ArticleDevelopmental biology2017
The C. elegans Spalt-like protein SEM-4 functions through the SoxC transcription factor SEM-2 to promote a proliferative blast cell fate in the postembryonic mesoderm.
Article in Developmental biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- eIF5A and polyamines restrict mRNA levels in response to ribosome stalls.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- A Coffin-Siris syndrome-associated mutation modeled in Caenorhabditis elegans affects multiple developmental processes.G3 (Bethesda, Md.) · 2025Article
- A function of Spalt proteins in heterochromatin organization and maintenance of genomic DNA integrity.Development (Cambridge, England) · 2025Article
- SEM-2/SoxC regulates multiple aspects of C. elegans postembryonic mesoderm development.PLoS genetics · 2025Article
- SEM-2/SoxC regulates multiple aspects ofbioRxiv : the preprint server for biology · 2024Article
- Investigation of Conserved Amino Acids in the EGL-15 5A Domain Required for Sex Myoblast Migration inmicroPublication biology · 2024Article
- Article
- Positive autoregulation ofDevelopment (Cambridge, England) · 2020Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Proper development of a multicellular organism relies on well-coordinated regulation of cell fate specification, cell proliferation and cell differentiation. The C. elegans postembryonic mesoderm provides a useful system for uncovering factors involved in these processes and for further dissecting their regulatory relationships. The single Spalt-like zinc finger containing protein SEM-4/SALL is known to be involved in specifying the proliferative sex myoblast (SM) fate. We have found that SEM-4/SALL is sufficient to promote the SM fate and that it does so in a cell autonomous manner. We further showed that SEM-4/SALL acts through the SoxC transcription factor SEM-2 to promote the SM fate. SEM-2 is known to promote the SM fate by inhibiting the expression of two BWM-specifying transcription factors. In light of recent findings in mammals showing that Sall4, one of the mammalian homologs of SEM-4, contributes to pluripotency regulation by inhibiting differentiation, our work suggests that the function of SEM-4/SALL proteins in regulating pluripotency versus differentiation appears to be evolutionarily conserved.
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