Journal article
Reciprocal asymmetry of SYS-1/β-catenin and POP-1/TCF controls asymmetric divisions in Caenorhabditis elegans
Proceedings of the National Academy of Sciences - PNAS, Vol.104(9), pp.3231-3236
02/27/2007
DOI: 10.1073/pnas.0611507104
PMCID: PMC1796998
PMID: 17296929
Abstract
β-Catenins are conserved regulators of metazoan development that function with TCF DNA-binding proteins to activate transcription. In
Caenorhabditis elegans
, SYS-1/β-catenin and POP-1/TCF regulate several asymmetric divisions, including that of the somatic gonadal precursor cell (SGP). In the distal but not the proximal SGP daughter, SYS-1/β-catenin and POP-1/TCF transcriptionally activate
ceh-22
to specify the distal fate. Here, we investigate the distribution of SYS-1/β-catenin and its regulation. Using a rescuing transgene, VNS::SYS-1, which fuses VENUS fluorescent protein to SYS-1, we find more VNS::SYS-1 in distal than proximal SGP daughters, a phenomenon we call “SYS-1 asymmetry.” In addition, SYS-1 asymmetry is seen in many other tissues, consistent with the idea that SYS-1 regulates asymmetric divisions broadly during
C. elegans
development. In particular, SYS-1 is more abundant in E than MS, and SYS-1 is critical for the endodermal fate. In all cases, SYS-1 is reciprocal to POP-1 asymmetry: cells with higher SYS-1 have lower POP-1, and vice versa. SYS-1 asymmetry is controlled posttranslationally and relies on frizzled and dishevelled homologs, which also control POP-1 asymmetry. Therefore, upstream regulators modulate the SYS-1 to POP-1 ratio by increasing SYS-1 and decreasing POP-1 within the same cell. By contrast, SYS-1 asymmetry does not rely on WRM-1, which appears specialized for POP-1 asymmetry. We suggest a two-pronged pathway for control of SYS-1:POP-1, which can robustly accomplish differential gene expression in daughters of an asymmetric cell division.
Details
- Title: Subtitle
- Reciprocal asymmetry of SYS-1/β-catenin and POP-1/TCF controls asymmetric divisions in Caenorhabditis elegans
- Creators
- Bryan T Phillips - Departments of Biochemistry andAmbrose R Kidd - Program in Cellular and Molecular Biology, University of Wisconsin, Madison, WI 53706; andRyan King - Program in Cellular and Molecular Biology, University of Wisconsin, Madison, WI 53706; andJeff Hardin - Zoology and Program in Cellular and Molecular Biology, University of Wisconsin, Madison, WI 53706; andJudith Kimble - Departments of Biochemistry and Program in Cellular and Molecular Biology, University of Wisconsin, Madison, WI 53706; and The Howard Hughes Medical Institute, University of Wisconsin, 433 Babcock Drive, Madison, WI 53706
- Resource Type
- Journal article
- Publication Details
- Proceedings of the National Academy of Sciences - PNAS, Vol.104(9), pp.3231-3236
- DOI
- 10.1073/pnas.0611507104
- PMID
- 17296929
- PMCID
- PMC1796998
- NLM abbreviation
- Proc Natl Acad Sci U S A
- ISSN
- 0027-8424
- eISSN
- 1091-6490
- Publisher
- National Academy of Sciences
- Language
- English
- Date published
- 02/27/2007
- Academic Unit
- Biology
- Record Identifier
- 9984217539402771
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