophila and vertebrates implies that this class of transcription factors functioned in a primitive ancestral form to specify neuronal cell fate, supporting the proposition that certain basic mechanisms of cell-type determination have been conserved through metazoan evolution.

We report here that the lin-32 gene of Caenorhabditis elegans, which encodes a bHLH protein of the Drosophila achaete-scute family of transcription factors, is necessary and in some cells sufficient for specification of the neuroblast cell fate.

Single-cell resolution expression profiling of TFs and genetic analysis revealed a differentiation gene battery (Atonh1/lin-32, Drg11/alr-1, Gfi1/pag-3, Lhx5/mec-3, and Pou4/unc-86) for AVM/PVM mechanosensory neurons.

Consistently, lin-32 is expressed throughout Q neuroblast lineage, suggesting that LIN-32 may promote different target gene expression.

We showed that LIN-32 functions in parallel with a storkhead TF, HAM-1, to regulate Q neuroblast asymmetric division, and that Q neuroblast migration is inhibited in lin-32 alleles.

Moreover, we show that lin-32 acts in parallel with cnd-1/ NeuroD1 and ngn-1/ Neurog1 in negatively regulating an AMsh glia fate.

Consistently, lin-32 is expressed throughout Q neuroblast lineage, suggesting that LIN-32 may promote different target gene expression.

Loss of lin-32 results in the selective loss of the expression of pan-neuronal markers and terminal selector-type transcription factors that confer neuron class-specific features.

The atonal ortholog lin-32 and the E/daughterless ortholog hlh-2 act to confer neural competence during ray development, but additional regulatory factors that control specific aspects of cell fate are largely unknown.

Mutations in seven genes either reduce (lin-14) or increase (lin-4, egl-44, egl-46, sem-4, ced-3 and ced-4) the number of touch receptor-like cells.

The atonal ortholog lin-32 and the E/daughterless ortholog hlh-2 act to confer neural competence during ray development, but additional regulatory factors that control specific aspects of cell fate are largely unknown.

We show that the transcription factor unc-130, a human FOXD3/4 ortholog, is required to optimize avoidance behavior depending on stimulus strength in Caenorhabditis elegans. unc-130 is necessary for both ON responses (calcium decreases) and OFF responses (calcium increases) in AIBs, central neurons of avoidance optimization.

Here, we identified the LIN-32/Atonal bHLH transcription factor as a key regulator of URXL/R oxygen-sensing neuron development in Caenorhabditis elegans.

Ray development requires the conserved atonal-family bHLH gene lin-32, which specifies the ray neuroblast and promotes the differentiation of its progeny.

At first, we observed that in both C. elegans Q neuroblasts and Drosophila lateral neuroectoderm, conserved NPB specifier Msx/vab-15 regulates Atoh1/lin-32, supporting the homology of mechanosensory neuron development in lateral neural border lineage of Ecdysozia.

Here, we show that ectopic expression of both HLH-12 and LIN-32 in cells with AC potential transiently transforms them into fDTC-like cells.

We showed that LIN-32 functions in parallel with a storkhead TF, HAM-1, to regulate Q neuroblast asymmetric division, and that Q neuroblast migration is inhibited in lin-32 alleles.