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Or tomato and to elicitor treatment of parsley cells Dyer et al., 1989; Henstrand et al., 1992 ; . Similarly, funga1 elicitor treatment of tobacco cells causes the coordinate induction of HMG-COAR ; , sesquiterpene cyclase, and the sesquiterpene capsidiol Chappelland Nable, 1987; Vogeli and Chappell, 1988 ; . In neither case are the responsible regulatory mechanisms known. The importance of salicylic acid SA ; as a signal molecule in the induction of pathogenesis-related PR ; proteinsand systemic aquired resistance SAR ; is well established Yalpani et al., 1991; Ryals et al., 1995 ; . For eyample, treatment of plants with SA or 2, 6-dichloroisonicotinic acid INA ; is sufficient to induce PR proteins and SAR Uknes et ai., 1992; Ryals et al., 1995 ; . Furthermore, NahG plants, which cannot accumulate significant amounts of SA due to the expression of the bacteria1nahG gene encoding bacterialsalicylate hydroxylase, fail to induce PR proteins and SAR upon pathogen infection Bowling et al., 1994; Delaney et al., 1994 ; . The mutants nprl for nonexpresser of PR genes ; and niml for noninducible immunity ; have been shown to be defective in the induction of PR proteins and SAR Cao et al., 1994; Delaney et al., 1995 ; . In this report, we show that F! syringae infection or abiotic elicitor treatment, but not infection with virulent viruses, induces camalexin coordinately with the mRNAs and proteins of the tryptophan pathway enzymes in Arabidopsis. In contrast to the known PR genes, SA appears to be required but is not sufficient for the coordinate induction. Arabidopsis trp mutants defective at different steps of the pathway accumulate similar levels of camalexin as the wild type, suggesting that the control of camalexin biosynthesis lies beyond the tryptophan biosynthetic pathway.
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