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   <subfield code="a">10.1007/s00425-015-2373-6</subfield>
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   <subfield code="a">Narciclasine, a potential allelochemical, affects subcellular trafficking of auxin transporter proteins and actin cytoskeleton dynamics in Arabidopsis roots</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Yanfeng Hu, Xiaofan Na, Jiaolong Li, Lijing Yang, Jia You, Xiaolei Liang, Jianfeng Wang, Liang Peng, Yurong Bi]</subfield>
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   <subfield code="a">Main conclusion : The present study documented the action of a potential allelochemical, narciclasine, on auxin transport in Arabidopsis by mainly affecting subcellular trafficking of PIN and AUX1 proteins and through interfering actin cytoskeletal organization. Narciclasine (NCS), an Amaryllidaceae alkaloid isolated from Narcissus tazetta bulbs, has potential allelopathic activity and affects auxin transport. However, little is known about the cellular mechanism of this inhibitory effect of NCS on auxin transport. The present study characterizes the effects of NCS at the cellular level using transgenic Arabidopsis plants harboring the promoters of PIN, in combination with PIN-GFP proteins or AUX1-YFP fusions. NCS treatment caused significant reduction in the abundance of PIN and AUX1 proteins at the plasma membrane (PM). Analysis of the subcellular distribution of PIN and AUX1 proteins in roots revealed that NCS induced the intracellular accumulation of auxin transporters, including PIN2, PIN3, PIN4, PIN7 and AUX1. However, other PM proteins, such as PIP2, BRI1, and low temperature inducible protein 6b (LTI6b), were insensitive to NCS treatment. NCS-induced PIN2 compartments were further defined using endocytic tracer FM 4-64 labeled early endosomes and suggested that this compound affects the endocytosis trafficking of PIN proteins. Furthermore, pharmacological analysis indicated that the brefeldin A (BFA)-insensitive pathway is employed in the cellular effects of NCS on PIN2 trafficking. Although NCS did not alter actin dynamics in vitro, it resulted in the depolymerization of the actin cytoskeleton in vivo. This disruption of actin filaments by NCS subsequently influences the actin-based vesicle motility. Hence, the elucidation of the specific role of NCS is useful for further understanding the mechanisms of allelopathy at the phytohormone levels.</subfield>
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   <subfield code="a">Springer-Verlag Berlin Heidelberg, 2015</subfield>
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   <subfield code="a">Allelochemical</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">Auxin</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">Auxin transport</subfield>
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   <subfield code="a">Actin cytoskeleton</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">ARF : ADP-ribosylation factor family of GTP-binding proteins</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">AUX1/LAX : AUXIN RESISTANT1/LIKE AUXIN RESISTANT</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">BFA : Brefeldin A</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">eEF1A : Elongation factor one alpha</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">GEF : Guanine nucleotide exchange factor</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">LatB : Latrunculin B</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">NCS : Narciclasine</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">PIN : PIN-FORMED auxin efflux carrier protein</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">PM : Plasma membrane</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">TIBA : 2,3,5-Triiodobenzoic acid</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">TryA23 : Tyrphostin A23</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">Hu</subfield>
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   <subfield code="u">Ministry of Education Key Laboratory of Cell Activities and Stress Adaptations, School of Life Sciences, Lanzhou University, 730000, Lanzhou, People's Republic of China</subfield>
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   <subfield code="a">Na</subfield>
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   <subfield code="u">Ministry of Education Key Laboratory of Cell Activities and Stress Adaptations, School of Life Sciences, Lanzhou University, 730000, Lanzhou, People's Republic of China</subfield>
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   <subfield code="a">Li</subfield>
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   <subfield code="u">Ministry of Education Key Laboratory of Cell Activities and Stress Adaptations, School of Life Sciences, Lanzhou University, 730000, Lanzhou, People's Republic of China</subfield>
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   <subfield code="a">Yang</subfield>
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   <subfield code="a">You</subfield>
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   <subfield code="u">School of Life Science, Northwest Normal University, 730070, Lanzhou, People's Republic of China</subfield>
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   <subfield code="D">Yurong</subfield>
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   <subfield code="t">Planta</subfield>
   <subfield code="d">Springer Berlin Heidelberg</subfield>
   <subfield code="g">242/6(2015-12-01), 1349-1360</subfield>
   <subfield code="x">0032-0935</subfield>
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   <subfield code="a">BK010053</subfield>
   <subfield code="b">XK010053</subfield>
   <subfield code="c">XK010000</subfield>
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   <subfield code="a">Metadata rights reserved</subfield>
   <subfield code="b">Springer special CC-BY-NC licence</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="D">1</subfield>
   <subfield code="a">research-article</subfield>
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