The Wound-Inducible Lls1 Gene from Maize is an Orthologue of the Arabidopsis Acd1 Gene, and the LLS1 Protein is Present in Non-Photosynthetic Tissues

The Wound-Inducible Lls1 Gene from Maize is an Orthologue of the Arabidopsis Acd1 Gene, and the... Previous studies indicated that the lethal leaf spot 1 lesion mimic locus of maize (ZmLls1) encodes a novel cell protective function in plants. Here we show that the accelerated cell death 1(acd1) locus of Arabidopsis thaliana corresponds to gene At3g44880 on chromosome 3. Proof that the Acd1 gene is an orthologue of ZmLls1 is provided by in vivo complementation of the acd1 mutant by the ZmLls1 gene. The Atlls1 lesion mimic phenotype was delayed in a chlorophyll a oxygenase (CAO) mutant chlorina1 background which is deficient in chlorophyll b synthesis. The interpretation that the cell protective function of LLS1 is linked with the removal of a phototoxic chlorophyll intermediate is supported by the recent report that the maize Lls1 gene encodes pheophorbide a oxygenase (PaO). Western blot analysis demonstrates that the LLS1 protein is present constitutively in all photosynthetic plant tissues. A transient increase in Lls1 gene expression by about 50-fold upon physical wounding of maize leaves indicates that the function of Lls1 is regulated in response to stress. We show that the LLS1 protein is also present at low levels in non-photosynthetic tissues including etiolated leaves suggesting that the ability to degrade chlorophyll exists in a standby mode in plant cells. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Plant Molecular Biology Springer Journals

The Wound-Inducible Lls1 Gene from Maize is an Orthologue of the Arabidopsis Acd1 Gene, and the LLS1 Protein is Present in Non-Photosynthetic Tissues

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Publisher
Kluwer Academic Publishers
Copyright
Copyright © 2004 by Kluwer Academic Publishers
Subject
Life Sciences; Biochemistry, general; Plant Sciences; Plant Pathology
ISSN
0167-4412
eISSN
1573-5028
D.O.I.
10.1023/B:PLAN.0000028789.51807.6a
Publisher site
See Article on Publisher Site

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