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.
journal_name
Proc Natl Acad Sci U S Aauthors
Gendre D,Oh J,Boutté Y,Best JG,Samuels L,Nilsson R,Uemura T,Marchant A,Bennett MJ,Grebe M,Bhalerao RPdoi
10.1073/pnas.1018371108subject
Has Abstractpub_date
2011-05-10 00:00:00pages
8048-53issue
19eissn
0027-8424issn
1091-6490pii
1018371108journal_volume
108pub_type
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