Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.31 (beta-glucuronidase)
 7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

All methyl-beta-D-galacturonide-positive mutants isolated from Escherichia coli K-12 carry constitutive mutations for beta-glucuronidase (UID) synthesis. Most of these mutants are specific for UID synthesis and are distributed in three classes according to the derepression level of UID. Each specific mutant carries a mutation(s) near uidA, the structural gene for UID, at min 30.5 of the E. coli K-12 linkage map. The expression of UID synthesis in F-merodiploid strains carrying these mutations permits discrimination between dominant and recessive constitutivity over the wild-type allele. The first kind of mutation (dominant) should affect the operator site uidO of the structural gene uidA; the second type of mutation (recessive) should affect a regulatory gene, uidR, operating through a negative control. The isolation of mutants bearing at this locus superrepressed mutations, which can revert to produce a constitutive phenotype, confirms the occurrence of such a regulatory gene. The partially derepressed uidR mutants of the first class are normally inducible and remain constitutive at low temperature; their UID has the same thermal sensitivity as in the wild-type strains. The occurrence of similar regulatory gene mutants has been recently described in the lactose system (Shineberg, 1974).
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PMID:Regulation of beta-glucuronidase synthesis in Escherichia coli K-12: constitutive mutants specifically derepressed for uidA expression. 77 33

Plants perceive subtle changes in light quality and quantity through a set of photoreceptors, including phytochromes and cryptochromes. Upon perception, these photoreceptors initiate signal transduction pathways leading to photomorphogenic changes in development. Using activation-tagging mutagenesis to identify novel light-signaling components, we have isolated a gain-of-function mutant, sob1-D (suppressor of phytochrome B-4 [phyB-4] dominant), which suppresses the long-hypocotyl phenotype of the phyB missense allele, phyB-4. The sob1-D mutant phenotype is caused by the overexpression of a Dof (DNA binding with one finger) transcription factor, OBF4 Binding Protein 3 (OBP3). A translational fusion between OBP3 and green fluorescent protein is nuclear localized in onion (Allium cepa) cells. Tissue-specific accumulation of an OBP3:OBP3-beta-glucuronidase translational fusion is regulated by light in Arabidopsis thaliana. Hypocotyls of transgenic lines with reduced OBP3 expression are less responsive to red light. This aberrant phenotype in red light requires functional phyB, suggesting that OBP3 is a positive regulator of phyB-mediated inhibition of hypocotyl elongation. Furthermore, these partial-loss-of-function lines have larger cotyledons. This light-dependent cotyledon phenotype is most dramatic in blue light and requires functional cryptochrome 1 (cry1), indicating that OBP3 is a negative regulator of cry1-mediated cotyledon expansion. These results suggest a model where OBP3 is a component in both phyB and cry1 signaling pathways, acting as a positive and negative regulator, respectively. An alternate, though not mutually exclusive, model places OBP3 as a general inhibitor of tissue expansion with phyB and cry1, differentially modulating OBP3's role in this response.
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PMID:The Dof transcription factor OBP3 modulates phytochrome and cryptochrome signaling in Arabidopsis. 1565 36