Abstract
Phytoplasmas, wall-less and phloem-restricted plant pathogens, are transmitted by insect vectors. They can infect many crops and cause severe symptoms. Plant may use a systemic defense system to fight against them. In periwinkles, PR1 is induced in both symptomatic and non-symptomatic parts when they are infected by PLY phytoplasma, and the non-symptomatic parts are more resistant to PLY phytoplasma infection than healthy controls. Both NPR1 and NPR3 play an important role in Systemic acquired resistance (SAR). When periwinkles are infected by PLY, CrNPR1 is moderately induced. In addition, silencing of CrNPR1 accelerates symptom progression of PLY, while silencing of CrNPR3 attenuates the progression. To further understand whether the functions of CrNPR1 and CrNPR3 are similar to their Arabidopsis homolog, AtNPR1, we generated Arabidopsis transgenic plants that overexpress AtNPR1, CrNPR1 or CrNPR3 in Col-0, npr1-1 and NahG backgrounds, and compared their defense responses to Pseudomonas syringae pv. tomato DC3000 (PstDC3000). The results showed that induction of PR1 was not restored after PstDC3000 infection in all transgenic lines in the NahG background, indicating that similar to AtNPR1, induction of PR1 mediated by CrNPR1 or CrNPR3 may depend on SA signaling. In addition, overexpressed CrNPR1 in npr1-1 seems to slightly restored the induction of PR1 expression; however, we need to repeat the experiment to confirm the results. We also did not observe the restored plant defense to PstDC3000 in all of the transgenic lines. Therefore, we failed to conclude whether CrNPR1 and CrNPR3 have a similar function to AtNPR1 to affect disease resistance of Arabidopsis to PstDC3000. In addition, NahG and npr1-1 lines were not more susceptible to Pst DC3000 infection than Col-0. The experimental conditions will need to be optimized to obtain consistent results, and the function of CrNPR1 and CrNPR3 will be concluded in the future. Because AtNPR1 enters nucleus in response to SA, the localization of CrNPR1 and CrNPR3 will also be examined in the future. Our results will extend our knowledge in plant defense mechanism against phytoplasma.
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