Expression of the rice CDPK-7 in sorghum: molecular and phenotypic analyses

Expression of the rice CDPK-7 in sorghum: molecular and phenotypic analyses Sorghum (Sorghum bicolor (L.) Moench) is an important source for food, feed, and possesses many agronomic attributes attractive for a biofuels feedstock. A warm season crop originating from the semi-arid tropics, sorghum is relatively susceptible to both cold and freezing stress. Enhancing the ability of sorghum to tolerate cold and freezing offers a route to expand the acreage for production, and provides a potential drought avoidance strategy during flowering, an important parameter for protection of yield. Targeted perturbation of the signal transduction pathway, that is triggered by exposure to abiotic stress in plants, has been demonstrated in model systems as an avenue to augment tolerance. Calcium-dependent protein kinases (CDPKs) are key players in a plant’s response to environmental assaults. To test the impact of modulating CDPK activity in sorghum as a means to enhanced abiotic stress tolerance, we introduced a constitutively expressed rice CDPK-7 (OsCDPK-7) gene construct. Sorghum transformants carrying this cassette, were not improved in cold or salt stress under the conditions tested. However, a lesion mimic phenotype and up-regulation of a number of pathogen related proteins, along with transcripts linked to photosynthesis were observed. These results demonstrate that modulating the Ca signaling cascade in planta via unregulated enhanced CDPK activity can lead to off-type effects likely due to the broadly integrated nature of these enzymes in signaling. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Plant Molecular Biology Springer Journals

Expression of the rice CDPK-7 in sorghum: molecular and phenotypic analyses

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Publisher
Springer Netherlands
Copyright
Copyright © 2011 by Springer Science+Business Media B.V.
Subject
Life Sciences; Biochemistry, general; Plant Pathology; Plant Sciences
ISSN
0167-4412
eISSN
1573-5028
D.O.I.
10.1007/s11103-011-9741-9
Publisher site
See Article on Publisher Site

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