Transgene-induced lesion mimic

Transgene-induced lesion mimic Lesion mimic, i.e., the spontaneous formation of lesions resembling hypersensitive response (HR) lesions in the absence of a pathogen, is a dramatic phenotype occasionally found to accompany the expression of different, mostly unrelated, transgenes in plants. Recent studies indicated that transgene-induced lesion formation is not a simple case of necrosis, i.e., direct killing of cells by the transgene product, but results from the activation of a programmed cell death (PCD) pathway. Moreover, activation of HR-like cell death by transgene expression is viewed as an important evidence for the existence of a PCD pathway in plants. The study of lesion mimic transgenes is important to our understanding of PCD and the signals that control it in plants. PCD-inducing transgenes may provide clues regarding the different entry points into the cell death pathway, the relationships between the different branches of the pathway (e.g., developmental or environmental), or the different mechanisms involved in its induction or execution. Cell death-inducing transgenes may also be useful in biotechnology. Some lesion mimic transgenes were found to be induced in plants a state of systemic acquired resistance (SAR). These genes can be used in the development of pathogen-resistant crops. Other cell death-inducing transgenes may be used as specific cell ablation tools. Although mainly revealed unintentionally, and at times considered `an adverse phenotype', lesion mimic transgenes should not be ignored because they may prove valuable for studying PCD as well as developing useful traits in different plants and crops. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Plant Molecular Biology Springer Journals

Transgene-induced lesion mimic

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Publisher
Kluwer Academic Publishers
Copyright
Copyright © 2000 by Kluwer Academic Publishers
Subject
Life Sciences; Biochemistry, general; Plant Sciences; Plant Pathology
ISSN
0167-4412
eISSN
1573-5028
D.O.I.
10.1023/A:1026544625898
Publisher site
See Article on Publisher Site

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