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Dev Cell. 2015 Jul 6;34(1):108-18. doi: 10.1016/j.devcel.2015.05.024. Epub 2015 Jun 18.

POS-1 Promotes Endo-mesoderm Development by Inhibiting the Cytoplasmic Polyadenylation of neg-1 mRNA.

Author information

1
Program in Molecular Medicine, RNA Therapeutics Institute and Howard Hughes Medical Institute, University of Massachusetts Medical School, 368 Plantation Street, Worcester, MA 01605, USA.
2
Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Worcester, MA 01605, USA.
3
Victorian Bioinformatics Consortium, Monash University, Clayton, Victoria 3800, Australia; Life Sciences Computation Centre, Victorian Life Sciences Computation Initiative, Carlton, Victoria 3053, Australia.
4
Developmental Biology Program, Sloan-Kettering Institute, New York, NY 10065, USA.
5
Department of Biology and Biotechnology, Worcester Polytechnic Institute, Life Science and Bioengineering Center, Gateway Park, 60 Prescott Street, Worcester, MA 01605, USA.
6
Department of Biochemistry and Molecular Biology, Monash University, Clayton, Victoria 3800, Australia.
7
Program in Molecular Medicine, RNA Therapeutics Institute and Howard Hughes Medical Institute, University of Massachusetts Medical School, 368 Plantation Street, Worcester, MA 01605, USA. Electronic address: craig.mello@umassmed.edu.

Abstract

The regulation of mRNA translation is of fundamental importance in biological mechanisms ranging from embryonic axis specification to the formation of long-term memory. POS-1 is one of several CCCH zinc-finger RNA-binding proteins that regulate cell fate specification during C. elegans embryogenesis. Paradoxically, pos-1 mutants exhibit striking defects in endo-mesoderm development but have wild-type distributions of SKN-1, a key determinant of endo-mesoderm fates. RNAi screens for pos-1 suppressors identified genes encoding the cytoplasmic poly(A)-polymerase homolog GLD-2, the Bicaudal-C homolog GLD-3, and the protein NEG-1. We show that NEG-1 localizes in anterior nuclei, where it negatively regulates endo-mesoderm fates. In posterior cells, POS-1 binds the neg-1 3' UTR to oppose GLD-2 and GLD-3 activities that promote NEG-1 expression and cytoplasmic lengthening of the neg-1 mRNA poly(A) tail. Our findings uncover an intricate series of post-transcriptional regulatory interactions that, together, achieve precise spatial expression of endo-mesoderm fates in C. elegans embryos.

PMID:
26096734
PMCID:
PMC4507413
DOI:
10.1016/j.devcel.2015.05.024
[Indexed for MEDLINE]
Free PMC Article

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