ArticleDevelopmental biology2014
CEH-28 activates dbl-1 expression and TGF-β signaling in the C. elegans M4 neuron.
Article in Developmental biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- TGF-β pathways in aging and immunity: lessons fromFrontiers in genetics · 2023Review
- Importance of TGFβ in Cancer and Nematode Infection and Their Interaction-Opinion.Biomolecules · 2022Review
- Reduced bone morphogenic protein signaling along the gut-neuron axis by heat shock factor promotes longevity.Aging cell · 2022Article
- Article
- Vitellogenins - Yolk Gene Function and Regulation inFrontiers in physiology · 2019Review
- The TGF-β Family inCold Spring Harbor perspectives in biology · 2017Review
- Regulation of C. elegans neuronal differentiation by the ZEB-family factor ZAG-1 and the NK-2 homeodomain factor CEH-28.PloS one · 2014Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
M4 is a multifunctional neuron in the Caenorhabditis elegans pharynx that can both stimulate peristaltic contractions of the muscles in the pharyngeal isthmus and function systemically to regulate an enhanced sensory response under hypoxic conditions. Here we identify a third function for M4 that depends on activation of the TGF-β family gene dbl-1 by the homeodomain transcription factor CEH-28. dbl-1 is expressed in M4 and a subset of other neurons, and we show CEH-28 specifically activates dbl-1 expression in M4. Characterization of the dbl-1 promoter indicates that CEH-28 targets an M4-specific enhancer within the dbl-1 promoter region, while expression in other neurons is mediated by separate regulatory sequences. Unlike ceh-28 mutants, dbl-1 mutants do not exhibit M4 synaptic and signaling defects. Instead, both ceh-28 and dbl-1 mutants exhibit morphological defects in the g1 gland cells located adjacent to M4 in the pharynx, and these defects can be partially rescued by M4-specific expression of dbl-1 in these mutants. Identical gland cell defects are observed in sma-6 and daf-4 mutants defective in the receptor for DBL-1, but they are not observed in sma-2 and sma-3 mutants lacking the R-Smads functioning downstream of this receptor. Together these results identify a novel neuroendocrine function for M4 and provide evidence for an R-Smad-independent mechanism for DBL-1 signaling in C. elegans.
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