|Citation||Mikl M, Cowan CR. Alternative 3' UTR selection controls PAR-5 homeostasis and cell polarity in C. elegans embryos. Cell Rep, 2014.|
|Short Description||Alternative 3' UTR selection controls PAR-5 homeostasis and cell polarity in C. elegans embryos. |
GEO Record: GSE59705 Platform: GPL13776
Download gene-centric, log2 transformed data: WBPaper00045705.ce.rs.csv
|# of Conditions||8|
|Full Description||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.