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Conserved Arabidopsis ECHIDNA protein mediates trans-Golgi-network trafficking and cell elongation

Conserved Arabidopsis ECHIDNA protein mediates trans-Golgi-network trafficking and cell elongation
Conserved Arabidopsis ECHIDNA protein mediates trans-Golgi-network trafficking and cell elongation
Multiple steps of plant growth and development rely on rapid cell elongation during which secretory and endocytic trafficking via the trans-Golgi network (TGN) plays a central role. Here, we identify the ECHIDNA (ECH) protein from Arabidopsis thaliana as a TGN-localized component crucial for TGN function. ECH partially complements loss of budding yeast TVP23 function and a Populus ECH complements the Arabidopsis ech mutant, suggesting functional conservation of the genes. Compared with wild-type, the Arabidopsis ech mutant exhibits severely perturbed cell elongation as well as defects in TGN structure and function, manifested by the reduced association between Golgi bodies and TGN as well as mislocalization of several TGN-localized proteins including vacuolar H+-ATPase subunit a1 (VHA-a1). Strikingly, ech is defective in secretory trafficking, whereas endocytosis appears unaffected in the mutant. Some aspects of the ech mutant phenotype can be phenocopied by treatment with a specific inhibitor of vacuolar H+-ATPases, concanamycin A, indicating that mislocalization of VHA-a1 may account for part of the defects in ech. Hence, ECH is an evolutionarily conserved component of the TGN with a central role in TGN structure and function.

secretory pathway, dwarf mutant, vacuolar defect
0027-8424
8048-8053
Gendre, Delphine
280ac5fd-29f9-4856-8bf0-851659bc6de1
Oh, Jaesung
763a2138-e7f9-466a-824e-a7df87b939f2
Boutte, Yuhann
5f8df443-5caa-430e-862d-2920cbac63f9
Best, Jacob G.
342a5836-182d-4453-8022-8006b097ef54
Samuels, Lacey
72c61e4f-4dc0-4188-a930-e06d5ef86e95
Nilsson, Robert
8ab590ac-bb36-49a0-9eb3-26299555e301
Uemura, Tomohiro
868874af-46dc-4c3f-9f0a-6f8dba3778f7
Marchant, Alan
3e54d51c-53b0-4df0-b428-2e73b071ee8e
Bennett, Malcolm J.
0b55f21b-a31d-406b-8b83-f06e2c451e32
Grebe, Markus
3b99935b-627b-4a6e-96e5-f16f6cfbf9df
Bhalerao, Rishikesh P.
7d29fc1b-920b-4f81-b805-14b4a45b7bb0
Gendre, Delphine
280ac5fd-29f9-4856-8bf0-851659bc6de1
Oh, Jaesung
763a2138-e7f9-466a-824e-a7df87b939f2
Boutte, Yuhann
5f8df443-5caa-430e-862d-2920cbac63f9
Best, Jacob G.
342a5836-182d-4453-8022-8006b097ef54
Samuels, Lacey
72c61e4f-4dc0-4188-a930-e06d5ef86e95
Nilsson, Robert
8ab590ac-bb36-49a0-9eb3-26299555e301
Uemura, Tomohiro
868874af-46dc-4c3f-9f0a-6f8dba3778f7
Marchant, Alan
3e54d51c-53b0-4df0-b428-2e73b071ee8e
Bennett, Malcolm J.
0b55f21b-a31d-406b-8b83-f06e2c451e32
Grebe, Markus
3b99935b-627b-4a6e-96e5-f16f6cfbf9df
Bhalerao, Rishikesh P.
7d29fc1b-920b-4f81-b805-14b4a45b7bb0

Gendre, Delphine, Oh, Jaesung, Boutte, Yuhann, Best, Jacob G., Samuels, Lacey, Nilsson, Robert, Uemura, Tomohiro, Marchant, Alan, Bennett, Malcolm J., Grebe, Markus and Bhalerao, Rishikesh P. (2011) Conserved Arabidopsis ECHIDNA protein mediates trans-Golgi-network trafficking and cell elongation. Proceedings of the National Academy of Sciences of the United States of America, 108 (19), 8048-8053. (doi:10.1073/pnas.1018371108). (PMID:21512130)

Record type: Article

Abstract

Multiple steps of plant growth and development rely on rapid cell elongation during which secretory and endocytic trafficking via the trans-Golgi network (TGN) plays a central role. Here, we identify the ECHIDNA (ECH) protein from Arabidopsis thaliana as a TGN-localized component crucial for TGN function. ECH partially complements loss of budding yeast TVP23 function and a Populus ECH complements the Arabidopsis ech mutant, suggesting functional conservation of the genes. Compared with wild-type, the Arabidopsis ech mutant exhibits severely perturbed cell elongation as well as defects in TGN structure and function, manifested by the reduced association between Golgi bodies and TGN as well as mislocalization of several TGN-localized proteins including vacuolar H+-ATPase subunit a1 (VHA-a1). Strikingly, ech is defective in secretory trafficking, whereas endocytosis appears unaffected in the mutant. Some aspects of the ech mutant phenotype can be phenocopied by treatment with a specific inhibitor of vacuolar H+-ATPases, concanamycin A, indicating that mislocalization of VHA-a1 may account for part of the defects in ech. Hence, ECH is an evolutionarily conserved component of the TGN with a central role in TGN structure and function.

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More information

Published date: 21 April 2011
Keywords: secretory pathway, dwarf mutant, vacuolar defect
Organisations: Biological Sciences

Identifiers

Local EPrints ID: 184787
URI: http://eprints.soton.ac.uk/id/eprint/184787
ISSN: 0027-8424
PURE UUID: 420b209b-e345-4b7a-bd94-16f2d14e0e89

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Date deposited: 09 May 2011 09:27
Last modified: 14 Mar 2024 03:09

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Contributors

Author: Delphine Gendre
Author: Jaesung Oh
Author: Yuhann Boutte
Author: Jacob G. Best
Author: Lacey Samuels
Author: Robert Nilsson
Author: Tomohiro Uemura
Author: Alan Marchant
Author: Malcolm J. Bennett
Author: Markus Grebe
Author: Rishikesh P. Bhalerao

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