Translational control of maternal mRNAs is a major form of gene regulation during germline development and embryogenesis. In Caenorhabditis elegans, the maternal gene
glp-1 encodes a homolog of the Notch transmembrane protein required for cell proliferation in the germline and cell fate specification in the embryo. The RNA binding proteins POS-1 and GLD-1 directly regulate the translation of GLP-1 protein by binding to the specific elements within the
glp-1 3' untranslated region (3' UTR). When POS-1 or GLD-1 binding is disrupted by mutation of their respective elements, the expression pattern of a
glp-1 3' UTR transgene changes in both the germline and in embryos. The mechanism by which POS-1 and GLD-1 mediate translation repression is not well understood. Previous work showed that loss of
pos-1 increases the average polyA tail length of endogenous
glp-1 transcripts in embryos. Here, we show that mutation of either the GLD-1 or POS-1 binding motifs in transgenic reporters does not change polyA site selection. This result rules out alternative polyA site usage as a mechanism of regulation. We also show that wild-type
glp-1 transgenic reporter embryos have a shorter average polyA tail length compared to mutant transgenic reporters in GLD-1 or POS-1 binding motifs. We further used our reporters to measure the effect of cytoplasmic polyA polymerases, deadenylases and translation initiation factors on the
glp-1 expression level and pattern. The results reveal that POS-1 and GLD-1 exert their effects through different pathways. Our studies provide insights of into the mechanism of
glp-1 post-transcriptional regulation in the germline and embryo.