Abstract
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.
Highlights
Caenorhabditis elegans embryogenesis begins with a series of polarized divisions that segregate germ cell precursors from cells that produce only somatic cell types
We refer to the asymmetrical localization of MEX-5 in the one-cell embryo and in later germline blastomeres as MEX-5 asymmetry, and to the degradation of MEX-5 in somatic blastomeres at and after the four-cell stage as somatic degradation
GFP:MEX-5 (82 kDa) is larger than GFP (27 kDa), this size difference alone would not be expected to appreciably impact simple diffusion; FRAP recovery rates for the diffusion of a 100 kDa protein are similar to that of GFP (Sprague and McNally, 2005), while the recovery rate for GFP:MEX-5 is much longer (>10-fold). We found that both ZF1 and ZF2 are required for the restricted mobility of MEX-5, and for MEX-5 asymmetry
Summary
Caenorhabditis elegans embryogenesis begins with a series of polarized divisions that segregate germ cell precursors from cells that produce only somatic cell types (reviewed by Gönczy and Rose, 2005). These divisions result in the asymmetric partitioning of several maternally provided proteins, such as PIE-1, which localizes exclusively to germ cell precursors (Mello et al, 1996). Understanding how polarity of the fertilized egg is established, and how this polarity leads to the asymmetric localization of proteins such as PIE-1, are major goals of research in C. elegans, and have provided general insights into mechanisms of cell and tissue polarity (for reviews, see Goldstein and Macara, 2007; Gönczy, 2008). A complex of anterior PAR proteins (PAR-3, PAR-6, PKC3) accumulates at the anterior cap, at least in part through association with the actomyosin network, while the kinase PAR-1 accumulates in a complementary pattern at the posterior cortex (for reviews, see Goldstein and Macara, 2007; Munro, 2006; Nance, 2005)
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