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Richard C Crain - One of the best experts on this subject based on the ideXlab platform.

  • abscisic acid induced phosphoinositide turnover in guard cell protoplasts of vicia faba
    Plant Physiology, 1996
    Co-Authors: Yunjung Choi, J F Kelleher, Sarah M. Assmann, Richard C Crain
    Abstract:

    Guard cell protoplasts of Vicia faba treated with 10 [mu]M (+)abscisic acid (ABA) in the light exhibited a 20% decrease in diameter within 1.5 h, from 24.1 to 19.6 [mu]m. Within 10 s of administration of ABA, a 90% increase in levels of inositol 1,4,5-trisphosphate was observed, provided that cells were treated with Li+, an inhibitor of inositol phosphatase activity, prior to incubation. Concomitantly, levels of 32P-labeled phosphatidylinositol 4,5-bisphosphate and phosphatidylinositol 4-phosphate decreased 20% compared to levels in control cells; levels of label in the membrane lipids phosphatidylcholine, phosphatidylethanolamine, and phosphatidylglycerol did not change significantly in response to ABA treatment. These results show that phosphoinositide turnover is activated in response to ABA in guard cells. We conclude that phosphoinositide signaling is likely to be a step in the Biochemical Cascade that couples ABA to guard cell shrinking and stomatal closure.

  • Abscisic Acid-lnduced Phosphoinositide Turnover in Cuard Cell Protoplasts of Vicia faba'
    1996
    Co-Authors: Youngsook Lee, J F Kelleher, Sarah M. Assmann, Young B. Choi, Sujeoung Suh, Joonsang Lee, Cheol O. Joe, Richard C Crain
    Abstract:

    Cuard cell protoplasts of Vicia faba treated with 10 p~ (+)abscisic acid (ABA) in the light exhibited a 20% decrease in diameter within 1.5 h, from 24.1 to 19.6 pm. Within 1 O s of administration of ABA, a 90% increase in levels of inositol 1,4,5-trisphosphate was observed, provided that cells were treated-with Li+, an inhibitor of inositol phosphatase activity, prior to incubation. Concomitantly, levels of 32P-labeled phosphatidylinositol 4,5-bisphosphate and phosphatidylinositol 4-phosphate decreased 20% compared to levels in control cells; levels of label in the membrane lipids phosphatidylcholine, phosphatidylethanolamine, and phosphatidylglycerol did not change significantly in response to ABA treatment. These results show that phosphoinositide turnover is activated in response to ABA in guard cells. We conclude that phosphoinositide signaling is likely to be a step in the Biochemical Cascade that couples ABA to guard cell shrinking and stomatal closure.

Yunjung Choi - One of the best experts on this subject based on the ideXlab platform.

  • abscisic acid induced phosphoinositide turnover in guard cell protoplasts of vicia faba
    Plant Physiology, 1996
    Co-Authors: Yunjung Choi, J F Kelleher, Sarah M. Assmann, Richard C Crain
    Abstract:

    Guard cell protoplasts of Vicia faba treated with 10 [mu]M (+)abscisic acid (ABA) in the light exhibited a 20% decrease in diameter within 1.5 h, from 24.1 to 19.6 [mu]m. Within 10 s of administration of ABA, a 90% increase in levels of inositol 1,4,5-trisphosphate was observed, provided that cells were treated with Li+, an inhibitor of inositol phosphatase activity, prior to incubation. Concomitantly, levels of 32P-labeled phosphatidylinositol 4,5-bisphosphate and phosphatidylinositol 4-phosphate decreased 20% compared to levels in control cells; levels of label in the membrane lipids phosphatidylcholine, phosphatidylethanolamine, and phosphatidylglycerol did not change significantly in response to ABA treatment. These results show that phosphoinositide turnover is activated in response to ABA in guard cells. We conclude that phosphoinositide signaling is likely to be a step in the Biochemical Cascade that couples ABA to guard cell shrinking and stomatal closure.

J F Kelleher - One of the best experts on this subject based on the ideXlab platform.

  • abscisic acid induced phosphoinositide turnover in guard cell protoplasts of vicia faba
    Plant Physiology, 1996
    Co-Authors: Yunjung Choi, J F Kelleher, Sarah M. Assmann, Richard C Crain
    Abstract:

    Guard cell protoplasts of Vicia faba treated with 10 [mu]M (+)abscisic acid (ABA) in the light exhibited a 20% decrease in diameter within 1.5 h, from 24.1 to 19.6 [mu]m. Within 10 s of administration of ABA, a 90% increase in levels of inositol 1,4,5-trisphosphate was observed, provided that cells were treated with Li+, an inhibitor of inositol phosphatase activity, prior to incubation. Concomitantly, levels of 32P-labeled phosphatidylinositol 4,5-bisphosphate and phosphatidylinositol 4-phosphate decreased 20% compared to levels in control cells; levels of label in the membrane lipids phosphatidylcholine, phosphatidylethanolamine, and phosphatidylglycerol did not change significantly in response to ABA treatment. These results show that phosphoinositide turnover is activated in response to ABA in guard cells. We conclude that phosphoinositide signaling is likely to be a step in the Biochemical Cascade that couples ABA to guard cell shrinking and stomatal closure.

  • Abscisic Acid-lnduced Phosphoinositide Turnover in Cuard Cell Protoplasts of Vicia faba'
    1996
    Co-Authors: Youngsook Lee, J F Kelleher, Sarah M. Assmann, Young B. Choi, Sujeoung Suh, Joonsang Lee, Cheol O. Joe, Richard C Crain
    Abstract:

    Cuard cell protoplasts of Vicia faba treated with 10 p~ (+)abscisic acid (ABA) in the light exhibited a 20% decrease in diameter within 1.5 h, from 24.1 to 19.6 pm. Within 1 O s of administration of ABA, a 90% increase in levels of inositol 1,4,5-trisphosphate was observed, provided that cells were treated-with Li+, an inhibitor of inositol phosphatase activity, prior to incubation. Concomitantly, levels of 32P-labeled phosphatidylinositol 4,5-bisphosphate and phosphatidylinositol 4-phosphate decreased 20% compared to levels in control cells; levels of label in the membrane lipids phosphatidylcholine, phosphatidylethanolamine, and phosphatidylglycerol did not change significantly in response to ABA treatment. These results show that phosphoinositide turnover is activated in response to ABA in guard cells. We conclude that phosphoinositide signaling is likely to be a step in the Biochemical Cascade that couples ABA to guard cell shrinking and stomatal closure.

Sarah M. Assmann - One of the best experts on this subject based on the ideXlab platform.

  • abscisic acid induced phosphoinositide turnover in guard cell protoplasts of vicia faba
    Plant Physiology, 1996
    Co-Authors: Yunjung Choi, J F Kelleher, Sarah M. Assmann, Richard C Crain
    Abstract:

    Guard cell protoplasts of Vicia faba treated with 10 [mu]M (+)abscisic acid (ABA) in the light exhibited a 20% decrease in diameter within 1.5 h, from 24.1 to 19.6 [mu]m. Within 10 s of administration of ABA, a 90% increase in levels of inositol 1,4,5-trisphosphate was observed, provided that cells were treated with Li+, an inhibitor of inositol phosphatase activity, prior to incubation. Concomitantly, levels of 32P-labeled phosphatidylinositol 4,5-bisphosphate and phosphatidylinositol 4-phosphate decreased 20% compared to levels in control cells; levels of label in the membrane lipids phosphatidylcholine, phosphatidylethanolamine, and phosphatidylglycerol did not change significantly in response to ABA treatment. These results show that phosphoinositide turnover is activated in response to ABA in guard cells. We conclude that phosphoinositide signaling is likely to be a step in the Biochemical Cascade that couples ABA to guard cell shrinking and stomatal closure.

  • Abscisic Acid-lnduced Phosphoinositide Turnover in Cuard Cell Protoplasts of Vicia faba'
    1996
    Co-Authors: Youngsook Lee, J F Kelleher, Sarah M. Assmann, Young B. Choi, Sujeoung Suh, Joonsang Lee, Cheol O. Joe, Richard C Crain
    Abstract:

    Cuard cell protoplasts of Vicia faba treated with 10 p~ (+)abscisic acid (ABA) in the light exhibited a 20% decrease in diameter within 1.5 h, from 24.1 to 19.6 pm. Within 1 O s of administration of ABA, a 90% increase in levels of inositol 1,4,5-trisphosphate was observed, provided that cells were treated-with Li+, an inhibitor of inositol phosphatase activity, prior to incubation. Concomitantly, levels of 32P-labeled phosphatidylinositol 4,5-bisphosphate and phosphatidylinositol 4-phosphate decreased 20% compared to levels in control cells; levels of label in the membrane lipids phosphatidylcholine, phosphatidylethanolamine, and phosphatidylglycerol did not change significantly in response to ABA treatment. These results show that phosphoinositide turnover is activated in response to ABA in guard cells. We conclude that phosphoinositide signaling is likely to be a step in the Biochemical Cascade that couples ABA to guard cell shrinking and stomatal closure.

Wendy H. Raskind - One of the best experts on this subject based on the ideXlab platform.

  • hereditary spastic paraplegia advances in genetic research
    Neurology, 1996
    Co-Authors: Terry Heimanpatterson, Franca Cambi, J. L. Haines, Mariepierre Dube, Margaret A Pericakvance, Afif Hentati, Denise A. Figlewicz, Thomas D. Bird, Wendy H. Raskind
    Abstract:

    Hereditary spastic paraplegia (HSP) is a diverse group of inherited disorders characterized by progressive lower-extremity spasticity and weakness. Insight into the genetic basis of these disorders is expanding rapidly. Uncomplicated autosomal dominant, autosomal recessive, and X-linked HSP are genetically heterogeneous: different genes cause clinically indistinguishable disorders. A locus for autosomal recessive HSP is on chromosome 8q. Loci for autosomal dominant HSP have been identified on chromosomes 2p, 14q, and 15q. One locus (Xq22) has been identified for X-linked, uncomplicated HSP and shown to be due to a proteolipoprotein gene mutation in one family. The existence of HSP families for whom these loci are excluded indicates the existence of additional, as yet unidentified HSP loci. There is marked clinical similarity among HSP families linked to each of these loci, suggesting that gene products from HSP loci may participate in a common Biochemical Cascade, which, if disturbed, results in axonal degeneration that is maximal at the ends of the longest CNS axons. Identifying the single gene defects that cause HSPs distal axonopathy may provide insight into factors responsible for development and maintenance of axonal integrity. We review clinical, genetic, and pathologic features of HSP and present differential diagnosis and diagnostic criteria of this important group of disorders. We discuss polymorphic microsatellite markers useful for genetic linkage analysis and genetic counseling in HSP. NEUROLOGY 1996;46: 1507-1514