Title

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

UMMS Affiliation

Program in Molecular Medicine; RNA Therapeutics Institute; Department of Biochemistry and Molecular Pharmacology

Publication Date

2015-07-06

Document Type

Article

Subjects

Animals; Caenorhabditis elegans; Caenorhabditis elegans Proteins; Carrier Proteins; Cell Differentiation; Cytoplasm; Gene Expression Regulation, Developmental; Germ Cells; Mesoderm; Nuclear Proteins; Polyadenylation; RNA, Helminth; RNA, Messenger

Disciplines

Cell Biology | Developmental Biology | Molecular Biology

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.

DOI of Published Version

10.1016/j.devcel.2015.05.024

Source

Dev Cell. 2015 Jul 6;34(1):108-18. doi: 10.1016/j.devcel.2015.05.024. Epub 2015 Jun 18. Link to article on publisher's site

Journal/Book/Conference Title

Developmental cell

Related Resources

Link to Article in PubMed

PubMed ID

26096734

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