No abstract

Salicylic acid (SA) is a defense hormone required for both local and systemic acquired resistance (SAR) in plants. Pathogen infections induce SA synthesis through up-regulating the expression of Isochorismate Synthase 1 (ICS1), which encodes a key enzyme in SA production. Here we report that both SAR Deficient 1 (SARD1) and CBP60g are key regulators for ICS1 induction and SA synthesis. Whereas knocking out SARD1 compromises basal resistance and SAR, overexpression of SARD1 constitutively activates defense responses. In the sard1-1 cbp60g-1 double mutant, pathogen-induced ICS1 upregulation and SA synthesis are blocked in both local and systemic leaves, resulting in compromised basal resistance and loss of SAR. Electrophoretic mobility shift assays showed that SARD1 and CBP60g represent a plant-specific family of DNA-binding proteins. Both proteins are recruited to the promoter of ICS1 in response to pathogen infections, suggesting that they control SA synthesis by regulating ICS1 at the transcriptional level.

-N leaching losses were not significantly affected by the two different rainfall treatments. The total NO 3 ) -N leaching loss was significantly related to the amoA gene copy numbers of the AOB DNA and to nitrification rate in the soil but not to that of the AOA. These results suggest that the DCD nitrification inhibitor is highly effective in decreasing NO 3 ) leaching under these different soil and rainfall conditions and that the amount of NO 3 ) -N leached is mainly related to the growth of the AOB population in the nitrogen rich urine patch soils of grazed grassland.