High impact information on CYP83B1

• CYP83B1, a cytochrome P450 at the metabolic branch point in auxin and indole glucosinolate biosynthesis in Arabidopsis [1].
• A T-DNA insertion in the CYP83B1 gene leads to plants with a phenotype that suggests severe auxin overproduction, whereas CYP83B1 overexpression leads to loss of apical dominance typical of auxin deficit [1].
• CYP83B1 N-hydroxylates indole-3-acetaldoxime to the corresponding aci-nitro compound, 1-aci-nitro-2-indolyl-ethane, with a K(m) of 3 microM and a turnover number of 53 min(-1) [1].
• The evidence suggests that red1 represents a putative phytochrome signal transduction mutant potentially specific to the phyB pathway [2].
• RED1 is necessary for phytochrome B-mediated red light-specific signal transduction in Arabidopsis [2].

Biological context of CYP83B1

• The knockout mutant of the CYP83B1 gene (rnt1-1) shows a strong auxin excess phenotype and are allelic to sur-2 [3].
• The involvement of two p450 enzymes, CYP83B1 and CYP83A1, in auxin homeostasis and glucosinolate biosynthesis [3].
• CYP83A1 and CYP83B1 heterologously expressed in yeast (Saccharomyces cerevisiae) cells show marked differences in their substrate specificity [3].
• CYP83A1 is the closest relative to CYP83B1 and shares 63% amino acid sequence identity [3].
• Analysis of indole-3-acetic acid (IAA) synthesis and metabolism in sur2 plants indicates that the mutation causes a conditional increase in the pool size of IAA through up-regulation of IAA synthesis [4].

Associations of CYP83B1 with chemical compounds

• Another cytochrome P450 enzyme, CYP83B1, funnels IAOx into IGS [5].
• Although expression of CYP83A1 under control of its endogenous promoter in the rnt1-1 background does not prevent the auxin excess and indole glucosinolate deficit phenotype caused by the lack of the CYP83B1 gene, ectopic overexpression of CYP83A1 using a 35S promoter rescues the rnt1-1 phenotype [3].
• The presence of putative auxin responsive cis-acting elements in the CYP83B1 promoter but not in the CYP83A1 promoter supports the suggestion that CYP83B1 has evolved to selectively metabolize a tryptophan-derived aldoxime intermediate shared with the pathway of auxin biosynthesis in Arabidopsis [3].
• The ability of CYP83A1 to metabolize aromatic oximes, albeit at small levels, explains the presence of indole glucosinolates at various levels in different developmental stages of the CYP83B1 knockout mutant, rnt1-1 [6].
• 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 [6].

Regulatory relationships of CYP83B1

• Constitutive and inducible over-expression of OBP2 activates expression of CYP83B1 [5].

Other interactions of CYP83B1

• However, indole-3-acetaldoxime has a 50-fold higher affinity toward CYP83B1 than toward CYP83A1 [3].

Analytical, diagnostic and therapeutic context of CYP83B1

• Analysis by gas chromatography coupled to mass spectrometry indicated increased levels of free indole-3-acetic acid correlated with a decreased level of bound auxin in the sur2 mutant [7].

References