First published online October 24, 2008
Development 135, 2201e (2008)
© The Company of Biologists Limited
MEX-5 takes its PARtners for asymmetry
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
p. 3665). 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.

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Related articles in Development:
- MEX-5 asymmetry in one-cell C. elegans embryos requires PAR-4- and PAR-1-dependent phosphorylation
- Jennifer R. Tenlen, Jeffrey N. Molk, Nitobe London, Barbara D. Page, and James R. Priess
Development 2008 135: 3665-3675.
[Abstract]
[Full Text]