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Showing papers on "Cobalamin transport published in 2009"


Journal ArticleDOI
TL;DR: W whole-genome microarrays were applied to characterize the transcriptome during growth with excess and limiting concentrations of the corrinoid cyanocobalamin and the effects of exposure to spent medium from a methanogenic chloroethene-dehalogenating enrichment culture (designated ANAS) imply that ANAS spent medium contains corrinoids forms different from cyanOCobalamin.
Abstract: Dehalococcoides ethenogenes strain 195 utilizes corrinoid-containing reductive dehalogenases to reduce the environmental pollutants tetrachloroethene and trichloroethene to ethene. Although corrinoids are essential for dehalogenation activity, strain 195 cannot biosynthesize corrinoids de novo. To improve our understanding of corrinoid physiology in this bacterium, whole-genome microarrays were applied to characterize the transcriptome during growth with excess and limiting concentrations of the corrinoid cyanocobalamin. Additional studies examined the effects of exposure to spent medium from a methanogenic chloroethene-dehalogenating enrichment culture (designated ANAS). Both excess cyanocobalamin and ANAS spent medium resulted in the downregulation of two genes (DET0125-0126) that are encoded downstream of a putative cobalamin riboswitch. In contrast, only ANAS spent medium resulted in the downregulation of three duplicated genes (DET0657-0659/DET0691-0693) encoded downstream of a second putative cobalamin riboswitch. These latter genes are predicted to be involved in synthesizing the lower ligand base that is attached to cobyric acid. It is also notable that only excess cyanocobalamin resulted in the downregulation of a predicted cobalamin transport system. Together, these results imply that ANAS spent medium contains corrinoid forms different from cyanocobalamin and that strain 195 adjusts its metabolism according to the corrinoid forms available for uptake.

58 citations


Journal ArticleDOI
TL;DR: Interestingly, urinary methylmalonic acid excretion was increased significantly during the first days of life suggesting that functional cobalamin deficiency is present also during fetal life, although not giving rise to clinical symptoms until well after birth.

25 citations