@article{11122, abstract = {Nuclear pore complexes (NPCs) are large multiprotein assemblies that allow traffic between the cytoplasm and the nucleus. During mitosis in higher eukaryotes, the Nuclear Envelope (NE) breaks down and NPCs disassemble. How NPCs reassemble and incorporate into the NE upon mitotic exit is poorly understood. We demonstrate a function for the conserved Nup107-160 complex in this process. Partial in vivo depletion of Nup133 or Nup107 via RNAi in HeLa cells resulted in reduced levels of multiple nucleoporins and decreased NPC density in the NE. Immunodepletion of the entire Nup107-160 complex from in vitro nuclear assembly reactions produced nuclei with a continuous NE but no NPCs. This phenotype was reversible only if Nup107-160 complex was readded before closed NE formation. Depletion also prevented association of FG-repeat nucleoporins with chromatin. We propose a stepwise model in which postmitotic NPC assembly initiates on chromatin via early recruitment of the Nup107-160 complex.}, author = {Walther, Tobias C. and Alves, Annabelle and Pickersgill, Helen and Loı̈odice, Isabelle and HETZER, Martin W and Galy, Vincent and Hülsmann, Bastian B. and Köcher, Thomas and Wilm, Matthias and Allen, Terry and Mattaj, Iain W. and Doye, Valérie}, issn = {0092-8674}, journal = {Cell}, keywords = {General Biochemistry, Genetics and Molecular Biology}, number = {2}, pages = {195--206}, publisher = {Elsevier}, title = {{The conserved Nup107-160 complex is critical for nuclear pore complex assembly}}, doi = {10.1016/s0092-8674(03)00235-6}, volume = {113}, year = {2003}, } @article{2989, abstract = {In contrast to animals, little is known about pattern formation in plants. Physiological and genetic data suggest the involvement of the phytohormone auxin in this process. Here, we characterize a novel member of the PIN family of putative auxin efflux carriers, Arabidopsis PIN4, that is localized in developing and mature root meristems. Atpin4 mutants are defective in establishment and maintenance of endogenous auxin gradients, fail to canalize externally applied auxin, and display various patterning defects in both embryonic and seedling roots. We propose a role for AtPIN4 in generating a sink for auxin below the quiescent center of the root meristem that is essential for auxin distribution and patterning.}, author = {Friml, Jirí and Benková, Eva and Blilou, Ikram and Wiśniewska, Justyna and Hamann, Thorsten and Ljung, Karin and Woody, Scott and Sandberg, Göran and Scheres, Ben and Jürgens, Gerd and Palme, Klaus}, issn = {0092-8674}, journal = {Cell}, number = {5}, pages = {661 -- 673}, publisher = {Cell Press}, title = {{AtPIN4 mediates sink-driven auxin gradients and root patterning in Arabidopsis}}, doi = {10.1016/S0092-8674(02)00656-6}, volume = {108}, year = {2002}, } @article{2586, abstract = {The role of inhibitory Golgi cells in cerebellar function was investigated by selectively ablating Golgi cells expressing human interleukin-2 receptor α subunit in transgenic mice, using the immunotoxin- mediated cell targeting technique. Golgi cell disruption caused severe acute motor disorders. These mice showed gradual recovery but retained a continuing inability to perform compound movements. Optical and electrical recordings combined with immunocytological analysis indicated that elimination of Golgi cells not only reduces GABA-mediated inhibition but also attenuates functional NMDA receptors in granule cells. These results demonstrate that synaptic integration involving both GABA inhibition and NMDA receptor activation is essential for compound motor coordination. Furthermore, this integration can adapt after Golgi cell elimination so as not to evoke overexcitation by the reduction of NMDA receptors.}, author = {Watanabe, Dai and Inokawa, Hitoshi and Hashimoto, Kouichi and Suzuki, Noboru and Kano, Masanobu and Shigemoto, Ryuichi and Hirano, Tomoo and Toyama, Keisuke and Kaneko, Satoshi and Yokoi, Mineto and Moriyoshi, Koki and Suzuki, Misao and Kobayashi, Kazuto and Nagatsu, Toshiharu and Kreitman, Robert and Pastan, Ira and Nakanishi, Shigetada}, issn = {0092-8674}, journal = {Cell}, number = {1}, pages = {17 -- 27}, publisher = {Cell Press}, title = {{Ablation of cerebellar Golgi cells disrupts synaptic integration involving GABA inhibition and NMDA receptor activation in motor coordination}}, doi = {10.1016/S0092-8674(00)81779-1}, volume = {95}, year = {1998}, } @article{6160, abstract = {Natural isolates of C. elegans exhibit either solitary or social feeding behavior. Solitary foragers move slowly on a bacterial lawn and disperse across it, while social foragers move rapidly on bacteria and aggregate together. A loss-of-function mutation in the npr-1 gene, which encodes a predicted G protein–coupled receptor similar to neuropeptide Y receptors, causes a solitary strain to take on social behavior. Two isoforms of NPR-1 that differ at a single residue occur in the wild. One isoform, NPR-1 215F, is found exclusively in social strains, while the other isoform, NPR-1 215V, is found exclusively in solitary strains. An NPR-1 215V transgene can induce solitary feeding behavior in a wild social strain. Thus, isoforms of a putative neuropeptide receptor generate natural variation in C. elegans feeding behavior.}, author = {de Bono, Mario and Bargmann, Cornelia I}, issn = {0092-8674}, journal = {Cell}, number = {5}, pages = {679--689}, publisher = {Elsevier}, title = {{Natural variation in a neuropeptide Y receptor homolog modifies social behavior and food response in C. elegans}}, doi = {10.1016/s0092-8674(00)81609-8}, volume = {94}, year = {1998}, } @article{2559, abstract = {Taking advantage of the restricted expression of metabotropic glutamate receptor subtype 6 (mGIuR6) in retinal ON bipolar cells, we generated knockout mice lacking mGIuR6 expression. The homozygous mutant mice showed a loss of ON responses but unchanged OFF responses to light. The mutant mice displayed no obvious changes in retinal cell organization nor in the projection of optic fibers to the brain. Furthermore, the mGIuR6-deficient mice showed visual behavioral responses to light stimulation as examined by shuttle box avoidance behavior experiments using light exposure as a conditioned stimulus. The results demonstrate that mGIuR6 is essential in synaptic transmission to the ON bipolar cell and that the OFF response provides an important means for transmitting visual information.}, author = {Masu, Masayuki and Iwakabe, Hideki and Tagawa, Yoshiaki and Miyoshi, Tomomitsu and Yamashita, Masayuki and Fukuda, Yutaka and Sasaki, Hitoshi and Hiroi, Kano and Nakamura, Yasuhisa and Shigemoto, Ryuichi and Takada, Masahiko and Nakamura, Kenji and Nakao, Kazuki and Katsuki, Motoya and Nakanishi, Shigetada}, issn = {0092-8674}, journal = {Cell}, number = {5}, pages = {757 -- 765}, publisher = {Cell Press}, title = {{Specific deficit of the ON response in visual transmission by targeted disruption of the mGIuR6 gene}}, doi = {10.1016/0092-8674(95)90354-2}, volume = {80}, year = {1995}, } @article{2554, abstract = {The retinal bipolar cell receiving glutamate transmission from photoreceptors mediates a key process in segregating visual signals into ON center and OFF center pathways. This transmission involves a G protein- coupled metabotropic glutamate receptor (mGluR). Immunocytochemical and immunoelectron microscopic studies indicate the restricted localization of a specific mGluR subtype, mGluR6, at the postsynaptic site of the rat rod bipolar cell. This specialization is developmentally regulated: mGluR6 is initially distributed in both the soma and dendrites and is finally concentrated on the postsynaptic site. The mGluR6 localization is reversed when photoreceptors degenerate in the mutant rat with retinal dystrophy. Evidence is thus presented indicating specialized, developmentally regulated receptor distribution in the central nervous system and the crucial role of mGluR6 in photoreceptor-bipolar cell synaptic transmission.}, author = {Nomura, Akinori and Shigemoto, Ryuichi and Nakamura, Yasuhisa and Okamoto, Naoyuki and Mizuno, Noboru and Nakanishi, Shigetada}, issn = {0092-8674}, journal = {Cell}, number = {3}, pages = {361 -- 369}, publisher = {Cell Press}, title = {{Developmentally regulated postsynaptic localization of a metabotropic glutamate receptor in rat rod bipolar cells}}, doi = {10.1016/0092-8674(94)90151-1}, volume = {77}, year = {1994}, }