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Cell Rep. 2014 Sep 11;8(5):1380-90. doi: 10.1016/j.celrep.2014.08.004. Epub 2014 Sep 4.

Alternative 3' UTR selection controls PAR-5 homeostasis and cell polarity in C. elegans embryos.

Author information

1
Research Institute of Molecular Pathology (IMP), 1030 Vienna, Austria. Electronic address: mmikl@gmx.at.
2
Research Institute of Molecular Pathology (IMP), 1030 Vienna, Austria. Electronic address: cowan@imp.ac.at.

Abstract

Cell polarity in one-cell C. elegans embryos guides asymmetric cell division and cell-fate specification. Shortly after fertilization, embryos establish two antagonistic cortical domains of PAR proteins. Here, we find that the conserved polarity factor PAR-5 regulates PAR domain size in a dose-dependent manner. Using quantitative imaging and controlled genetic manipulation, we find that PAR-5 protein levels reflect the cumulative output of three mRNA isoforms with different translational efficiencies mediated by their 3' UTRs. 3' UTR selection is regulated, influencing PAR-5 protein abundance. Alternative splicing underlies the selection of par-5 3' UTR isoforms. 3' UTR splicing is enhanced by the SR protein kinase SPK-1, and accordingly, SPK-1 is required for wild-type PAR-5 levels and PAR domain size. Precise regulation of par-5 isoform selection is essential for polarization when the posterior PAR network is compromised. Together, strict control of PAR-5 protein levels and feedback from polarity to par-5 3' UTR selection confer robustness to embryo polarization.

PMID:
25199833
DOI:
10.1016/j.celrep.2014.08.004
[Indexed for MEDLINE]
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