Change search
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
The conserved Arabidopsis ECHIDNA protein mediates trans-Golgi-network trafficking and cell elongation
Swedish University of Agricultural Sciences, Umeå.
Swedish University of Agricultural Sciences, Umeå.
Swedish University of Agricultural Sciences, Umeå.
University of British Columbia, Vancouver.
Show others and affiliations
2011 (English)In: Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, E-ISSN 1091-6490, Vol. 108, no 19, p. 8048-8053Article in journal (Refereed) Published
Abstract [en]

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.

Place, publisher, year, edition, pages
2011. Vol. 108, no 19, p. 8048-8053
Identifiers
URN: urn:nbn:se:ltu:diva-9819DOI: 10.1073/pnas.1018371108Local ID: 8818fa75-b77b-4a54-867f-be5636e740aeOAI: oai:DiVA.org:ltu-9819DiVA, id: diva2:982757
Note
Upprättat; 2011; 20130207 (robnil)Available from: 2016-09-29 Created: 2016-09-29 Last updated: 2018-05-28Bibliographically approved

Open Access in DiVA

No full text in DiVA

Other links

Publisher's full text

Authority records BETA

Nilsson, Robert

Search in DiVA

By author/editor
Nilsson, Robert
In the same journal
Proceedings of the National Academy of Sciences of the United States of America

Search outside of DiVA

GoogleGoogle Scholar

doi
urn-nbn

Altmetric score

doi
urn-nbn
Total: 11 hits
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf