| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
|
First published online December 9, 2005; 10.1104/pp.105.071399 Plant Physiology 140:59-66 (2006) © 2006 American Society of Plant Biologists OPEN ACCESS ARTICLE
The Photorespiratory Arabidopsis shm1 Mutant Is Deficient in SHM11,[W],[OA]Department of Plant Biology, Michigan State University, East Lansing, Michigan 48824–1312 (L.M.V., H.V., A.P.M.W.); Department of Biological Sciences, Dartmouth College, Hanover, New Hampshire 03755–3576 (A.J., C.R.M.); and Botanisches Institut der Universität zu Köln, D–50931 Koln, Germany (P.R.)
Mitochondrial serine hydroxymethyltransferase (SHMT), combined with glycine decarboxylase, catalyzes an essential sequence of the photorespiratory C2 cycle, namely, the conversion of two molecules of glycine into one molecule each of CO2, NH4+, and serine. The Arabidopsis (Arabidopsis thaliana) mutant shm (now designated shm1-1) is defective in mitochondrial SHMT activity and displays a lethal photorespiratory phenotype when grown at ambient CO2, but is virtually unaffected at elevated CO2. The Arabidopsis genome harbors seven putative SHM genes, two of which (SHM1 and SHM2) feature predicted mitochondrial targeting signals. We have mapped shm1-1 to the position of the SHM1 gene (At4g37930). The mutation is due to a G
1 This work was supported by the Deutsche Forschungsgemeinschaft (postdoctoral research fellowship to L.M.V. and grant no. WE2231/2–1 to A.P.M.W.), the National Science Foundation (grant no. MCB–0348074 to A.P.M.W.), and the U.S. Department of Agriculture (grant no. 2002–01392 to C.R.M.). 2 These authors contributed equally to the paper. The author responsible for distribution of materials integral to the findings presented in this article in accordance with journal policy described in the Instructions for Authors (http://www.plantphysiol.org) is: Andreas P.M. Weber (aweber{at}msu.edu). [W] The online version of this article contains Web-only data. [OA] Open Access articles can be viewed online without a subscription. Article, publication date, and citation information can be found at www.plantphysiol.org/cgi/doi/10.1104/pp.105.071399. * Corresponding author; e-mail aweber{at}msu.edu; fax 517–432–5294. Received September 12, 2005; returned for revision September 12, 2005; accepted October 25, 2005. This article has been cited by other articles:
|
|||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ASPB Publications | PLANT PHYSIOLOGY® | THE PLANT CELL | |
|---|---|---|---|
A transition at the 5' splice site of intron 6 of SHM1, causing aberrant splicing and a premature termination of translation. A T-DNA insertion allele of SHM1, shm1-2, and the F1 progeny of a genetic cross between shm1-1 and shm1-2 displayed the same conditional lethal phenotype as shm1-1. Expression of wild-type SHM1 under the control of either the cauliflower mosaic virus 35S or the SHM1 promoter in shm1-1 abrogated the photorespiratory phenotype of the shm mutant, whereas overexpression of SHM2 or expression of SHM1 under the control of the SHM2 promoter did not rescue the mutant phenotype. Promoter-
-glucuronidase analyses revealed that SHM1 is predominantly expressed in leaves, whereas SHM2 is mainly transcribed in the shoot apical meristem and roots. Our findings establish SHM1 as the defective gene in the Arabidopsis shm1-1 mutant. 
