Format

Send to

Choose Destination
See comment in PubMed Commons below
Plant J. 2003 Feb;33(4):677-90.

AtBXL1, a novel higher plant (Arabidopsis thaliana) putative beta-xylosidase gene, is involved in secondary cell wall metabolism and plant development.

Author information

1
Laboratoire de Biologie Cellulaire - Institut National de la Recherche Agronomique, Route de St-Cyr 78026 Versailles Cedex, France.

Erratum in

  • Plant J. 2003 May;34(3):393.

Abstract

To investigate mechanisms involved in cell wall development, an Arabidopsis T-DNA insertion mutant collection was screened to identify mutants with beta-glucuronidase fusion gene expression in tissues undergoing secondary cell wall thickening. This promoter-trapping strategy allowed the isolation of a transformant containing the GUS coding sequence inserted 700 bp upstream of the ATG of a putative beta-xylosidase gene. The transformant has no phenotype as the expression of the gene was not disrupted by the insertion. The analysis of the predicted protein, AtBXL1, suggests its targeting to the extracellular matrix and its involvement in cell wall metabolism through a putative activity towards xylans. The 2-kb promoter sequence of AtBXL1 was fused to the GUS coding sequence and introduced into wild-type Arabidopsis thaliana. GUS expression was shown to be restricted to tissues undergoing secondary cell wall formation. Beta-xylosidase activity was associated with the cell wall-enriched fraction of different organs of wild-type plants. The level of activity correlates with transcript accumulation of AtBXL1 and other AtBXL1-related genes. Transgenic plants expressing the AtBXL1 cDNA in antisense orientation were generated. Lines exhibiting the highest decrease in AtBXL1 transcript accumulation and beta-xylosidase activity had phenotypic alterations. This newly identified gene is proposed to be involved in secondary cell wall hemicellulose metabolism and plant development.

PMID:
12609041
[Indexed for MEDLINE]
Free full text
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Wiley
    Loading ...
    Support Center