期刊
DEVELOPMENT
卷 136, 期 17, 页码 2933-2944出版社
COMPANY BIOLOGISTS LTD
DOI: 10.1242/dev.040204
关键词
C. elegans; Left/right asymmetry; Neuronal development; Transcriptional regulation
资金
- NIH [R01NS039996-05, R01NS050266-03, NS054540-01]
- Francis Goelet Fellowship
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [F31NS054540, R01NS039996, R01NS050266] Funding Source: NIH RePORTER
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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