A phosphate-starvation inducible β-glucosidase gene (psr3.2) isolated from Arabidopsis thaliana is a member of a distinct subfamily of the BGA family

A phosphate-starvation inducible β-glucosidase gene (psr3.2) isolated from Arabidopsis thaliana... We have previously isolated a phosphate starvation-response (psr) cDNA clone, psr3.1, from Brassica nigra which encodes a β-glucosidase. Southern blots of Arabidopsis thaliana genomic DNA probed with the psr3.1 cDNA indicated that this gene exists as a single locus. A genomic library of A. thaliana was screened at high stringency to isolate the corresponding genomic clone. The resultant clone was coined psr3.2 because of its sequence divergence from isolated psr3.1 cDNA clones. Northern blotting with probes derived from the coding region of the genomic clone showed that this gene is expressed at high levels in Pi-starved roots and the enhancement occurred within two days of growth in medium lacking Pi. The expression of this gene is repressed by heat shock and anaerobic conditions, and it is not significantly induced by high salinity, or by nitrogen or sulfur deprivation. Sequence analysis of the genomic clone revealed the existence of 13 exons interrupted by 12 AT-rich introns and it possessed a high homology with the B. nigra psr3.1 as well as various other β-glucosidase genes from other species. Sequence similarity and divergence percentages between the deduced amino acid sequences of the psr3 clones and other β-glycosidases suggests that they should be included along with two other Brassicaceae genes in a distinct subfamily of the BGA glycosidase gene family. The presence of an endoplasmic reticulum retention signal at the carboxy terminus indicates the likely cellular location of PSR3.2. The possible metabolic and regulatory roles of this enzyme during the Pi-starvation response are discussed. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Plant Molecular Biology Springer Journals

A phosphate-starvation inducible β-glucosidase gene (psr3.2) isolated from Arabidopsis thaliana is a member of a distinct subfamily of the BGA family

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Publisher
Kluwer Academic Publishers
Copyright
Copyright © 1997 by Kluwer Academic Publishers
Subject
Life Sciences; Biochemistry, general; Plant Sciences; Plant Pathology
ISSN
0167-4412
eISSN
1573-5028
D.O.I.
10.1023/A:1005865406382
Publisher site
See Article on Publisher Site

Abstract

We have previously isolated a phosphate starvation-response (psr) cDNA clone, psr3.1, from Brassica nigra which encodes a β-glucosidase. Southern blots of Arabidopsis thaliana genomic DNA probed with the psr3.1 cDNA indicated that this gene exists as a single locus. A genomic library of A. thaliana was screened at high stringency to isolate the corresponding genomic clone. The resultant clone was coined psr3.2 because of its sequence divergence from isolated psr3.1 cDNA clones. Northern blotting with probes derived from the coding region of the genomic clone showed that this gene is expressed at high levels in Pi-starved roots and the enhancement occurred within two days of growth in medium lacking Pi. The expression of this gene is repressed by heat shock and anaerobic conditions, and it is not significantly induced by high salinity, or by nitrogen or sulfur deprivation. Sequence analysis of the genomic clone revealed the existence of 13 exons interrupted by 12 AT-rich introns and it possessed a high homology with the B. nigra psr3.1 as well as various other β-glucosidase genes from other species. Sequence similarity and divergence percentages between the deduced amino acid sequences of the psr3 clones and other β-glycosidases suggests that they should be included along with two other Brassicaceae genes in a distinct subfamily of the BGA glycosidase gene family. The presence of an endoplasmic reticulum retention signal at the carboxy terminus indicates the likely cellular location of PSR3.2. The possible metabolic and regulatory roles of this enzyme during the Pi-starvation response are discussed.

Journal

Plant Molecular BiologySpringer Journals

Published: Sep 29, 2004

References

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