The Experts below are selected from a list of 53571 Experts worldwide ranked by ideXlab platform
Alan Hall - One of the best experts on this subject based on the ideXlab platform.
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cdc42 regulates gsk 3beta and adenomatous polyposis coli to control Cell Polarity
Nature, 2003Co-Authors: Sandrine Etiennemanneville, Alan HallAbstract:Cell Polarity is a fundamental property of all Cells. In higher eukaryotes, the small GTPase Cdc42, acting through a Par6-atypical protein kinase C (aPKC) complex, is required to establish Cellular asymmetry during epithelial morphogenesis, asymmetric Cell division and directed Cell migration. However, little is known about what lies downstream of this complex. Here we show, through the use of primary rat astrocytes in a Cell migration assay, that Par6-PKCzeta interacts directly with and regulates glycogen synthase kinase-3beta (GSK-3beta) to promote polarization of the centrosome and to control the direction of Cell protrusion. Cdc42-dependent phosphorylation of GSK-3beta occurs specifically at the leading edge of migrating Cells, and induces the interaction of adenomatous polyposis coli (Apc) protein with the plus ends of microtubules. The association of Apc with microtubules is essential for Cell polarization. We conclude that Cdc42 regulates Cell Polarity through the spatial regulation of GSK-3beta and Apc. This role for Apc may contribute to its tumour-suppressor activity.
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cdc42 regulates gsk 3beta and adenomatous polyposis coli to control Cell Polarity
Nature, 2003Co-Authors: Sandrine Etiennemanneville, Alan HallAbstract:Cell Polarity is a fundamental property of all Cells. In higher eukaryotes, the small GTPase Cdc42, acting through a Par6–atypical protein kinase C (aPKC) complex, is required to establish Cellular asymmetry during epithelial morphogenesis, asymmetric Cell division and directed Cell migration1,2,3,4,5. However, little is known about what lies downstream of this complex. Here we show, through the use of primary rat astrocytes in a Cell migration assay, that Par6–PKCζ interacts directly with and regulates glycogen synthase kinase-3β (GSK-3β) to promote polarization of the centrosome and to control the direction of Cell protrusion. Cdc42-dependent phosphorylation of GSK-3β occurs specifically at the leading edge of migrating Cells, and induces the interaction of adenomatous polyposis coli (Apc) protein with the plus ends of microtubules. The association of Apc with microtubules is essential for Cell polarization. We conclude that Cdc42 regulates Cell Polarity through the spatial regulation of GSK-3β and Apc. This role for Apc may contribute to its tumour-suppressor activity.
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Cell Polarity par6 apkc and cytoskeletal crosstalk
Current Opinion in Cell Biology, 2003Co-Authors: Sandrine Etiennemanneville, Alan HallAbstract:Par6 and atypical protein kinase C are key players in the establishment of Cell Polarity. First discovered in Caenorhabditis elegans, the function of this protein complex is conserved in all multiCellular organisms. Recent work is beginning to throw light on how it converts information generated by extraCellular cues into intraCellular asymmetry.
Sandrine Etiennemanneville - One of the best experts on this subject based on the ideXlab platform.
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cdc42 regulates gsk 3beta and adenomatous polyposis coli to control Cell Polarity
Nature, 2003Co-Authors: Sandrine Etiennemanneville, Alan HallAbstract:Cell Polarity is a fundamental property of all Cells. In higher eukaryotes, the small GTPase Cdc42, acting through a Par6-atypical protein kinase C (aPKC) complex, is required to establish Cellular asymmetry during epithelial morphogenesis, asymmetric Cell division and directed Cell migration. However, little is known about what lies downstream of this complex. Here we show, through the use of primary rat astrocytes in a Cell migration assay, that Par6-PKCzeta interacts directly with and regulates glycogen synthase kinase-3beta (GSK-3beta) to promote polarization of the centrosome and to control the direction of Cell protrusion. Cdc42-dependent phosphorylation of GSK-3beta occurs specifically at the leading edge of migrating Cells, and induces the interaction of adenomatous polyposis coli (Apc) protein with the plus ends of microtubules. The association of Apc with microtubules is essential for Cell polarization. We conclude that Cdc42 regulates Cell Polarity through the spatial regulation of GSK-3beta and Apc. This role for Apc may contribute to its tumour-suppressor activity.
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cdc42 regulates gsk 3beta and adenomatous polyposis coli to control Cell Polarity
Nature, 2003Co-Authors: Sandrine Etiennemanneville, Alan HallAbstract:Cell Polarity is a fundamental property of all Cells. In higher eukaryotes, the small GTPase Cdc42, acting through a Par6–atypical protein kinase C (aPKC) complex, is required to establish Cellular asymmetry during epithelial morphogenesis, asymmetric Cell division and directed Cell migration1,2,3,4,5. However, little is known about what lies downstream of this complex. Here we show, through the use of primary rat astrocytes in a Cell migration assay, that Par6–PKCζ interacts directly with and regulates glycogen synthase kinase-3β (GSK-3β) to promote polarization of the centrosome and to control the direction of Cell protrusion. Cdc42-dependent phosphorylation of GSK-3β occurs specifically at the leading edge of migrating Cells, and induces the interaction of adenomatous polyposis coli (Apc) protein with the plus ends of microtubules. The association of Apc with microtubules is essential for Cell polarization. We conclude that Cdc42 regulates Cell Polarity through the spatial regulation of GSK-3β and Apc. This role for Apc may contribute to its tumour-suppressor activity.
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Cell Polarity par6 apkc and cytoskeletal crosstalk
Current Opinion in Cell Biology, 2003Co-Authors: Sandrine Etiennemanneville, Alan HallAbstract:Par6 and atypical protein kinase C are key players in the establishment of Cell Polarity. First discovered in Caenorhabditis elegans, the function of this protein complex is conserved in all multiCellular organisms. Recent work is beginning to throw light on how it converts information generated by extraCellular cues into intraCellular asymmetry.
Enrico Scarpella - One of the best experts on this subject based on the ideXlab platform.
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coordination of tissue Cell Polarity by auxin transport and signaling
eLife, 2019Co-Authors: Carla Verna, Sree Janani Ravichandran, Megan G. Sawchuk, Nguyen Manh Linh, Enrico ScarpellaAbstract:Plants coordinate the Polarity of hundreds of Cells during vein formation, but how they do so is unclear. The prevailing hypothesis proposes that GNOM, a regulator of membrane trafficking, positions PIN-FORMED auxin transporters to the correct side of the plasma membrane; the resulting Cell-to-Cell, polar transport of auxin would coordinate tissue Cell Polarity and induce vein formation. Contrary to predictions of the hypothesis, we find that vein formation occurs in the absence of PIN-FORMED or any other interCellular auxin-transporter; that the residual auxin-transport-independent vein-patterning activity relies on auxin signaling; and that a GNOM-dependent signal acts upstream of both auxin transport and signaling to coordinate tissue Cell Polarity and induce vein formation. Our results reveal synergism between auxin transport and signaling, and their unsuspected control by GNOM in the coordination of tissue Cell Polarity during vein patterning, one of the most informative expressions of tissue Cell polarization in plants.
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coordination of tissue Cell Polarity by auxin transport and signaling
bioRxiv, 2019Co-Authors: Sree Janani Ravichandran, Megan G. Sawchuk, Nguyen Manh Linh, Carla Verna, Enrico ScarpellaAbstract:Abstract Coordination of Polarity between Cells in tissues is key to multiCellular organism development. In animals, coordination of this tissue Cell Polarity often requires direct Cell-Cell interactions and Cell movements, which are precluded in plants by a wall that separates Cells and holds them in place; yet plants coordinate the Polarity of hundreds of Cells during the formation of the veins in their leaves. Overwhelming experimental evidence suggests that the plant signaling molecule auxin coordinates tissue Cell Polarity to induce vein formation, but how auxin does so is unclear. The prevailing hypothesis proposes that GNOM, a regulator of vesicle formation during protein trafficking, positions auxin transporters of the PIN-FORMED family to the correct side of the plasma membrane. The resulting Cell-to-Cell, polar transport of auxin would coordinate tissue Cell Polarity and would induce vein formation. Here we tested this hypothesis by means of a combination of Cellular imaging, molecular genetic analysis, and chemical induction and inhibition. Contrary to predictions of the hypothesis, we find that auxin-induced vein formation occurs in the absence of PIN-FORMED proteins or any known interCellular auxin transporter, that the residual auxin-transport-independent vein-patterning activity relies on auxin signaling, and that a GNOM-dependent signal that coordinates tissue Cell Polarity to induce vein formation acts upstream of both auxin transport and signaling. Our results reveal synergism between auxin transport and signaling, and their unsuspected control by GNOM, in the coordination of tissue Cell Polarity during vein patterning, one of the most spectacular and informative expressions of tissue Cell polarization in plants.
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coordination of Cell Polarity and the patterning of leaf vein networks
Current Opinion in Plant Biology, 2018Co-Authors: Nguyen Manh Linh, Carla Verna, Enrico ScarpellaAbstract:During development, the behavior of Cells in tissues is coordinated along specific orientations or directions by coordinating the polar localization of components in those Cells. The coordination of such Cell Polarity is perhaps nowhere more spectacular than in developing leaves, where the Polarity of hundreds of Cells is coordinated in the leaf epidermis and inner tissue to pattern vein networks. Available evidence suggests that the spectacular coordination of Cell Polarity that patterns vein networks is controlled by auxin transport and levels, and by genes that have been implicated in the polar localization of auxin transporters.
Helena E Richardson - One of the best experts on this subject based on the ideXlab platform.
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abnormalities in Cell proliferation and apico basal Cell Polarity are separable in drosophila lgl mutant clones in the developing eye
Developmental Biology, 2007Co-Authors: Nicola A Grzeschik, Helena E Richardson, Nancy Amin, Julie Secombe, Anthony M BrumbyAbstract:Abstract In homozygous mutants of Drosophila lethal-2-giant larvae (lgl), tissues lose apico-basal Cell Polarity and exhibit ectopic proliferation. Here, we use clonal analysis in the developing eye to investigate the effect of lgl null mutations in the context of surrounding wild-type tissue. lgl− clones in the larval eye disc exhibit ectopic expression of the G1–S regulator, Cyclin E, and ectopic proliferation, but do not lose apico-basal Cell Polarity. Decreasing the perdurance of Lgl protein in larval eye disc clones, by forcing extra proliferation of lgl− tissue (using a Minute background), leads to a loss in Cell Polarity and to more extreme ectopic Cell proliferation. Later in development at the pupal stage, lgl mutant photoreceptor Cells show aberrant apico-basal Cell Polarity, but this is not associated with ectopic proliferation, presumably because Cells are differentiated. Thus in a clonal context, the ectopic proliferation and Cell Polarity defects of lgl− mutants are separable. Furthermore, lgl− mosaic eye discs have alterations in the normal patterns of apoptosis: in larval discs some lgl− and wild-type Cells at the clonal boundary undergo apoptosis and are excluded from the epithelia, but apoptosis is decreased elsewhere in the disc, and in pupal retinas lgl− tissue shows less apoptosis.
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dlg scribble and lgl in Cell Polarity Cell proliferation and cancer
BioEssays, 2003Co-Authors: Patrick O Humbert, Sarah M Russell, Helena E RichardsonAbstract:Dlg (Discs large), Scrib (Scribble) and Lgl (Lethal giant larvae) are evolutionarily conserved components of a common genetic pathway that link the seemingly disparate functions of Cell Polarity and Cell proliferation in epithelial Cells. dlg, scrib and lgl have been identified as tumour suppressor genes in Drosophila, mutations of which cause similar phenotypes, involving disruption of Cell Polarity and neoplastic overgrowth of tissues. The molecular mechanisms by which Dlg, Scrib and Lgl proteins regulate Cell proliferation are not clear, but there is some evidence that epithelial polarisation is required for this regulation. Dlg, Scrib and Lgl are highly conserved between human and Drosophila, and we discuss evidence that these proteins also play a role in cancer progression in humans.
Carla Verna - One of the best experts on this subject based on the ideXlab platform.
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coordination of tissue Cell Polarity by auxin transport and signaling
eLife, 2019Co-Authors: Carla Verna, Sree Janani Ravichandran, Megan G. Sawchuk, Nguyen Manh Linh, Enrico ScarpellaAbstract:Plants coordinate the Polarity of hundreds of Cells during vein formation, but how they do so is unclear. The prevailing hypothesis proposes that GNOM, a regulator of membrane trafficking, positions PIN-FORMED auxin transporters to the correct side of the plasma membrane; the resulting Cell-to-Cell, polar transport of auxin would coordinate tissue Cell Polarity and induce vein formation. Contrary to predictions of the hypothesis, we find that vein formation occurs in the absence of PIN-FORMED or any other interCellular auxin-transporter; that the residual auxin-transport-independent vein-patterning activity relies on auxin signaling; and that a GNOM-dependent signal acts upstream of both auxin transport and signaling to coordinate tissue Cell Polarity and induce vein formation. Our results reveal synergism between auxin transport and signaling, and their unsuspected control by GNOM in the coordination of tissue Cell Polarity during vein patterning, one of the most informative expressions of tissue Cell polarization in plants.
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coordination of tissue Cell Polarity by auxin transport and signaling
bioRxiv, 2019Co-Authors: Sree Janani Ravichandran, Megan G. Sawchuk, Nguyen Manh Linh, Carla Verna, Enrico ScarpellaAbstract:Abstract Coordination of Polarity between Cells in tissues is key to multiCellular organism development. In animals, coordination of this tissue Cell Polarity often requires direct Cell-Cell interactions and Cell movements, which are precluded in plants by a wall that separates Cells and holds them in place; yet plants coordinate the Polarity of hundreds of Cells during the formation of the veins in their leaves. Overwhelming experimental evidence suggests that the plant signaling molecule auxin coordinates tissue Cell Polarity to induce vein formation, but how auxin does so is unclear. The prevailing hypothesis proposes that GNOM, a regulator of vesicle formation during protein trafficking, positions auxin transporters of the PIN-FORMED family to the correct side of the plasma membrane. The resulting Cell-to-Cell, polar transport of auxin would coordinate tissue Cell Polarity and would induce vein formation. Here we tested this hypothesis by means of a combination of Cellular imaging, molecular genetic analysis, and chemical induction and inhibition. Contrary to predictions of the hypothesis, we find that auxin-induced vein formation occurs in the absence of PIN-FORMED proteins or any known interCellular auxin transporter, that the residual auxin-transport-independent vein-patterning activity relies on auxin signaling, and that a GNOM-dependent signal that coordinates tissue Cell Polarity to induce vein formation acts upstream of both auxin transport and signaling. Our results reveal synergism between auxin transport and signaling, and their unsuspected control by GNOM, in the coordination of tissue Cell Polarity during vein patterning, one of the most spectacular and informative expressions of tissue Cell polarization in plants.
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coordination of Cell Polarity and the patterning of leaf vein networks
Current Opinion in Plant Biology, 2018Co-Authors: Nguyen Manh Linh, Carla Verna, Enrico ScarpellaAbstract:During development, the behavior of Cells in tissues is coordinated along specific orientations or directions by coordinating the polar localization of components in those Cells. The coordination of such Cell Polarity is perhaps nowhere more spectacular than in developing leaves, where the Polarity of hundreds of Cells is coordinated in the leaf epidermis and inner tissue to pattern vein networks. Available evidence suggests that the spectacular coordination of Cell Polarity that patterns vein networks is controlled by auxin transport and levels, and by genes that have been implicated in the polar localization of auxin transporters.