1.14.13.237	up	enzyme expression is increased under jasmonic acid treatment (0.1 mM)	
1.14.13.237	up	isoforms FMOGS-OX1, FMOGS-OX2, FMOGS-OX6, and MYB28 show upregulation (5fold) toward absisic acid, isoforms FMOGS-OX5, FMOGS-OX6, and FMOGS-OX7 toward 20 mM 20 mM 1-aminocyclopropane-1-carboxylic acid, isoform FMOGS-OX1 toward 0.05 mM methyl jasmonate, isoform FMOGS-OX7 toward 0.2 mM salicylic acid, and isoforms FMOGS-OX2 and FMOGS-OX5 toward 0.1 mM iodoacetic acid	
1.14.13.237	up	expression of isoforms FMOGS-OX2 and FMOGS-OX4 is induced by glucose treatment, independent of transcription factors MYB28/29 and MYC2/3/4. Glucose-triggered upregulation of FMOGS-OX2 and FMOGS-OX4 is partially regulated by abscisic acid through the key negative regulators ABI1 and ABI2, and the positive regulator SnRK2, but not via the transcription factor ABI5	
1.14.13.237	up	the expression of FMOGS-OX2 and FMOGS-OX4 is induced by glucose treatment, independent of MYB28/29 and MYC2/3/4, the transcription factors that positively regulate aliphatic GSL biosynthesis. Glucose treatment of the abscisic acid (ABA)-related mutants indicated that glucose-triggered upregulation of FMOGS-OX2 and FMOGS-OX4 was partially regulated by ABA through the key negative regulators ABI1 and ABI2, and the positive regulator SnRK2, but not via the transcription factor ABI5. In wild-type plants, glucose treatment drastically reduces the accumulation of 4-methylthiobutyl (4MT) GSL, whereas a decrease in 4MT GSL is not observed in the fmogs-ox2, abi1-1, abi2-1, aba2-1, or aba3-1 mutants. This result indicates that the decreased accumulation of 4MT GSL by glucose treatment is attributed to upregulation of FMOGS-OX2 via the ABA signaling pathway. The expression of the FMOGS-OX2 and FMOGS-OX4 genes is induced by glucose treatment independent of the MYB and MYC transcription factors