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First published online 8 October 2008
doi: 10.1242/dev.027060
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1 Molecular and Cellular Biology Program, University of Washington, Seattle, WA
98195, USA.
2 Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle,
WA 98109, USA.
3 Howard Hughes Medical Institute, Seattle, WA 98109, USA.
4 Department of Biology, University of Washington, Seattle, WA 98195, USA.
Author for correspondence (e-mail:
jpriess{at}fhcrc.org)
Accepted 9 September 2008
Anteroposterior polarity in early C. elegans embryos is required for the specification of somatic and germline lineages, and is initiated by a sperm-induced reorganization of the cortical cytoskeleton and PAR polarity proteins. Through mechanisms that are not understood, the kinases PAR-1 and PAR-4, and other PAR proteins cause the cytoplasmic zinc finger protein MEX-5 to accumulate asymmetrically in the anterior half of the one-cell embryo. We show that MEX-5 asymmetry requires neither vectorial transport to the anterior, nor protein degradation in the posterior. MEX-5 has a restricted mobility before fertilization and in the anterior of one-cell embryos. However, MEX-5 mobility in the posterior increases as asymmetry develops, presumably allowing accumulation in the anterior. The MEX-5 zinc fingers and a small, C-terminal domain are essential for asymmetry; the zinc fingers restrict MEX-5 mobility, and the C-terminal domain is required for the increase in posterior mobility. We show that a crucial residue in the C-terminus, Ser 458, is phosphorylated in vivo. PAR-1 and PAR-4 kinase activities are required for the phosphorylation of S458, providing a link between PAR polarity proteins and the cytoplasmic asymmetry of MEX-5.
Key words: MEX-5, PAR-1, PAR-4, CCCH zinc finger proteins, C. elegans
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