Minisymposium 18: Plant defense signaling

Abs # 33004: Role of lipids in systemic acquired resistance

Presenter:	Shah, Jyoti , shah@ksu.edu
Authors	Shah, Jyoti  (A)   Nandi, Ashis  (A)   Krothapalli, Kartikeya  (A)   Makandar, Ragiba  (A)   Morton, Jessica  (A)   Omoluabi, Ozozoma  (A)   Buseman, Christen  (A)   Baughman, Ethan  (A)   Welti, Ruth  (A)
Affiliations:	(A): Division of Biology and the Molecular, Cellular and Developmental Biology Program, Kansas State University, Manhattan, Kansas 66506, USA

Systemic acquired resistance (SAR) is an induced response activated in the distal organs of a plant by the prior exposure of another organ to a necrotizing pathogen. SAR confers enhanced resistance to a broad-spectrum of pathogens. An unknown signal produced in the pathogen-inoculated organ traverses to the distal naive organs, where it activates SAR. SAR is accompanied by the elevated level of expression of a subgroup of the pathogenesis-related (PR) genes, some of which encode proteins with antimicrobial activities. There is an increase in the content of salicylic acid (SA) in the organs that manifest SAR. This increase in SA content is essential for the activation of SAR. Moreover, the application of SA or its functional analog, benzothiadiazole (BTH), induces a SAR-type response in the tissue to which it is applied. The Arabidopsis NPR1 gene is required for the activation of SAR. In addition to SAR, SA and NPR1 have an important role in the basal resistance to pathogens, also. Recent studies suggest an important role for plant lipids in the activation of SAR. A putative lipid-transfer protein, DIR1, and a SA-binding lipase, SABP2, are required for the activation of SAR in Arabidopsis and tobacco, respectively (Maldonado, et al. Nature 419: 399-402, 2002; Kumar and Klessig, Proc. Natl. Acad. Sci. USA 100: 16101-16106, 2003). Previously, we have shown that a recessive mutation in the Arabidopsis SSI2 gene, which encodes a fatty acid desaturase, constitutively activates an SAR-like defense response in the ssi2 mutant plant (Shah et al. Plant J 25: 563-574, 2001). In contrast, SAR is compromised in the sfd1 mutant, which was identified as a suppressor of ssi2 (Nandi et al. Plant Cell 15: 2383-2398, 2003; Nandi et al. Plant Cell 16: 465-477, 2004). SFD1 is required for the SAR-associated accumulation of SA. However, SFD1 is not directly involved in SA synthesis as SA does accumulate to high levels in the pathogen-inoculated leaves of the sfd1 mutant. Glycerolipid composition is altered in the sfd1 mutant plant. SFD1 encodes a dihydroxyacetone phosphate (DHAP) reductase that catalyzes the synthesis of glycerol-3-phosphate, which provides the glycerol backbone in glycerolipids. Our results suggest that a lipid-derived molecule is required either for the synthesis/translocation of the mobile signal and/or for the perception of the mobile signal in SAR.