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First published online January 22, 2010; doi:10.3732/ajb.0900233
American Journal of Botany 97: 357-364 (2010)
© 2010 Botanical Society of America, Inc.
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Brief Communication

Genetic analyses of cell death in maize (Zea mays, Poaceae) leaves reveal a distinct pathway operating in the camouflage1 mutant1

Mingshu Huang2,3 and David M. Braun2,4

2 Department of Biology, Pennsylvania State University, University Park, Pennsylvania 16802 USA 3 Current address: Department of Plant Biology, Cornell University, Ithaca, New York 14850 USA

ABSTRACT

Controlled cell death is vital for many physiological processes in plants, such as xylem development, the hypersensitive response (HR), and senescence; however, the pathways governing cell death are incompletely understood. Studies of mutants that display a cell-death phenotype have greatly contributed to our knowledge of how this process is regulated. The maize camouflage1 (cf1) mutant displays the novel phenotype of cell-specific death of bundle sheath (BS) cells in discrete yellow leaf tissues. To investigate the BS cell death in cf1 mutants, we characterized potential underlying factors. Hydrogen peroxide (H2O2) is known to be involved in many cell-death events in plants, including the HR. However, in vivo staining found no accumulation of H2O2 in cf1 mutant leaves. Additionally, genetic analyses determined that functional chloroplasts are required for cf1 BS cell death. These results demonstrate that cf1 BS cell death occurs via a distinct pathway from that seen in a functionally related maize mutant or in the HR, suggesting that cell death in maize leaves can be caused by multiple mechanisms.

Key Words: bundle sheath cells • cf1 • chloroplast • programmed cell death • reactive oxygen species • Zea mays

Received for publication 6 August 2009. Accepted for publication 11 November 2009.

FOOTNOTES

1 The authors thank T. Omeis and S. Harkcom for excellent plant care. We also thank two anonymous reviewers for improvements to the manuscript and the members of the Braun and McSteen laboratories for discussion of the data and comments on the manuscript. This research was supported by start-up funds provided to D. Braun by Penn State University.

4 Author for correspondence (e-mail: dbraun{at}psu.edu)


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