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Verfasst von:Fecht-Bartenbach, Jennifer von der [VerfasserIn]   i
 Schumacher, Karin [VerfasserIn]   i
Titel:Function of the anion transporter AtCLC-d in the trans-Golgi network
Verf.angabe:Jennifer von der Fecht-Bartenbach, Martin Bogner, Melanie Krebs, York-Dieter Stierhof, Karin Schumacher, Uwe Ludewig
Umfang:9 S.
Fussnoten:Gesehen am 09.05.2017
Titel Quelle:Enthalten in: The plant journal
Jahr Quelle:2007
Band/Heft Quelle:50(2007), 3, S. 466-474
ISSN Quelle:1365-313X
Abstract:Anion transporting proteins of the CLC type are involved in anion homeostasis in a variety of organisms. CLCs from Arabidopsis have been shown to participate in nitrate accumulation and storage. In this study, the physiological role of the functional chloride transporter AtCLC-d from Arabidopsis was investigated. AtCLC-d is weakly expressed in various tissues, including the root. When transiently expressed as a GFP fusion in protoplasts, it co-localized with the VHA-a1 subunit of the proton-transporting V-type ATPase in the trans-Golgi network (TGN). Stable expression in plants showed that it co-localized with the endocytic tracer dye FM4-64 in a brefeldin A-sensitive compartment. Immunogold electron microscopy confirmed the localization of AtCLC-d to the TGN. Disruption of the AtCLC-d gene by a T-DNA insertion did not affect the nitrate and chloride contents. The overall morphology of these clcd-1 plants was similar to that of the wild-type, but root growth on synthetic medium was impaired. Moreover, the sensitivity of hypocotyl elongation to treatment with concanamycin A, a blocker of the V-ATPase, was stronger in the clcd-1 mutant. These phenotypes could be complemented by overexpression of AtCLC-d in the mutant background. The results suggest that the luminal pH in the trans-Golgi network is adjusted by AtCLC-d-mediated transport of a counter anion such as Cl− or NO3−.
DOI:doi:10.1111/j.1365-313X.2007.03061.x
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Kostenfrei: Verlag: http://dx.doi.org/10.1111/j.1365-313X.2007.03061.x
 Kostenfrei: Verlag: http://onlinelibrary.wiley.com/doi/10.1111/j.1365-313X.2007.03061.x/abstract
 DOI: https://doi.org/10.1111/j.1365-313X.2007.03061.x
Datenträger:Online-Ressource
Sprache:eng
K10plus-PPN:1558370935
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