Wdpcp, a PCP Protein Required for Ciliogenesis, Regulates Directional Cell Migration and Cell Polarity by Direct Modulation of the Actin Cytoskeleton
http://www.plosbiology.org/article/info%3Adoi%2F10.1371%2Fjournal.pbio.1001720
This article discusses how cilia and ciliogenesis play a role in planar cell polarity. Planar cell polarity (PCP) regulates cell alignment for cell movement during embryonic development. which requires PCP and PCP effector proteins. These proteins coincidentally play an important role in ciliogenesis. After further research on PCP effectors, it was found that Wdpcp regulates both ciliogenesis AND cell movement; unfortunately the mechanism of this protein is relatively unknown. Studies of Wdpcp were executed by depriving mice of these genes. The Wdpcp depleted mice exibited cardiac outflow tracts and cochlea defects. Also, scientists found out that Wdpcp is useful for the recruitment of proteins responsible for ciliogenesis. Wdpcp is also found in cytoskeleton where is found in actin as well as focal adhesions. In the mice without Wdpcp, a actin filaments were unable to get recruited, this associates with decreased membrane "ruffling", failure to establish cell polarity, as well as a loss of directional cell migration. This allows scientist to believe that PCP defects in Wdpcp are caused by a direct of actin cytoskeleton, and not because of of a loss of cilia. This claim was fortified when Wdpcp mutant cochlea has normal kinocilia yet still has PCP defects.
This article discusses how cilia and ciliogenesis play a role in planar cell polarity. Planar cell polarity (PCP) regulates cell alignment for cell movement during embryonic development. which requires PCP and PCP effector proteins. These proteins coincidentally play an important role in ciliogenesis. After further research on PCP effectors, it was found that Wdpcp regulates both ciliogenesis AND cell movement; unfortunately the mechanism of this protein is relatively unknown. Studies of Wdpcp were executed by depriving mice of these genes. The Wdpcp depleted mice exibited cardiac outflow tracts and cochlea defects. Also, scientists found out that Wdpcp is useful for the recruitment of proteins responsible for ciliogenesis. Wdpcp is also found in cytoskeleton where is found in actin as well as focal adhesions. In the mice without Wdpcp, a actin filaments were unable to get recruited, this associates with decreased membrane "ruffling", failure to establish cell polarity, as well as a loss of directional cell migration. This allows scientist to believe that PCP defects in Wdpcp are caused by a direct of actin cytoskeleton, and not because of of a loss of cilia. This claim was fortified when Wdpcp mutant cochlea has normal kinocilia yet still has PCP defects.
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