Skip Navigation


JXB Advance Access originally published online on September 5, 2005
Journal of Experimental Botany 2005 56(420):2661-2671; doi:10.1093/jxb/eri259
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
56/420/2661    most recent
eri259v1
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (4)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Ezaki, B.
Right arrow Articles by Nakashima, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ezaki, B.
Right arrow Articles by Nakashima, S.
Agricola
Right arrow Articles by Ezaki, B.
Right arrow Articles by Nakashima, S.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author [2005]. Published by Oxford University Press [on behalf of the Society for Experimental Biology]. All rights reserved. For Permissions, please e-mail: journals.permissions@oupjournals.org

RESEARCH PAPER

Functions of two genes in aluminium (Al) stress resistance: repression of oxidative damage by the AtBCB gene and promotion of efflux of Al ions by the NtGDI1gene

Bunichi Ezaki*, Kiyokuni Sasaki, Hideaki Matsumoto and Susumu Nakashima

Research Institute for Bioresources, Okayama University, 2-20-1, Chuou, Kurashiki, Okayama 710-0046, Japan

* To whom correspondence should be addressed. Fax: +86 434 1249. E-mail: bezaki{at}rib.okayama-u.ac.jp

The functions of two genes whose expression provides tolerance to aluminium (Al) stress were investigated using plants and Saccharomyces cerevisiae (yeast): the Arabidopsis thaliana blue copper binding gene (AtBCB) and Nicotiana tabacum guanosine diphosphate (GDP) dissociation inhibitor gene (NtGDI1). To determine the localization of these proteins, each gene was fused to the green fluorescent protein (GFP) gene and introduced into onion epidermal cells. AtBCB was localized to cell membrane region and NtGDI1 to cytoplasm. Transgenic lines over-expressing the AtBCB gene showed constitutive lignin production in whole roots. By contrast, wild-type Arabidopsis (Ler) produced a negligible level of lignin and enhanced lignin production in the root-tip region by Al stress. Compared with Ler, the AtBCB-expressing lines showed a lower deposition of malon dialdehyde after Al stress. Microscopic observation of the Al-treated roots indicated that the deposition of lipid peroxides was clearly low in the area where lignin accumulated. It was proposed that lipid peroxidation caused by Al stress was diminished by the formation of lignin. Expression of the NtGDI1 gene in yeast complemented the temperature-sensitive phenotype of a sec19 mutant at 37 °C. This gene also complemented an Al-sensitive phenotype shown by the sec19 mutant at the permissive temperature of 32 °C. These results suggested that the yeast Sec19 vesicle transport system has a function in providing basal Al resistance in yeast by the export of Al ions. It was also proposed that over-expression of the NtGDI1 protein activates an Al efflux system that protects Arabidopsis against Al toxicity.

Key words: Aluminium (Al) ion stress, Al resistance mechanism, Arabidopsis thaliana, AtBCB gene, lignin, NtGDI1 gene, oxidative stress, Saccharomyces cerevisiae, sec19 gene, vesicle transport system


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.