Skip Navigation

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
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 (6)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Jun, J. H.
Right arrow Articles by Nam, H. G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Jun, J. H.
Right arrow Articles by Nam, H. G.
Agricola
Right arrow Articles by Jun, J. H.
Right arrow Articles by Nam, H. G.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Plant and Cell Physiology, 2002, Vol. 43, No. 3 323-330
© 2002 Oxford University Press

Involvement of the VEP1 Gene in Vascular Strand Development in Arabidopsis thaliana

Ji Hyung Jun, Chan Man Ha and Hong Gil Nam1

Division of Molecular Life Sciences, Pohang University of Science and Technology, Hyoja Dong, Pohang, Kyungbuk, 790-784 Korea

A dominant mutant line characterized by abnormal leaf venation pattern was isolated from a transgenic Arabidopsis plant pool that was generated with Agrobacterium culture harboring an Arabidopsis antisense cDNA library. In the mutant line, the phenotype was due to antisense suppression of a gene we named VEP1 (Vein Patterning). The predicted amino acid sequence of the gene contained a motif related to the mammalian death domain that is found in the apoptotic machinery. Reduced expression of the VEP1 gene resulted in the reduced complexity of the venation pattern of the cotyledons and foliar leaves, which was mainly due to the reduced number of the minor veins and their incomplete connection. The analysis of mutant embryos indicated that the phenotype was originated, at least in part, from a defect in the procambium patterning. In the mutant, the stem and root were thinner than those in wild type. This phenotype was associated with reduced vascular development. The promoter activity of the VEP1 gene was detected preferentially in the vascular regions. We propose that the death domain-containing protein VEP1 functions as a positive element required for vascular strand development in Arabidopsis thaliana.

1 Corresponding author: E-mail, hgn@bric.postech.ac.kr; Fax, +82-54-279-5972.


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


This article has been cited by other articles:


Home page
Plant Physiol.Home page
G. Wang, U. Ellendorff, B. Kemp, J. W. Mansfield, A. Forsyth, K. Mitchell, K. Bastas, C.-M. Liu, A. Woods-Tor, C. Zipfel, et al.
A Genome-Wide Functional Investigation into the Roles of Receptor-Like Proteins in Arabidopsis
Plant Physiology, June 1, 2008; 147(2): 503 - 517.
[Abstract] [Full Text] [PDF]


Home page
Plant CellHome page
C. M. Ha, J. H. Jun, H. G. Nam, and J. C. Fletcher
BLADE-ON-PETIOLE1 and 2 Control Arabidopsis Lateral Organ Fate through Regulation of LOB Domain and Adaxial-Abaxial Polarity Genes
PLANT CELL, June 1, 2007; 19(6): 1809 - 1825.
[Abstract] [Full Text] [PDF]


Home page
Plant Physiol.Home page
N. K. Clay and T. Nelson
Arabidopsis thickvein Mutation Affects Vein Thickness and Organ Vascularization, and Resides in a Provascular Cell-Specific Spermine Synthase Involved in Vein Definition and in Polar Auxin Transport
Plant Physiology, June 1, 2005; 138(2): 767 - 777.
[Abstract] [Full Text] [PDF]


Home page
DevelopmentHome page
C. M. Ha, G.-T. Kim, B. C. Kim, J. H. Jun, M. S. Soh, Y. Ueno, Y. Machida, H. Tsukaya, and H. G. Nam
The BLADE-ON-PETIOLE 1 gene controls leaf pattern formation through the modulation of meristematic activity in Arabidopsis
Development, January 1, 2003; 130(1): 161 - 172.
[Abstract] [Full Text] [PDF]



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.