The Arabidopsis NPR1 gene that controls systemic acquired resistance encodes a novel protein containing ankyrin repeats

Hui Cao, Jane Glazebrook, Joseph D. Clarke, Sigrid Volko, Xinnian Dong

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The Arabidopsis NPR1 gene controls the onset of systemic acquired resistance (SAR), a plant immunity, to a broad spectrum of pathogens that is normally established after a primary exposure to avirulent pathogens. Mutants with defects in NPR1 fail to respond to various SAR-inducing treatments, displaying little expression of pathogenesis-related (PR) genes and exhibiting increased susceptibility to infections. NPR1 was cloned using a map-based approach and was found to encode a novel protein containing ankyrin repeats. The lesion in one npr1 mutant allele disrupted the ankyrin consensus sequence, suggesting that these repeats are important for NPR1 function. Furthermore, transformation of the cloned wild-type NPR1 gene into npr1 mutants not only complemented the mutations, restoring the responsiveness to SAR induction with respect to PR-gene expression and resistance to infections, but also rendered the transgenic plants more resistant to infection by P. syringae in the absence of SAR induction.

Original languageEnglish (US)
Pages (from-to)57-63
Number of pages7
Issue number1
StatePublished - Jan 10 1997

Bibliographical note

Funding Information:
We thank S. Bowling for helping with the infection experiments and with preparation of the manuscript; F. Katagiri for providing the Arabidopsis cDNA library; J. Ecker and H. Goodman for providing the YACs, the YAC-end clones, and the RFLP markers; Ciba-Geigy LTD for the gift of INA; D. F. Klessig for communicating data prior to publication; V. Bennett and N. Pavletich for informative discussions on ankyrin repeats; and F. M. Ausubel for many helpful discussions and critical reading of the manuscript. This work was supported by USDA grant 95-37301-1917 and a grant by Monsanto Co. to X. D. at Duke University and by NIH grant GM48707 and NRICGP grant 940-1199 awarded to F. M. Ausubel at MGH.


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