Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2011 Apr;155(4):1762-8.
doi: 10.1104/pp.110.171694. Epub 2011 Feb 10.

Interconnection between methyl salicylate and lipid-based long-distance signaling during the development of systemic acquired resistance in Arabidopsis and tobacco

Po-Pu Liu  1 , Caroline C von Dahl, Sang-Wook Park, Daniel F Klessig
Affiliations

Interconnection between methyl salicylate and lipid-based long-distance signaling during the development of systemic acquired resistance in Arabidopsis and tobacco

Po-Pu Liu et al. Plant Physiol. 2011 Apr.
No abstract available

PubMed Disclaimer

Figures

Figure 1.
Figure 1.
Characterization of wild-type Ws-2 and Atdir1-1 plants. A, AtBSMT1 gene expression in primary infected and systemic leaves was analyzed at the indicated times in hours postmock (M) or Psm AvrRpt2 cor- (I) infection of 3- to 4-week-old wild-type Ws-2 or Atdir1-1 plants. Eukaryotic Translation Initiation Factor4a (EIF4a) was used as an internal control in the reverse transcriptase-PCR assays. AtBSMT1 and EIF4a were amplified using 25 and 20 cycles, respectively. Two independent experiments were analyzed with similar results. B, MeSA. C, SA. D, SAG contents were quantified in primary infected and systemic leaves of Psm AvrRpt2 cor--infected 3- to 4-week-old plants at the indicated times. Asterisks in B, C, and D indicate statistically significant differences (* = P < 0.05, ** = P < 0.01, Student’s t test) between levels in Atdir1-1 versus wild-type Ws-2 for each time point. Mean ± sd values are presented. Two independent experiments were analyzed with similar results.
Figure 2.
Figure 2.
Characterization of the tobacco homlogs of AtDIR1. A, Restoration of SAR proficiency in Atdir1-1 by CaMV 35S-driven expression of NtDIR1, NtDIR2, and NtDIR3. T2 transgenic plants were used for SAR analysis. The CaMV 35S-driven EV served as the control. Asterisks indicate statistically significant differences (* = P < 0.01, Student’s t test) in the growth of virulent Pst in plants induced for SAR by prior infection with Psm AvrRpt2 cor- as compared to plants that received an initial mock inoculation and therefore were not induced for SAR. Mean ± sd values are presented. B, The pHANNIBAL construct for silencing of NtDIR1, NtDIR2, and NtDIR3 contains approximately 300 nucleotides of each of the three NtDIRs arranged sequentially. C, Analysis of SAR in three transgenic lines, RNAi::NtDIRs #9, RNAi::NtDIRs #10, and RNAi::NtDIRs #11, which contain a single insertion of the pHANNIBAL RNAi construct shown in B. SAR was determined as percent reduction in the size of TMV lesions formed after a secondary infection on plants induced for SAR by prior TMV infection, as compared to lesions formed on plants that had received a mock inoculation and therefore were not induced for SAR. Plants transformed with the pHANNIBAL RNAi::EV served as a control. D, The silencing efficiency of NtDIRs in RNAi::NtDIRs #9, RNAi::NtDIRs #10, and RNAi::NtDIRs #11. The same plants were used in C. Elongation factor 1α (EF1α) was used as an internal control in reverse transcriptase-PCR assays. NtDIR1, NtDIR2, and NtDIR3 were amplified using 25 cycles, while 20 cycles was used for EF1α. E, NtSAMT1 gene expression was analyzed in the primary infected and systemic leaves of 6-week-old wild-type and RNAi::NtDIRs #9 plants at the indicated times. NtSAMT1 and EF1α were amplified using 36 and 25 cycles, respectively. Two independent experiments were analyzed with similar results in A, C, D, and E.
Figure 3.
Figure 3.
Working model of the interrelationship between MeSA and lipid-based, long-distance signaling for SAR. After pathogen attack, SA levels rise in the primary infected tissue. SA is partially converted to MeSA by AtBSMT1 (1). MSE can demethylate MeSA to reform SA; however, the rising levels of SA inhibit MSE by binding in its active site pocket (2). The accumulating MeSA is translocated to the uninoculated systemic tissue (3). In the primary infected tissue, AtDIR1 and an AtSFD1-dependent lipid form a complex, denoted XY (4), which is translocated to the systemic tissue (5). In the systemic tissue, MSE activity converts biologically inactive MeSA to active SA (6). To facilitate SA accumulation, and thereby SAR development, AtBSMT1 expression is directly or indirectly suppressed by the DIR1-lipid derivative complex, XY (7).
Figure 4.
Figure 4.
Exogenous MeSA induced SAR in wild-type Ws-2, but not in Atdir1-1 or in NtDIR-silenced tobacco. A, Three days prior to infection, 0, 3.3, and 6.6 μm MeSA were infiltrated into lower leaves of wild-type Ws-2 and Atdir1-1 plants to induced resistance to subsequent challenge by Pst. As a positive control, SAR was induced in one set of plants by infection with Psm AvrRpt2 cor-. Asterisks indicate statistically significant differences (* = P < 0.05, ** = P < 0.01, Student’s t test) in Pst growth between untreated (or mock-infected) plants versus MeSA-treated (or Psm AvrRpt2 cor- infected) plants. B, MeSA (0 or 5 μm) was infiltrated into lower leaves of wild-type or RNAi::NtDIRs #9 tobacco; 5 d posttreatment upper, untreated leaves were inoculated with TMV. Lesion sizes were measured 5 d postinfection (dpi). Pictures showing representative TMV lesions were taken 5 dpi. Tobacco plants induced for SAR via a primary infection with TMV served as a positive control. Two independent experiments were analyzed with similar results in A and B.
See this image and copyright information in PMC

References

    1. Attaran E, Zeier TE, Griebel T, Zeier J. (2009) Methyl salicylate production and jasmonate signaling are not essential for systemic acquired resistance in Arabidopsis. Plant Cell 21: 954–971 - PMC - PubMed
    1. Browse J, Somerville CR. (1991) Glycerolipid metabolism, biochemistry and regulation. Annu Rev Plant Physiol Mol Biol 42: 467–506
    1. Chaturvedi R, Krothapalli K, Makandar R, Nandi A, Sparks AA, Roth MR, Welti R, Shah J. (2008) Plastid omega3-fatty acid desaturase-dependent accumulation of a systemic acquired resistance inducing activity in petiole exudates of Arabidopsis thaliana is independent of jasmonic acid. Plant J 54: 106–117 - PubMed
    1. Jung HW, Tschaplinski TJ, Wang L, Glazebrook J, Greenberg JT. (2009) Priming in systemic plant immunity. Science 324: 89–91 - PubMed
    1. Kachroo A, Venugopal SC, Lapchyk L, Falcone D, Hildebrand D, Kachroo P. (2004) Oleic acid levels regulated by glycerolipid metabolism modulate defense gene expression in Arabidopsis. Proc Natl Acad Sci USA 101: 5152–5157 - PMC - PubMed

Publication types

Associated data

LinkOut - more resources