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Dev Biol. 2015 Aug 1;404(1):66-79. doi: 10.1016/j.ydbio.2015.04.025. Epub 2015 May 8.

MED GATA factors promote robust development of the C. elegans endoderm.

Author information

1
Biology Department, University of California, Riverside, Riverside, CA 92521, United States. Electronic address: mmaduro@ucr.edu.
2
Biology Department, University of California, Riverside, Riverside, CA 92521, United States.
3
Cell, Molecular and Developmental Biology Graduate Program, University of California, Riverside, Riverside, CA, United States.
4
MARCU-STAR Program, University of California, Riverside, Riverside, CA, United States.
5
Graduate Program in Bioinformatics and Systems Biology, University of California, San Diego, La Jolla, CA, United States.
6
Section of Ecology, Behavior, and Evolution, Division of Biology, University of California, San Diego, La Jolla, CA, United States.

Abstract

The MED-1,2 GATA factors contribute to specification of E, the progenitor of the Caenorhabditis elegans endoderm, through the genes end-1 and end-3, and in parallel with the maternal factors SKN-1, POP-1 and PAL-1. END-1,3 activate elt-2 and elt-7 to initiate a program of intestinal development, which is maintained by positive autoregulation. Here, we advance the understanding of MED-1,2 in E specification. We find that expression of end-1 and end-3 is greatly reduced in med-1,2(-) embryos. We generated strains in which MED sites have been mutated in end-1 and end-3. Without MED input, gut specification relies primarily on POP-1 and PAL-1. 25% of embryos fail to make intestine, while those that do display abnormal numbers of gut cells due to a delayed and stochastic acquisition of intestine fate. Surviving adults exhibit phenotypes consistent with a primary defect in the intestine. Our results establish that MED-1,2 provide robustness to endoderm specification through end-1 and end-3, and reveal that gut differentiation may be more directly linked to specification than previously appreciated. The results argue against an "all-or-none" description of cell specification, and suggest that activation of tissue-specific master regulators, even when expression of these is maintained by positive autoregulation, does not guarantee proper function of differentiated cells.

KEYWORDS:

C. elegans; Cell specification; Endoderm; GATA factors; Gene regulation; Gene regulatory networks; Robustness

PMID:
25959238
PMCID:
PMC4469534
DOI:
10.1016/j.ydbio.2015.04.025
[Indexed for MEDLINE]
Free PMC Article

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