Skip Navigation


Plant and Cell Physiology Advance Access first published online on February 14, 2006
This version published online on February 20, 2006
Plant and Cell Physiology, doi:10.1093/pcp/pcj020
This Article
Right arrow Advance Access manuscript (PDF)
Right arrow Supplementary Data
Right arrow All Versions of this Article:
47/4/513    most recent
pcj020v2
pcj020v1
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 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 arrowRequest Permissions
Google Scholar
Right arrow Articles by Nakajima, K.
Right arrow Articles by Hashimoto, T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Nakajima, K.
Right arrow Articles by Hashimoto, T.
Agricola
Right arrow Articles by Nakajima, K.
Right arrow Articles by Hashimoto, T.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Plant and Cell Physiology 2006 © The Japanese Society of Plant Physiologists (JSPP); all rights reserved.
Received January 11, 2006
Accepted February 6, 2006

Regular Paper

Role of the SPIRAL1 Gene Family in Anisotropic Growth of Arabidopsis thaliana

Keiji Nakajima 1, Tomomi Kawamura 1, and Takashi Hashimoto 1 *

1 Graduate School of Biological Sciences, Nara Institute of Science and Technology, 8916-5 Takayama, Ikoma, Nara 630-0192, Japan

* To whom correspondence should be addressed.
Takashi Hashimoto, E-mail: hasimoto{at}bs.naist.jp


  Abstract

Arabidopsis spiral1 (spr1) mutants show a right-handed helical growth phenotype in roots and etiolated hypocotyls due to impaired directional growth of rapidly expanding cells. SPR1 encodes a small protein with as yet unknown biochemical functions, though its localization to cortical microtubules (MTs) suggests that SPR1 maintains directional cell expansion by regulating cortical MT functions. The Arabidopsis genome contains five SPR1-LIKE (SP1L) genes that share high sequence identity in amino- and carboxy-terminal regions. Overexpression of SP1Ls rescued the helical growth phenotype of spr1, indicating that SPR1 and SP1L proteins share the same biochemical functions. Expression analyses revealed that SPR1 and SP1Ls are transcribed in partially overlapping tissues. A combination of spr1 and sp1l mutations resulted in randomly oriented cortical MT arrays and isotropic expansion of epidermal cells. These observations suggest that SPR1 and SP1Ls act redundantly in maintaining the cortical MT organization essential for anisotropic cell growth, and that the helical growth phenotype of spr1 results from a partially compromised state of cortical MTs. Additionally, inflorescence stems of spr1 sp1l multiple mutants showed a right-handed tendril-like twining growth, indicating that a directional winding response may be conferred to the non-directional nutational movement by modulating the expression of SPR1 homologs.

Keywords: Arabidopsis thaliana; cell expansion; cytoskeleton; microtubule; SPIRAL1.
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
 ANN BOT (LOND)Home page
L. Guo, C.-M. K. Ho, Z. Kong, Y.-R. J. Lee, Q. Qian, and B. Liu
Evaluating the microtubule cytoskeleton and its interacting proteins in monocots by mining the rice genome
Ann. Bot., February 1, 2009; 103(3): 387 - 402.
[Abstract] [Full Text] [PDF]

Home page
 GeneticsHome page
C. Ma, J. Tran, C. Li, L. Ganesan, D. Wood, and N. Morrissette
Secondary Mutations Correct Fitness Defects in Toxoplasma gondii With Dinitroaniline Resistance Mutations
Genetics, October 1, 2008; 180(2): 845 - 856.
[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.