Gravitropism and Lateral Root Emergence are Dependent on the Trans-Golgi Network Protein TNO1

被引:4
作者
Roy, Rahul [1 ,2 ]
Bassham, Diane C. [1 ,2 ,3 ]
机构
[1] Iowa State Univ, Dept Genet Dev & Cell Biol, Ames, IA 50011 USA
[2] Iowa State Univ, Interdept Genet Program, Ames, IA USA
[3] Iowa State Univ, Inst Plant Sci, Ames, IA USA
基金
美国国家航空航天局;
关键词
auxin; trans-Golgi network; lateral root; gravitropism; tethering factor; AUXIN TRANSPORT; SNARE PROTEINS; ENDOMEMBRANE SYSTEM; PLANT DEVELOPMENT; ARABIDOPSIS; TRAFFICKING; CELLS; ACID; ENDOCYTOSIS; VESICLE;
D O I
10.3389/fpls.2015.00969
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
The trans-Golgi network (TGN) is a dynamic organelle that functions as a relay station for receiving endocytosed cargo, directing secretory cargo, and trafficking to the vacuole. TON-localized SYP41-interacting protein (TNO1) is a large, TGN-localized, coiled-coil protein that associates with the membrane fusion protein SYP41, a target SNARE, and is required for efficient protein trafficking to the vacuole. Here, we show that a tool mutant has auxin transport related defects. Mutant roots have delayed lateral root emergence, decreased gravitropic bending of plant organs and increased sensitivity to the auxin analog 2,4-dichlorophenoxyacetic acid and the natural auxin 3-indoleacetic acid. Auxin asymmetry at the tips of elongating stage II lateral roots was reduced in the tool mutant, suggesting a role for TNO1 in cellular auxin transport during lateral root emergence. During gravistimulation, tool roots exhibited delayed auxin transport from the columella to the basal epidermal cells. Endocytosis to the TGN was unaffected in the mutant, indicating that bulk endocytic defects are not responsible for the observed phenotypes. Together these studies demonstrate a role for TNO1 in mediating auxin responses during root development and gravistimulation, potentially through trafficking of auxin transport proteins.
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页数:13
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