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Information on EC 1.14.99.36 - beta-carotene 15,15'-monooxygenase and Organism(s) Mus musculus and UniProt Accession Q9JJS6
for references in articles please use BRENDA:EC1.14.99.36deleted. Now classified as EC 1.13.11.63, beta-carotene 15,15'-dioxygenase
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1.14.99.36 beta-carotene 15,15'-monooxygenaseSynonyms
beta-carotene 15,15'-dioxygenase, 
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topGENERAL INFORMATION 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
evolution
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BCMO1 is a member of an evolutionary well-conserved family of carotenoid cleavage oxygenases
malfunction
physiological function
metabolism
physiological function
additional information
malfunction
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BCMO1 knock-out mice become vitamin A deficient despite expressing BCDO2. Hepatic BCDO2 expression is significantly elevated in BCMO1 KO mice compared with wild-type mice, leading to a significant increase in beta-apo-12'-carotenal or beta-apo-10'-carotenal concentration. BCMO1 KO mice reveal a large accumulation of beta-carotene in tissues (liver, lung, adipose tissue) of animals on a beta-carotene-enriched diet. Increased susceptibility of BCMO1 KO mice to diet induced obesity, coupled with increased expression of PPAR-gamma-induced genes. Knockout of BCMO1 alters serum lipid levels and leads to the development of liver steatosis in mice
malfunction
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Bcmo1-/- mice show increased expression of Bcdo2 in adipocytes and beta-10'-apocarotenol accumulates as the major beta-carotene derivative. Bcmo1-/- mice have a lower average body weight than wild-type mice
malfunction
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genetic disruption of BCO1 results in beta-carotene accumulation and vitamin A deficiency accompanied by a BCO2-dependent production of minor amounts of beta-apo-10'-carotenol, which can be esterified and transported by the same proteins as vitamin A but with a lower affinity and slower reaction kinetics. all-trans-Retinol treatment of vitamin A-deprived Bco1-/- mice decreases hepatic retinol-binding protein levels
malfunction
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lack of CMOI in the developing tissues further exacerbates the severity of vitamin A deficiency and thus the embryonic malformations of retinol-binding protein-deficient mice, phenotypes, overview
malfunction
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reduced BCMO1 expression in normal preneoplastic intestine of folate-deficient tumor-prone mice. A mouse model develops intestinal tumors after low dietary folate
physiological function
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BCMO1 catalyzes the symmetric cleavage of carotenoids. BCMO1 is the key enzyme for beta-carotene conversion into vitamin A. BCMO1-dependent decrease in PPAR-gamma target gene expression is observed during beta-carotene supplementation in inguinal white adipose tissue. The intestine-specific transcription factor intestine-specific homeobox in mouse intestine is an important regulator of BCMO1 expression. Activation of intestine-specific homeobox results in repression of SR-BI and BCMO1 expression thereby controlling beta-carotene absorption as well as vitamin A production
physiological function
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beta,beta-carotene 15,15'-monooxygenase and its substrate beta-carotene modulate migration and invasion in colorectal carcinoma cells. Increased beta-carotene consumption is linked to antitumor effects. Retinoic acid reduces the invasiveness in cancer, through inhibition of matrix metalloproteinases
physiological function
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beta-carotene plays an important role in the control of body adiposity in mice. The enzyme is a critical molecular player for the regulation of peroxisome proliferator-activated receptor gamma activity in adipocytes
physiological function
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beta-carotene-15,15'-oxygenase BCO1, but not beta-carotene-9',10'-oxygenase BCO2, is critical for retinoid homeostasis. In wild-type mice, beta-apo-10'-carotenol is converted to retinoids by BCO1
physiological function
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CMOI is expressed in embryonic tissues, suggesting that beta-carotene provides retinoids locally during development. CMOI exerts an additional function on retinoid metabolism by influencing retinyl ester formation via modulation of lecithin:retinol acyltransferase activity, at least in developing tissues
metabolism
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Bcmo1 and retinal dehydrogenase 1 are key enzymes in the retinoid metabolism of inguinal white adipose tissue
metabolism
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carotenoids and apo-carotenoids are converted to retinal by beta-carotene 15,15'-dioxygenase, BCDO, by beta-carotene 15,15'-monooxygenase, BCMO, and by apo-carotenoid 15,15'-oxygenase, ACO, EC 1.14.99.41
physiological function
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beta,beta-carotene 15,15'-monooxygenase-1, BCMO1, is a key enzyme in vitamin A metabolism in mammals. BCMO1 plays a significant physiological role in the local regulation of vitamin A and retinal in reproduction and development. Model of the putative mechanism for the regulation of BCMO1 by dietary fat and PPARgamma, overview
physiological function
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carotenoid 15,15'-oxygenases produce retinal from carotenoids
additional information
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dietary beta-carotene downregulates peroxisome proliferator-activated receptor gamma and peroxisome proliferator-activated receptor gamma target genes in adipose tissue of wild-type mice. Supplementation of beta-carotene alters gene expression profiles in wild-type but not in Bcmo1-/- mice
additional information
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beta-carotene represses Ppar gamma and CCAAT/enhancer-binding protein alpha expression in mature adipocytes
EXPRESSION
ORGANISM
UNIPROT
LITERATURE
Isx, intestine specific homeobox, participates in the maintenance of vitamin A by regulating Bcmo1 expression in the intestine
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severe vitamin A deficiency markedly decreases intestine-specific transcription factor intestine-specific homeobox expression accompanied by an increase in BCMO1 expression in duodenum and jejunum
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Release 2023.1 (January 2023)
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