EC Number   |
General Information |
Reference |
|---|
  1.14.14.45 | physiological function |
a CYP83B1 knockout mutant, rnt1-1, leads to the the presence of indole glucosinolates at various levels in different developmental stages. Plants overexpressing CYP83B1 contain elevated levels of aliphatic glucosinolates derived from methionine homologs, whereas the level of indole glucosinolates is almost constant in the overexpressing lines |
741196 |
| 1.14.14.45 | physiological function |
a T-DNA insertion in the CYP83B1 gene leads to plants with a phenotype that suggests severe auxin overproduction. Mutant seedlings are characterized by increased hypocotyl length, epinastic cotyledons, exfoliation of the hypocotyl, adventitious root formation from the hypocotyl, enhanced secondary root and root hair formation, and eventually callus formation and increasing disintegration of the seedling. Mutant seedlings contain reduced levels of indole glucosinolates. CYP83B1 overexpression leads to loss of apical dominance typical of auxin deficit |
741148 |
| 1.14.14.45 | physiological function |
aliphatic oximes derived from chain-elongated homologs of methionine are efficiently metabolized by isoform CYP83A1, whereas CYP83B1 metabolizes these substrates with very low efficiency. Aromatic oximes derived from phenylalanine, tryptophan, and tyrosine are metabolized by both enzymes, although CYP83B1 has higher affinity for these substrates than CYP83A1. Plants overexpressing CYP83B1 contain elevated levels of aliphatic glucosinolates derived from methionine homologs, whereas the level of indole glucosinolates is almost constant in the overexpressing lines |
741196 |
| 1.14.14.45 | physiological function |
inactivation of CYP83B1 leads to plants with a phenotype that suggests severe auxin overproduction, whereas CYP83B1 overexpression leads to loss of apical dominance typical of auxin deficit |
743440 |
| 1.14.14.45 | physiological function |
knockout of CYP83B1 leads to a strong auxin excess phenotype |
743483 |
| 1.14.14.45 | physiological function |
lack of the CYP83B1 gene product leads to auxin excess and indole glucosinolate deficit, ectopic overexpression of CYP83A1 using a 35S promoter rescues phenotype. Indole-3-acetaldoxime has a 50-fold higher affinity toward CYP83B1 than toward CYP83A1, EC 1.14.14.43. Both enzymes also metabolize the phenylalanine- and tyrosine-derived aldoximes. Indole-3-acetaldoxime is the physiological substrate for CYP83B1 |
741195 |
| 1.14.14.45 | physiological function |
model for the biosynthesis of Trp-derived glucosinolates and camalexin in Arabidopsis thaliana. The two first enzymes in biosynthesis are cytochromes P450 of the families CYP79 and CYP83, respectively. They convert the amino acids to activated aldoximes that react spontaneously with thiols to form thiol conjugates |
741152 |
| 1.14.14.45 | physiological function |
mutant plants have constitutively activated expression of the Atr1 Myb factor gene. The Atr1D mutant enhances the adventitious root formation of Cyp83B1 mutants, and Axr1, involved in RUB1 post-translational modifications, is necessary for cyp83B1 5-methyl tryptophan resistance. Cyp83B1 mutants have lesion-mimic phenotypes, suggesting that multiple stress pathways are activated by loss of Cyp83B1 function |
740514 |
| 1.14.14.45 | physiological function |
reduced epidermal fluorescence5 (ref5-1) mutant, identified leading to plants with defects in soluble phenylpropanoid accumulation, has a missense mutation in CYP83B1 and displays defects in glucosinolate biosynthesis and in phenylpropanoid accumulation |
741163 |
| 1.14.14.45 | physiological function |
the two key glucosinolate synthetic genes CYP83A1 and CYP83B1 are highly conserved within the Brassicaceae family |
740546 |
