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First published online November 14, 2008; 10.1104/pp.108.128348

Plant Physiology 149:286-296 (2009)
© 2009 American Society of Plant Biologists

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A Germin-Like Protein Gene Family Functions as a Complex Quantitative Trait Locus Conferring Broad-Spectrum Disease Resistance in Rice1,[W],[OA]

Patricia M. Manosalva2, Rebecca M. Davidson, Bin Liu, Xiaoyuan Zhu, Scot H. Hulbert, Hei Leung and Jan E. Leach*

Bioagricultural Sciences and Pest Management and Program in Plant Molecular Biology, Colorado State University, Fort Collins, Colorado 80523–1177 (P.M.M., R.M.D, J.E.L.); Plant Pathology, Kansas State University, Manhattan, Kansas 66502–5502 (P.M.M.); Rice Research Institute and Plant Protection Institute, Guangdong Academy of Agricultural Sciences, Guangzhou 510640, People's Republic of China (B.L., X.Z.); Plant Pathology, Washington State University, Pullman, Washington 99164 (S.H.H.); and Plant Breeding, Genetics, and Biotechnology, International Rice Research Institute, Los Banos, 4031 Laguna, Philippines (H.L.)

Plant disease resistance governed by quantitative trait loci (QTL) is predicted to be effective against a broad spectrum of pathogens and long lasting. Use of these QTL to improve crop species, however, is hindered because the genes contributing to the trait are not known. Five disease resistance QTL that colocalized with defense response genes were accumulated by marker-aided selection to develop blast-resistant varieties. One advanced backcross line carrying the major-effect QTL on chromosome (chr) 8, which included a cluster of 12 germin-like protein (OsGLP) gene members, exhibited resistance to rice (Oryza sativa) blast disease over 14 cropping seasons. To determine if OsGLP members contribute to resistance and if the resistance was broad spectrum, a highly conserved portion of the OsGLP coding region was used as an RNA interference trigger to silence a few to all expressed chr 8 OsGLP family members. Challenge with two different fungal pathogens (causal agents of rice blast and sheath blight diseases) revealed that as more chr 8 OsGLP genes were suppressed, disease susceptibility of the plants increased. Of the 12 chr 8 OsGLPs, one clustered subfamily (OsGER4) contributed most to resistance. The similarities of sequence, gene organization, and roles in disease resistance of GLP family members in rice and other cereals, including barley (Hordeum vulgare) and wheat (Triticum aestivum), suggest that resistance contributed by the chr 8 OsGLP is a broad-spectrum, basal mechanism conserved among the Gramineae. Natural selection may have preserved a whole gene family to provide a stepwise, flexible defense response to pathogen invasion.


1 This work was supported by the U.S. Department of Agriculture-Cooperative State Research, Extension, and Education Service-National Research Initiative (grant no. 2003–01551), the Cereal Comparative Genomics Initiative, a U.S. Agency for International Development Linkage Project, and the Kansas State and Colorado State Experiment Stations. R.M.D. was supported by the U.S. Department of Agriculture-Cooperative State Research, Extension, and Education Service-National Research Initiative (Rice-CAP grant no. 2004–35317–14867) and a Ford Foundation Diversity Fellowship. Field studies were funded by a Guangdong Academy of Agricultural Sciences (B.L., X.Z.) and International Rice Research Institute (H.L.) collaborative project.

2 Present address: Boyce Thompson Institute for Plant Research, Tower Road, Ithaca, NY 14853.

The author responsible for distribution of materials integral to the findings presented in this article in accordance with the policy described in the Instructions for Authors (www.plantphysiol.org) is: Jan Leach (jan.leach{at}colostate.edu).

[W] The online version of this article contains Web-only data.

[OA] Open Access articles can be viewed online without a subscription.

www.plantphysiol.org/cgi/doi/10.1104/pp.108.128348

* Corresponding author; e-mail jan.leach{at}colostate.edu.

Received August 22, 2008; accepted November 9, 2008; published November 14, 2008.




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