ArticleDevelopment (Cambridge, England)2009
The C. elegans Tailless/TLX transcription factor nhr-67 controls neuronal identity and left/right asymmetric fate diversification.
Article in Development (Cambridge, England), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed.
- Continuous negative autoregulation fine-tunes dosage-sensitive transcription factor expression to maintain post-mitotic neuron identity.bioRxiv : the preprint server for biology · 2026Article
- Neurogenesis in Caenorhabditis elegans.Genetics · 2024Review
- A lineage-resolved cartography of microRNA promoter activity in C. elegans empowers multidimensional developmental analysis.Nature communications · 2024Article
- Maintenance of neuronal identity in C. elegans and beyond: Lessons from transcription and chromatin factors.Seminars in cell & developmental biology · 2024Review
- Article
- Widespread employment of conserved C. elegans homeobox genes in neuronal identity specification.PLoS genetics · 2022Article
- Article
- A 4D single-cell protein atlas of transcription factors delineates spatiotemporal patterning during embryogenesis.Nature methods · 2021Article
- Combinatorial Action of Temporally Segregated Transcription Factors.Developmental cell · 2020Article
- Modular Organization ofGenetics · 2020Article
- Transcription factor autoregulation is required for acquisition and maintenance of neuronal identity.Development (Cambridge, England) · 2019Article
- RPM-1 and DLK-1 regulate pioneer axon outgrowth by controlling Wnt signaling.Development (Cambridge, England) · 2018Article
- CONSERVED AND EXAPTED FUNCTIONS OF NUCLEAR RECEPTORS IN ANIMAL DEVELOPMENT.Nuclear receptor research · 2017Article
- Article
- A map of terminal regulators of neuronal identity in Caenorhabditis elegans.Wiley interdisciplinary reviews. Developmental biology · 2016Review
- Invasive Cell Fate Requires G1 Cell-Cycle Arrest and Histone Deacetylase-Mediated Changes in Gene Expression.Developmental cell · 2015Article
- Of Fighting Flies, Mice, and Men: Are Some of the Molecular and Neuronal Mechanisms of Aggression Universal in the Animal Kingdom?PLoS genetics · 2015Review
- The Evolutionarily Conserved LIM Homeodomain Protein LIM-4/LHX6 Specifies the Terminal Identity of a Cholinergic and Peptidergic C. elegans Sensory/Inter/Motor Neuron-Type.PLoS genetics · 2015Article
- MicroRNAs: Not "Fine-Tuners" but Key Regulators of Neuronal Development and Function.Frontiers in neurology · 2015Review
- Two distinct types of neuronal asymmetries are controlled by the Caenorhabditis elegans zinc finger transcription factor die-1.Genes & development · 2014Article
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4 authors.
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Abstract
An understanding of the molecular mechanisms of cell fate determination in the nervous system requires the elucidation of transcriptional regulatory programs that ultimately control neuron-type-specific gene expression profiles. We show here that the C. elegans Tailless/TLX-type, orphan nuclear receptor NHR-67 acts at several distinct steps to determine the identity and subsequent left/right (L/R) asymmetric subtype diversification of a class of gustatory neurons, the ASE neurons. nhr-67 controls several broad aspects of sensory neuron development and, in addition, triggers the expression of a sensory neuron-type-specific selector gene, che-1, which encodes a zinc-finger transcription factor. Subsequent to its induction of overall ASE fate, nhr-67 diversifies the fate of the two ASE neurons ASEL and ASER across the L/R axis by promoting ASER and inhibiting ASEL fate. This function is achieved through direct expression activation by nhr-67 of the Nkx6-type homeobox gene cog-1, an inducer of ASER fate, that is inhibited in ASEL through the miRNA lsy-6. Besides controlling bilateral and asymmetric aspects of ASE development, nhr-67 is also required for many other neurons of diverse lineage history and function to appropriately differentiate, illustrating the broad and diverse use of this type of transcription factor in neuronal development.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.