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Mol Biol Cell 2011 Jun 15;2212:2042-53. doi: 10.1091/mbc.E10-10-0844.
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Atypical protein kinase C controls sea urchin ciliogenesis.

Prulière G , Cosson J , Chevalier S , Sardet C , Chenevert J .

The atypical protein kinase C (aPKC) is part of the conserved aPKC/PAR6/PAR3 protein complex, which regulates many cell polarity events, including the formation of a primary cilium at the apical surface of epithelial cells. Cilia are highly organized, conserved, microtubule-based structures involved in motility, sensory processes, signaling, and cell polarity. We examined the distribution and function of aPKC in the sea urchin embryo, which forms a swimming blastula covered with motile cilia. We found that in the early embryo aPKC is uniformly cortical and becomes excluded from the vegetal pole during unequal cleavages at the 8- to 64-cell stages. During the blastula and gastrula stages the kinase localizes at the base of cilia, forming a ring at the transition zone between the basal body and the elongating axoneme. A dose-dependent and reversible inhibition of aPKC results in mislocalization of the kinase, defective ciliogenesis, and lack of swimming. Thus, as in the primary cilium of differentiated mammalian cells, aPKC controls the growth of motile cilia in invertebrate embryos. We suggest that aPKC might function to phosphorylate kinesin and so activate the transport of intraflagellar vesicles.

PubMed ID: 21508313
PMC ID: PMC3113769
Article link: Mol Biol Cell

Genes referenced: LOC100887844 LOC115919910 LOC115925415 LOC586799 LOC594566 pbrm1 pkcl2 pole taf12 tubgcp2

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References [+] :
Alford, Cell polarity emerges at first cleavage in sea urchin embryos. 2009, Pubmed, Echinobase