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- Volume 24, 2008
Annual Review of Cell and Developmental Biology - Volume 24, 2008
Volume 24, 2008
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Protein Kinases: Starting a Molecular Systems View of Endocytosis
Vol. 24 (2008), pp. 501–523More LessThe field of endocytosis is in strong need of formal biophysical modeling and mathematical analysis. At the same time, endocytosis must be much better integrated into cellular physiology to understand the former's complex behavior in such a wide range of phenotypic variations. Furthermore, the concept that endocytosis provides the space-time for signal transduction can now be experimentally addressed. In this review, we discuss these principles and argue for a systematic and top-down approach to study the endocytic membrane system. We provide a summary of published observations on protein kinases regulating endocytic machinery components and discuss global unbiased approaches to further map out kinase regulatory networks. In particular, protein phosphorylation is at the heart of controlling the physical properties of endocytosis and of integrating these physical properties into the signal transduction networks of the cell to allow a fine-tuned response to the continuously varying physiological conditions of a cell.
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Comparative Aspects of Animal Regeneration
Vol. 24 (2008), pp. 525–549More LessMost but not all phyla include examples of species that are able to regenerate large sections of the body plan. The mechanisms underlying regeneration on this scale are currently being studied in a variety of contexts in both vertebrates and invertebrates. Regeneration generally involves the formation of a wound epithelium after transection or injury, followed by the generation of regenerative progenitor cells and morphogenesis to give the regenerate. Common mechanisms may exist in relation to each of these aspects. For example, the initial proliferation of progenitor cells often depends on the nerve supply, whereas morphogenesis reflects the generation of positional disparity between adjacent cells—the principle of intercalation. These mechanisms are reviewed here across a range of contexts. We also consider the evolutionary origins of regeneration and how regeneration may relate to both agametic reproduction and to ontogeny.
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Cell Polarity Signaling in Arabidopsis
Vol. 24 (2008), pp. 551–575More LessCell polarization is intimately linked to plant development, growth, and responses to the environment. Major advances have been made in our understanding of the signaling pathways and networks that regulate cell polarity in plants owing to recent studies on several model systems, e.g., tip growth in pollen tubes, cell morphogenesis in the leaf epidermis, and polar localization of PINs. From these studies we have learned that plant cells use conserved mechanisms such as Rho family GTPases to integrate both plant-specific and conserved polarity cues and to coordinate the cytoskeketon dynamics/reorganization and vesicular trafficking required for polarity establishment and maintenance. This review focuses upon signaling mechanisms for cell polarity formation in Arabidopsis, with an emphasis on Rho GTPase signaling in polarized cell growth and how these mechanisms compare with those for cell polarity signaling in yeast and animal systems.
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Hunter to Gatherer and Back: Immunological Synapses and Kinapses as Variations on the Theme of Amoeboid Locomotion
Vol. 24 (2008), pp. 577–596More LessThe immunological synapse was initially defined as a stable cell-cell junction composed of three concentric supramolecular activation clusters (SMACs) enriched in particular components: a central SMAC with clustered antigen receptors and kinases, a peripheral SMAC rich in β2 integrin adhesion molecule LFA-1, and a distal SMAC marked by a critical tyrosine phosphatase. In the past year the SMACs have each been identified with functional modules of amoeboid motility, and the stability of the immunological synapse has been revealed as a reconfiguration of the motile apparatus from an asymmetric hunting mode, a kinapse, to a symmetric gathering mode, the synapse. The genetic control of this process involves actinomyosin regulators PKCθ and WASp. Crtam is involved in postsynaptic polarity in early kinapses prior to cell division. It is unlikely that the immune system is unique in using symmetrization to stop migration without inactivating motile machinery.
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Dscam-Mediated Cell Recognition Regulates Neural Circuit Formation
Vol. 24 (2008), pp. 597–620More LessThe Dscam family of immunoglobulin cell surface proteins mediates recognition events between neurons that play an essential role in the establishment of neural circuits. The Drosophila Dscam1 locus encodes tens of thousands of cell surface proteins via alternative splicing. These isoforms exhibit exquisite isoform-specific binding in vitro that mediates homophilic repulsion in vivo. These properties provide the molecular basis for self-avoidance, an essential developmental mechanism that allows axonal and dendritic processes to uniformly cover their synaptic fields. In a mechanistically similar fashion, homophilic repulsion mediated by Drosophila Dscam2 prevents processes from the same class of cells from occupying overlapping synaptic fields through a process called tiling. Genetic studies in the mouse visual system support the view that vertebrate DSCAM also promotes both self-avoidance and tiling. By contrast, DSCAM and DSCAM-L promote layer-specific targeting in the chick visual system, presumably through promoting homophilic adhesion. The fly and mouse studies underscore the importance of homophilic repulsion in regulating neural circuit assembly, whereas the chick studies suggest that DSCAM proteins may mediate a variety of different recognition events during wiring in a context-dependent fashion.
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Previous Volumes
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Volume 40 (2024)
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Volume 39 (2023)
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Volume 38 (2022)
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Volume 37 (2021)
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Volume 36 (2020)
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Volume 35 (2019)
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Volume 34 (2018)
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Volume 33 (2017)
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Volume 32 (2016)
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Volume 31 (2015)
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Volume 30 (2014)
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Volume 29 (2013)
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Volume 28 (2012)
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Volume 27 (2011)
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Volume 26 (2010)
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Volume 25 (2009)
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Volume 24 (2008)
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Volume 23 (2007)
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Volume 22 (2006)
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Volume 21 (2005)
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Volume 20 (2004)
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Volume 19 (2003)
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Volume 18 (2002)
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Volume 17 (2001)
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Volume 16 (2000)
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Volume 15 (1999)
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Volume 14 (1998)
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Volume 13 (1997)
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Volume 12 (1996)
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Volume 11 (1995)
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Volume 10 (1994)
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Volume 9 (1993)
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Volume 8 (1992)
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Volume 7 (1991)
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Volume 6 (1990)
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Volume 5 (1989)
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Volume 4 (1988)
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Volume 3 (1987)
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Volume 2 (1986)
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Volume 1 (1985)
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Volume 0 (1932)