This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Supplemental material
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Google Scholar
Right arrow Articles by Kaya, A.
Right arrow Articles by Koc, A.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kaya, A.
Right arrow Articles by Koc, A.

 Previous Article  |  Next Article 

Molecular and Cellular Biology, July 2009, p. 3665-3674, Vol. 29, No. 13
0270-7306/09/$08.00+0     doi:10.1128/MCB.01646-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Identification of a Novel System for Boron Transport: Atr1 Is a Main Boron Exporter in Yeast{triangledown} ,{dagger}

Alaattin Kaya,1,2 Huseyin C. Karakaya,1 Dmitri E. Fomenko,2 Vadim N. Gladyshev,2 and Ahmet Koc1*

Department of Molecular Biology and Genetics, Izmir Institute of Technology, 35430 Urla, Izmir, Turkey,1 Department of Biochemistry and Redox Biology Center, University of Nebraska, Lincoln, Nebraska 685882

Received 22 October 2008/ Returned for modification 20 January 2009/ Accepted 20 April 2009

Boron is a micronutrient in plants and animals, but its specific roles in cellular processes are not known. To understand boron transport and functions, we screened a yeast genomic DNA library for genes that confer resistance to the element in Saccharomyces cerevisiae. Thirty boron-resistant transformants were isolated, and they all contained the ATR1 (YML116w) gene. Atr1 is a multidrug resistance transport protein belonging to the major facilitator superfamily. C-terminal green fluorescent protein-tagged Atr1 localized to the cell membrane and vacuole, and ATR1 gene expression was upregulated by boron and several stress conditions. We found that atr1{Delta} mutants were highly sensitive to boron treatment, whereas cells overexpressing ATR1 were boron resistant. In addition, atr1{Delta} cells accumulated boron, whereas ATR1-overexpressing cells had low intracellular levels of the element. Furthermore, atr1{Delta} cells showed stronger boron-dependent phenotypes than mutants deficient in genes previously reported to be implicated in boron metabolism. ATR1 is widely distributed in bacteria, archaea, and lower eukaryotes. Our data suggest that Atr1 functions as a boron efflux pump and is required for boron tolerance.


* Corresponding author. Mailing address: Department of Molecular Biology and Genetics, Izmir Institute of Technology, 35430 Urla, Izmir, Turkey. Phone: 90-232-750 7544. Fax: 90-232-750 7509. E-mail: ahmetkoc{at}iyte.edu.tr

{triangledown} Published ahead of print on 4 May 2009.

{dagger} Supplemental material for this article may be found at http://mcb.asm.org/.


Molecular and Cellular Biology, July 2009, p. 3665-3674, Vol. 29, No. 13
0270-7306/09/$08.00+0     doi:10.1128/MCB.01646-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.