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CELL BIOLOGY AND SIGNAL TRANSDUCTION

Downstream Divergence of the Ethylene Signaling Pathway for Harpin-Stimulated Arabidopsis Growth and Insect Defense¹

Department of Plant Pathology, Nanjing Agricultural University, Nanjing 210095, China (H.-P.D., J.P., Z.B., G.C., H.D.); and Department of Plant Pathology, Cornell University, Ithaca, New York 14853 (X.M., J.M.B., S.V.B.)

Ethylene (ET) signal transduction may regulate plant growth and defense, depending on which components are recruited into the pathway in response to different stimuli. We report here that the ET pathway controls both insect resistance (IR) and plant growth enhancement (PGE) in Arabidopsis (Arabidopsis thaliana) plants responding to harpin, a protein produced by a plant pathogenic bacterium. PGE may result from spraying plant tops with harpin or by soaking seeds in harpin solution; the latter especially enhances root growth. Plants treated similarly develop resistance to the green peach aphid (Myzus persicae). The salicylic acid pathway, although activated by harpin, does not lead to PGE and IR. By contrast, PGE and IR are induced in both wild-type plants and genotypes that have defects in salicylic acid signaling. In response to harpin, levels of jasmonic acid (JA) decrease, and the COI1 gene, which is indispensable for JA signal transduction, is not expressed in wild-type plants. However, PGE and IR are stimulated in the JA-resistant mutant jar1-1. In the wild type, PGE and IR develop coincidently with increases in ET levels and the expression of several genes essential for ET signaling. The ET receptor gene ETR1 is required because both phenotypes are arrested in the etr1-1 mutant. Consistently, inhibition of ET perception nullifies the induction of both PGE and IR. The signal transducer EIN2 is required for IR, and EIN5 is required for PGE because IR and PGE are impaired correspondingly in the ein2-1 and ein5-1 mutants. Therefore, harpin activates ET signaling while conscribing EIN2 and EIN5 to confer IR and PGE, respectively.

² These authors contributed equally to the paper.

³ Present address: College of Life Sciences, Nanjing Normal University, 122 Ninghai Road, Nanjing 210097, China.

⁴ Present address: Institute of Genetics and Developmental Biology, Chinese Academy of Science, 1 Anwai-Datun Road, Beijing 100101, China.

Article, publication date, and citation information can be found at www.plantphysiol.org/cgi/doi/10.1104/pp.104.048900.

^* Corresponding author; e-mail hsdong{at}njau.edu.cn; fax 86–(25)–84395246.

Received June 30, 2004; returned for revision September 11, 2004; accepted September 20, 2004.

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