ArticlePloS one2014
Regulation of C. elegans neuronal differentiation by the ZEB-family factor ZAG-1 and the NK-2 homeodomain factor CEH-28.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 22 citations in OpenAlex.
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- Deciphering the underlying mechanisms of the pharyngeal pumping motions inProceedings of the National Academy of Sciences of the United States of America · 2024Article
- The enteric nervous system of theeLife · 2022Article
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- Molecular Effects of Silver Nanoparticles on Monogenean Parasites: Lessons fromInternational journal of molecular sciences · 2020Article
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- Inhibition of cell fate repressors secures the differentiation of the touch receptor neurons ofDevelopment (Cambridge, England) · 2018Article
- Characterization of the crawling activity of Caenorhabditis elegans using a Hidden Markov model.Theory in biosciences = Theorie in den Biowissenschaften · 2015Article
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Authors and funding
2 authors at 1 institution in 1 country.
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Abstract
The C. elegans pharyngeal neuron M4 is a multi-functional cell that acts as a cholinergic motor neuron to stimulate peristaltic pharyngeal muscle contraction and as a neuroendocrine cell secreting neuropeptides and growth factors to affect other cells both inside and outside the pharynx. The conserved transcription factors ZAG-1 and CEH-28 are co-expressed in M4 through most of development, and here we examine how these factors contribute to M4 differentiation. We find ZAG-1 functions upstream of CEH-28 in a branched pathway to activate expression of different sets of M4 differentiation markers. CEH-28 activates expression of the growth factor genes dbl-1 and egl-17, and the neuropeptide genes flp-5 and flp-2, while ZAG-1 activates expression of the serotonin receptor ser-7, as well as expression of ceh-28 and its downstream targets. Other markers of M4 differentiation are expressed normally in both zag-1 and ceh-28 mutants, including the neuropeptide gene flp-21 and the acetylcholine biosynthetic gene unc-17. Unlike ceh-28 mutants, zag-1 mutants completely lack peristaltic muscle contractions resulting from broader defects in M4 differentiation. Despite these defects, neither ZAG-1 nor CEH-28 are terminal selectors of the M4 phenotype, and we suggest they function in a hierarchy to regulate different aspects of M4 differentiation.
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