Anteroposterior polarity in the C. elegans embryo begins with the sperm-induced formation of an anterior cortical actomyosin cap and the asymmetric cortical localisation of the PAR polarity proteins. The subsequent accumulation of the zinc finger protein MEX-5 in the anterior cytoplasm converts this cortical asymmetry into cytoplasmic mRNA and protein asymmetries, but what establishes MEX-5 asymmetry? Tenlen and co-workers now uncover a novel link between the PAR polarity proteins and this asymmetry (see ). MEX-5 has restricted mobility before fertilisation and in the anterior of one-cell embryos, they report, but in the embryo's posterior its mobility increases as asymmetry develops. They show that a C-terminal domain is required for this increased mobility and identify a crucial residue (Ser458) in the domain that is phosphorylated in vivo. Because the kinase activities of PAR-1 and PAR-4 are required to phosphorylate this residue, the researchers suggest that its phosphorylation might be the elusive link between the PAR proteins and the cytoplasmic asymmetry of MEX-5.
