1 September 2004 Host gene expression in response to Egyptian broomrape (Orobanche aegyptiaca)
Amanda A. Griffitts, Carole L. Cramer, James H. Westwood
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Selective control of Egyptian broomrape is extremely difficult because the close association between host crop and parasite limits the use of most mechanical and herbicidal approaches. However, this host–parasite interaction can also form the basis of the simplest control strategy: parasite-resistant crops. Although much work has been conducted to identify and characterize mechanisms of parasite resistance, varieties with stable resistance are still unavailable for most affected crops. The development of resistant crops can be accelerated by genetic engineering to the extent that important aspects of the host–parasite interaction are understood. In this study, we characterize a variety of gene promoter elements with respect to parasite induction and expression pattern. Studies were conducted using transgenic plants expressing fusions of the β-glucuronidase reporter gene with promoter elements from several genes. Promoters from genes known to have increased expression in response to pathogen attack or wounding showed localized, induced expression after parasitism. These included phenylalanine ammonia lyase, chalcone synthase, sesquiterpene cyclase, and HMG1 (3-hydroxy-3-methylglutaryl CoA reductase). In contrast, the systemic acquired resistance–associated gene PR-1a was not induced by parasitism. Non–defense-related genes varied in response, with squalene synthase being repressed, whereas farnesyltransferase was highly expressed in the region of parasite attachment. These results demonstrate a range of expression, both in intensity and tissue specificity, in response to parasitism.

Nomenclature: Egyptian broomrape, Orobanche aegyptiaca Pers. OROAG.

Amanda A. Griffitts, Carole L. Cramer, and James H. Westwood "Host gene expression in response to Egyptian broomrape (Orobanche aegyptiaca)," Weed Science 52(5), 697-703, (1 September 2004). https://doi.org/10.1614/WS-03-155R
Received: 20 November 2003; Accepted: 1 February 2004; Published: 1 September 2004
genetic engineering
isoprenoid pathway
parasitic plant
phenylpropanoid pathway
PR protein
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