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Salicylic acid (SA) and nitric oxide (NO) are key signal molecules involved in the reduction of Al accumulation in many plants. The purpose of this study was to investigate whether they could reduce the root content of Al and/or its binding to the root cell wall (CW) fractions in Panax notoginseng, and to investigate the corresponding regulatory mechanisms. Effects of Al treatments on the endogenous SA and NO contents of P. notoginseng were detected. Exogenous SA and paclobutrazol (PAC, a SA synthesis inhibitor) treatments were conducted to test the effects on endogenous NO content; exogenous sodium nitroprusside (SNP, a NO doner) and 2-phenyl-4,4,5,5-tetramethyl- imidazoline-1-oxyl-3-oxyde (cPTIO, a NO synthesis inhibitor) treatments were conducted to test the effects on endogenous SA content. Pectin methyltransferase (PMT) and pectin methylesterase (PME) activity and the gene expression, pectin methylesterification degree (PMD), pectin content, and the accumulation of Al in roots were also studied under the treatments described above. Al stress induced a significant increase of the activity and expression of phenylalanine ammonia-lyase (PAL), and promoted the significant increase of endogenous SA content of P. notoginseng roots. The Al promoted accumulation of endogenous NO could be enhanced by exogenous SA treatment, but was reduced by PAC. Accumulation of endogenous NO that promoted by Al could be enhanced by exogenous SA treatment, but was reduced by PAC treatment. However, SNP or cPTIO treatments had no significant effect on the Al-induced endogenous SA content of P. notoginseng. This showed that NO acted downstream of SA signaling of P. notoginseng under Al stress. Al stress can increase the activity and genes expression of PME in the roots of P. notoginseng, reduce PMD, increase CW pectin content, and thus, the binding capacity of CW pectin to Al was enhanced in P. notoginseng roots. Exogenous SA or SNP both reduced the Al-binding capacity of root CW pectin by decreasing the pectin content, and increased the PMD by inhibiting the genes expression and activity of PME. The effects of PAC or cPTIO on the above-mentioned indicators under Al stress were opposite to that of exogenous SA or SNP treatments. The Al stress induced accumulation of pectin and the reduction of PMD in the root CW of P. notoginseng could be reversed by the treatments of exogenous SA or SNP, then the Al contents in root CW pectin were reduced. Al stress activated the endogenous SA and NO signaling pathways in P. notoginseng, and NO acted downstream of SA. It showed that the Al-activated NO-SA signaling pathway contributed in the reduction of Al binding to the root under Al stress.

Panax notoginseng is normally cultivated in acidic red soil with high soluble Al, however, the distribution pattern of Al in P. notoginseng is unknown. The aim of this study is to investigate the Al distribution in different organs of P. notoginseng grown in different acid soil, in order to get a deeper insight into the Al tolerance mechanism in this species. P. notoginseng was sampled from different sites and subjected to Al determination. Al tolerance and accumulation were investigated by exposing the seedlings to different Al concentrations in hydroponic solution. The expression of pectin methylesterase genes was determined by quantitative RT-PCR. The soil pH ranged from 4.68 to 6.13. The total Al concentration in soil was 76.7–168.5 g·kg−1 and active Al was 1.34–5.01 g·kg−1. Al concentration differed with organs of P. notoginseng, following the order: rootlet > rhizome > main root > leaf and stem. Furthermore, Al concentration in the cell wall, organelle and cytoplasmic supernatant of P. notoginseng was approximately 15:2:1 and most Al in the cell wall was bound to pectin component. Al treatment significantly increased the content of pectin and enhanced the expression of PME3, PME7, and PME40 of P. notoginseng root. P. notoginseng was able to grow under high active Al condition and accumulated high Al in its underground parts. The pectin component in the cell wall was the major binding site of Al of P. notoginseng root.