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      Microtubules induce self-organization of polarized PAR domains in C. elegans zygotes

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          Abstract

          A hallmark of polarized cells is the segregation of the PAR polarity regulators into asymmetric domains at the cell cortex 1, 2 . Antagonistic interactions involving two conserved kinases, atypical protein kinase C (aPKC) and PAR-1, have been implicated in polarity maintenance 1, 2 , but the mechanisms that initiate the formation of asymmetric PAR domains are not understood. Here, we describe one pathway used by the sperm-donated centrosome to polarize the PAR proteins in Caenorhabditis elegans zygotes. Before polarization, cortical aPKC excludes PAR-1 kinase and its binding partner PAR-2 by phosphorylation. During symmetry breaking, microtubules nucleated by the centrosome locally protect PAR-2 from phosphorylation by aPKC, allowing PAR-2 and PAR-1 to access the cortex nearest the centrosome. Cortical PAR-1 phosphorylates PAR-3, causing the PAR-3/aPKC complex to leave the cortex. Our findings illustrate how microtubules, independent of actin dynamics, stimulate the self-organization of PAR proteins by providing local protection against a global barrier imposed by aPKC.

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          Most cited references37

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          The PAR proteins: fundamental players in animal cell polarization.

          The par genes were discovered in genetic screens for regulators of cytoplasmic partitioning in the early embryo of C. elegans, and encode six different proteins required for asymmetric cell division by the worm zygote. Some of the PAR proteins are localized asymmetrically and form physical complexes with one another. Strikingly, the PAR proteins have been found to regulate cell polarization in many different contexts in diverse animals, suggesting they form part of an ancient and fundamental mechanism for cell polarization. Although the picture of how the PAR proteins function remains incomplete, cell biology and biochemistry are beginning to explain how PAR proteins polarize cells.
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            Cortical flows powered by asymmetrical contraction transport PAR proteins to establish and maintain anterior-posterior polarity in the early C. elegans embryo.

            The C. elegans PAR proteins PAR-3, PAR-6, and PKC-3 are asymmetrically localized and have essential roles in cell polarity. We show that the one-cell C. elegans embryo contains a dynamic and contractile actomyosin network that appears to be destabilized near the point of sperm entry. This asymmetry initiates a flow of cortical nonmuscle myosin (NMY-2) and F-actin toward the opposite, future anterior, pole. PAR-3, PAR-6, and PKC-3, as well as non-PAR proteins that associate with the cytoskeleton, appear to be transported to the anterior by this cortical flow. In turn, PAR-3, PAR-6, and PKC-3 modulate cortical actomyosin dynamics and promote cortical flow. PAR-2, which localizes to the posterior cortex, inhibits NMY-2 from accumulating at the posterior cortex during flow, thus maintaining asymmetry by preventing inappropriate, posterior-directed flows. Similar actomyosin flows accompany the establishment of PAR asymmetries that form after the one-cell stage, suggesting that actomyosin-mediated cortical flows have a general role in PAR asymmetry.
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              Cell polarity in eggs and epithelia: parallels and diversity.

              Cell polarity, the generation of cellular asymmetries, is necessary for diverse processes in animal cells, such as cell migration, asymmetric cell division, epithelial barrier function, and morphogenesis. Common mechanisms generate and transduce cell polarity in different cells, but cell type-specific processes are equally important. In this review, we highlight the similarities and differences between the polarity mechanisms in eggs and epithelia. We also highlight the prospects for future studies on how cortical polarity interfaces with other cellular processes, such as morphogenesis, exocytosis, and lipid signaling, and how defects in polarity contribute to tumor formation. Copyright 2010 Elsevier Inc. All rights reserved.
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                Author and article information

                Journal
                100890575
                21417
                Nat Cell Biol
                Nat. Cell Biol.
                Nature Cell Biology
                1465-7392
                1476-4679
                7 September 2011
                9 October 2011
                1 May 2012
                : 13
                : 11
                : 1361-1367
                Affiliations
                Department of Molecular Biology and Genetics, Howard Hughes Medical Institute, Center for Cell Dynamics, Johns Hopkins University School of Medicine, 725 N. Wolfe St., PCTB 706, Baltimore, MD 21205, USA
                Article
                nihpa322844
                10.1038/ncb2354
                3208083
                21983565
                f147834d-7f46-48a5-947c-2f12baa1eabb

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                Cell biology
                Cell biology

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