AAL1

AAL1 (F1800-0169) (0-200 μM; 3 days) inhibits root and hypocotyl growth of dark-grown Arabidopsis thaliana Col-0 seedlings, with an IC₅₀ of 20 μM for root growth and 50 μM for hypocotyl growth, but does not inhibit apical hook growth at concentrations below 180 μM^[1].
AAL1 (10-20 μM; 6 d; 16 h light/8 h dark) promotes hypocotyl elongation in Col-0 and yuc1/2/4/6 seedlings, indicating that this effect is independent of YUCCA-mediated auxin biosynthesis^[1].
The inhibitory effect of AAL1 (50 or 100 μM; 3 d; dark culture) on root growth is significantly attenuated in tir1-1 seedlings, whereas yuc1/2/4/6 shows no significant resistance to AAL1, which supports that the biological function of AAL1 depends on the auxin receptor TIR1 rather than auxin biosynthesis^[1].
AAL1 (50 μM; 0.5 or 3 h; dark-cultured Col-0 seedlings) increases the expression of auxin-responsive genes ARF19, IAA2 and GH3.3, with a significant elevation already observed at 0.5 h^[1].
AAL1 (0.5-3 h; DII-VENUS transgenic seedlings) rapidly reduces the DII-VENUS fluorescence signal, with obvious degradation observable within 0.5 h; its effect is weaker than that of 2,4-D and IAA, which supports that AAL1 is involved in TIR1-mediated degradation of auxin signaling proteins^[1].
Root and hypocotyl growth inhibition induced by AAL1 (100 μM; 3 d; dark culture) is partially reversed by the auxin efflux inhibitor NPA (0.05-0.2 μM); in addition, multiple aux1 mutants show reduced sensitivity to AAL1, indicating that the action of AAL1 depends on auxin influx and efflux transport systems^[1].
The inhibition of seedling root and hypocotyl growth induced by AAL1 (100 μM; 3 d; dark culture) can be significantly partially reversed by Tyr or Phe (200 μM), while Trp does not exert the same reversing effect^[1].
After treatment with AAL1 (100 μM; seeds imbibed at 4°C for 3 d, followed by germination in the dark at 22°C for 3 d), LC-MS detects a chemical with the same mass and retention time as AAL1 in seedlings, supporting that AAL1 mainly functions in an unmodified form^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.