1.14.13.237	up	enzyme expression is increased under jasmonic acid treatment (0.1 mM)	743177	
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	-, 765621	
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	742595	
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	-, 765621