rmal profile used consisted of an initial denaturation step at 95uC for 10 min, followed by 40 cycles of 95uC for 15 s, 59uC for 30 s, and 72uC for 30 s. To verify amplification of one specific target cDNA, a melting-curve RS 1 chemical information analysis was included according to the thermal profile suggested by the manufacturer. The amount of plant RNA in each sample was normalized using eEF1a as internal control. Nucleotide sequences of all primers used are listed in Results ABA Negatively Regulates Resistance to Xoo To substantiate this hypothesis, we quantified the level of basal and fluridone-inducible Xoo resistance in plants silenced for the MAP kinase gene OsMPK5. One of the better studied MAP kinases Role of ABA in Rice Defense against Xoo in rice, OsMPK5 has been shown to function as a positive regulator of ABA signaling in rice. Accordingly, OsMPK5 RNAi plants are partially ABA-insensitive and display reduced expression of ABA-responsive genes. As shown in Temporal Dynamics of ABA Biosynthesis and Signaling in Response to Xoo Inoculation To gain more insight into the mechanism of ABA-induced Xoo susceptibility, we monitored the steady-state mRNA levels of several ABA biosynthetic and ABA responsive genes in control and ABA-pretreated IRBB3 leaves at various times after inoculation with PXO99. As shown in ABA Negatively Regulates Xoo Resistance by Attenuating SA-mediated Defenses Role of ABA in Rice Defense against Xoo To test this hypothesis, we monitored the temporal expression patterns of three SA regulatory genes in control and ABA-treated IRBB3 leaves following PXO99 infection. Besides OsWRKY45 and OsNPR1, these genes included OsWRKY13, a well-characterized transcription factor gene functioning upstream of OsWRKY45 and OsNPR1. Consistent with the expression profiles reported in other studies, expression of OsWRKY45 
and OsNPR1 responded only weakly to Xoo inoculation. However, both genes were several-fold down-regulated in pathogen-inoculated leaves pretreated with ABA. Interestingly, ABA-mediated suppression of OsWRKY45 was evident at 4 11784156 and 8 dpi only, which is in line with the upregulation of ABA biosynthesis and ABA signaling genes at these time points. In contrast, expression of OsWRKY13 was not responsive to ABA treatment at any time point, suggesting that ABA antagonizes SA-mediated Xoo resistance downstream of OsWRKY13. This notion was further supported by the different effects of ABA pretreatment on BLB development in transgenic rice lines overexpressing OsNPR1 and OsWRKY13. Consistent with previous studies, both OsNPR1OX and OsWRKY13-OX lines exhibited increased resistance to Xoo compared to the respective wild-types. However, while ABA application significantly promoted disease development in both WT and OsWRKY13-OX backgrounds, overexpressing OsNPR1 fully blocked ABA-inducible Xoo susceptibility. Collectively, 5 Role of ABA in Rice Defense against Xoo these data further confirm mutually antagonistic 11078888 SA-ABA crosstalk during leaf blight infection and strengthen the hypothesis that ABA suppresses SA defenses downstream of OsWRKY13 but upstream of OsNPR1. Fluridone-inducible Xoo Resistance is Independent of SA The observation that ABA induces Xoo susceptibility, at least in part, by antagonizing the SA pathway prompted us to check whether ABA-lowering fluridone induces resistance by de-repressing SA-mediated immune responses. To address this hypothesis, we initially checked the impact of fluridone application on the expression of the SA m