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First published online October 24, 2008


Development 135, 2201e (2008)
© The Company of Biologists Limited
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In this issue

MEX-5 takes its PARtners for asymmetry


Figure 1

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]  




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