ArticlePloS one2014
Uncoupling different characteristics of the C. elegans E lineage from differentiation of intestinal markers.
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 11 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Meta-analysis of Caenorhabditis elegans single-cell developmental data reveals multi-frequency oscillation in gene activation.Bioinformatics (Oxford, England) · 2020Pooled it
- Cell lineage-resolved embryonic morphological map reveals signaling associated with cell fate and size asymmetry.Nature communications · 2025Article
- Evolutionary Change in Gut Specification inJournal of developmental biology · 2023Review
- Cell-based allometry: an approach for evaluation of complexity in morphogenesis.Quantitative biology (Beijing, China) · 2023Article
- Reciprocal signaling by Wnt and Notch specifies a muscle precursor in the C. elegans embryo.Development (Cambridge, England) · 2017Article
- cdc-25.4, a Caenorhabditis elegans Ortholog of cdc25, Is Required for Male Mating Behavior.G3 (Bethesda, Md.) · 2016Article
- Timing of Tissue-specific Cell Division Requires a Differential Onset of Zygotic Transcription during Metazoan Embryogenesis.The Journal of biological chemistry · 2016Article
- Article
- Quantitative Differences in Nuclear β-catenin and TCF Pattern Embryonic Cells in C. elegans.PLoS genetics · 2015Article
- MED GATA factors promote robust development of the C. elegans endoderm.Developmental biology · 2015Article
- Systems-level quantification of division timing reveals a common genetic architecture controlling asynchrony and fate asymmetry.Molecular systems biology · 2015Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
In the 4-cell C. elegans embryo, a signal from P2 to its anterior sister, EMS, specifies the posterior daughter of EMS, E, as the sole founder cell for intestine. The P2-to-EMS signal restricts high level zygotic expression of the redundant GATA transcription factors, END-1 and END-3, to only the E lineage. Expression of END-1 or END-3 in early blastomeres is sufficient to drive intestinal differentiation. We show here that a number of E lineage characteristics, which are also regulated through P2-EMS signaling, can be uncoupled from intestine development, and each with a different sensitivity to specific perturbations of the P2-EMS signal. For example, we show that the extended cell cycle in Ea and Ep depends on the P2-induced high level expression of the cell cycle regulator, WEE-1.1, in E. A mutation in wee-1.1 results in shortened Ea and Ep cell cycles, but has no effect upon intestinal differentiation or embryogenesis. Furthermore, it has been shown previously that the total number of E lineage cell divisions is regulated by a mechanism dependent upon E being specified as the intestinal founder cell. We now show, however, that cell division counting can be uncoupled from intestine differentiation in the E lineage. Many mutations in P2-EMS signal genes exhibit nonfully-penetrant defects in intestinal differentiation. When embryos with those mutations generate intestinal cells, they often make too many intestinal cells. In addition, at the level of individual embryos, expression of end-1 and end-3, and another very early E-specific zygotic gene, sdz-23, exhibit stochastic and discordant defects in P2-EMS signaling mutants. We show here that sdz-23 is expressed close to wildtype levels in embryos deleted of both end-1 and end-3. sdz-23 does not appear to function in intestine development, raising the intriguing possibility that the P2-EMS interaction has downstream molecular consequences within the E lineage independent of end-1/3 and intestinal development.
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