beginning and then a sharp decrease, but it has noobvious influenceon
gluconapin and sinigrin (Fig. 1A). No significant changes in the content
of individual and total aliphatic and indole glucosinolates were ob-
served after Ethrel and 1-MCP (Fig. 1A).
The effects of SA treatments on glucosinolates varied with the dif-
ferent SA treatment methods (Fig. 1B). A steady increase in 4-
methoxyglucobrassicin content was observed by all SA treatments
with a peak value at 6 d after treatment. In contrast, the content
of 4-methoxyglucobrassicin at 6 d after treatment was 7.38 fold
(SA/SA), 7.43 fold (Control/SA) and 6.65 fold (SA/Control) higher, re-
spectively. Moreover, glucobrassicin showed a notable decline after
SA/SA and Control/SA treatments. SA/Control treatment significantly
increased the contents of gluconapin and sinigrin at 6 d. Similar to
the effect of MeJA treatment, progoitrin was notably induced at the
beginning and then declined among all three SA treatments (Fig. 1B).
beginning and then a sharp decrease, but it has noobvious influenceongluconapin and sinigrin (Fig. 1A). No significant changes in the contentof individual and total aliphatic and indole glucosinolates were ob-served after Ethrel and 1-MCP (Fig. 1A).The effects of SA treatments on glucosinolates varied with the dif-ferent SA treatment methods (Fig. 1B). A steady increase in 4-methoxyglucobrassicin content was observed by all SA treatmentswith a peak value at 6 d after treatment. In contrast, the contentof 4-methoxyglucobrassicin at 6 d after treatment was 7.38 fold(SA/SA), 7.43 fold (Control/SA) and 6.65 fold (SA/Control) higher, re-spectively. Moreover, glucobrassicin showed a notable decline afterSA/SA and Control/SA treatments. SA/Control treatment significantlyincreased the contents of gluconapin and sinigrin at 6 d. Similar tothe effect of MeJA treatment, progoitrin was notably induced at thebeginning and then declined among all three SA treatments (Fig. 1B).
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