Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.23 (beta-galactosidase)
 14,648 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The gene ileR+, considered to encode a transacting protein involved in the regulation of the thr and ilv operons of Escherichia coli, has been cloned and localized to a 1.2 Kb BglII-SalI fragment of DNA. In strains harboring attenuation-defective fusions of lacZ to the promoter regions of the thr and ilv operons, ileR mutations lead to beta-galactosidase levels higher than those of the deattenuated parental strains. Reduced utilization of the thr and ilv promoters was observed in ileR cells harboring either ilvR+ plasmids or plasmids leading to the hyperproduction of Trp repressor. These results support the idea that ileR+ encodes a repressor protein that negatively affects the expression of the thr and ilv operons. Two additional trans-acting positive regulatory elements that act at the thr and ilv promoters have been identified by an analysis of deletion mutants. It thus appears that there exist positive as well as negative controlling elements that can act independently of attenuation to modulate the ilv and thr operons.
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PMID:New regulatory genes involved in the control of transcription initiation at the thr and ilv promoters of Escherichia coli K-12. 609 66

The positive regulatory gene (phoM) for alkaline phosphatase of Escherichia coli was cloned on a mini-F plasmid pMF3 from the E. coli chromosome by a shotgun method. The hybrid plasmid pTHR32, which carries 10.8 kb chromosomal DNA, complemented both phoM and thrB mutations. The restriction map was constructed. Based upon this information, several PhoM- deletion plasmids and smaller PhoM+ plasmids were constructed in vitro. By examining the phenotypes and the physical maps of these plasmids, we could define the phoM gene locus in a 2.5 kb region on the restriction map of the cloned chromosomal DNA fragment. The PhoM+ plasmid not only enabled a phoM- -phoR- double mutant to express phoA (the structural gene for the alkaline phosphatase) but also phoB (another positive regulatory gene for phoA). These results are consistent with a model for genetic regulation of phoA expression that proposes that both the phoM and phoR gene products activate phoB expression under phosphate starved conditions, and PhoB protein, in turn, activates phoA expression. The phoM gene product was identified by the maxicell method as a protein with a molecular weight of 60,000. A hybrid plasmid that carries a phoM'-'lacZ fused gene on mini-F vector pMF3 was constructed in vitro. This plasmid enabled us to study phoM gene expression by measuring the beta-galactosidase level in the cells. The plasmid was introduced into various regulatory mutants related to the phosphate regulon, and phoM gene expression in these strains was studied under conditions of limited or excess phosphate. It was found that phoM expression was not regulated by phosphate nor by any of the pho genes. The transcriptional direction of phoM was found to be clockwise toward the thr operon on the E. coli genetic map. The fusion gene product interfered with phoB and phoA expression in the phoR mutants. Overproduction of PhoM protein increased phoB and phoA expression only in the phoR mutants. The implications of these findings are discussed.
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PMID:Cloning and characterization of the alkaline phosphatase positive regulatory gene (phoM) of Escherichia coli. 638 64

Following heat shock the expression of heat shock genes is regulated by the heat shock transcription factor, HSF, known to bind to arrays of the heat shock element, NGAAN, upstream of the heat shock genes. Phosphorylation of HSF is necessary for its activation. We report that the treatment of Chinese hamster HA-1 cells with 250 nM of okadaic acid (OA), a ser/thr phosphatase inhibitor, leads to an increase in activated HSF after heat shock. This is followed by the activation of the transcription of heat shock genes as assayed by the increase in the synthesis of beta-galactosidase in an HA-1 cell line containing the heat shock promoter ligated to the beta-galactosidase gene. To investigate the specificity of OA, we used other phosphatase inhibitors. We found that treatment of HA-1 cells with 500 microM of sodium vanadate, an inhibitor of tyr/phosphatases, resulted in a three to fivefold reduction in HSF activation and binding to the heat shock element following heat shock. Such reduction in HSF activation virtually abolished beta-galactosidase induction. Reduced HSP synthesis was further confirmed by SDS-PAGE and Western blot analysis using anti-HSP-70 and 28 antibodies. Sodium vanadate treatment of heat shocked cells greatly reduced levels of thermotolerance. These results show that ser/thr and specifically tyr/phosphatase inhibitors modulate the signal transduction pathway of HSF activation.
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PMID:Inhibitors of tyrosine and Ser/Thr phosphatases modulate the heat shock response. 817 93

Elevated osmolality and pCO(2) have been shown to alter sialylation in a protein-specific manner. In Chinese hamster ovary (CHO)MT2-l-8 cells, tPA sialylation changed only slightly from 40 to 250 mm Hg pCO(2), whereas neural cell adhesion molecule polysialic acid (NCAM PSA) content decreased by up to 70% at 250 mm Hg pCO(2), pH 7.2. NCAM PSA content also decreased with increasing NaCl or NH(4)Cl concentration. This suggests that PSA content is a sensitive indicator of conditions that may alter glycosylation. Amino acids and their derivatives have been used to protect hybridoma and CHO cell growth under hyperosmotic stress. We examined the impact of osmoprotectants on NCAM PSA content in CHO MT2-1-8 cells under hyperosmolality (up to 545 mOsm/kg) and at 195 and 250 mm Hg pCO(2). NCAM PSA content at 545 mOsm/kg was at least two-fold greater in the presence of glycine betaine or L-proline compared to that without osmoprotectant. Surprisingly, in the presence of 20 mM glycine betaine, PSA levels were 50-60% of the control level for osmolalities ranging from 320 to 545 mOsm/kg. Thus, glycine betaine inhibits NCAM polysialylation at osmolalities below 435 mOsm/kg and is beneficial at higher osmolalities. In contrast to glycine betaine, L-proline increased PSA content by 25-120% relative to the unprotected culture at < or =545 mOsm/kg. The decrease in NCAM PSA levels of CHO MT2-1-8 cells cultured at 195 mm Hg pCO(2)-435 mOsm/kg was not mitigated by the presence of 25 mM glycine betaine, glycine, or L-threonine, even though all of these compounds enhanced cell growth. At 250 mm Hg pCO(2), all osmoprotectants tested (20 mM L-threonine, L-proline, glycine, or glycine betaine) increased NCAM polysialylation, with 20 mM glycine betaine restoring NCAM PSA to near control levels. Thus, osmoprotectants may (partially) offset changes in glycosylation, as well as the inhibition of growth, in cells under environmental stress. Supernatant beta-galactosidase levels, which increase upon alkalization of acidic organelles, did not differ significantly under elevated pCO(2) and hyperosmolality from that at control conditions.
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PMID:Effects of osmoprotectant compounds on NCAM polysialylation under hyperosmotic stress and elevated pCO(2). 1178 9

Schwartz, Norman M. (Yale University, New Haven, Conn.). Suppression of a lac o degrees mutation in Escherichia coli. J. Bacteriol. 88:996-1001. 1964.-A class of pro(-) markers which can be cotransduced with lac map close to the i side of the lac region. The relative order of markers transferred by Hfr H is thr leu proA proB lac proC ade. Nine of ten slowgrowing lactose-utilizing revertants of a lac o degrees mutant are suppressed mutants. The time of entry of su-lac o-5 from an Hfr H derivative is 27 min. Su-lac o-5 is separated from the lac region by a 10-min interval. Su-lac o-5 is unstable, restores 7% of the wild-type level of beta-galactosidase activity, suppresses a try(-) mutation, and has a deleterious effect upon growth rate. The primary lac o degrees mutation is interpreted as being a z(-) polarity mutation which constitutes nonsense. Su-lac o-5 could act at the level of messenger ribonucleic acid translation converting nonsense to sense by promoting mistakes in protein synthesis.
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PMID:SUPPRESSION OF A LAC O-O MUTATION IN ESCHERICHIA COLI. 1421 65

The Salmonella tdc operon encodes enzymes belonging to a metabolic pathway that degrades L-serine and L-threonine. The upregulation of the tdc operon and increased virulence of Salmonella grown under oxygen-limiting conditions prompted us to investigate the role of the tdc operon in the pathogenesis of Salmonella Typhimurium. A Salmonella strain carrying a null mutation in tdcA, which encodes the transcriptional activator of the tdc operon, was impaired in mice infected intraperitoneally with the bacterium. In addition, the Salmonella tdcA mutant showed reduced replication compared with the parental strain in cultured animal cells, although their growth rates were similar in various culture media. To understand the function of TdcA in pathogenesis, we performed two-dimensional gel electrophoresis and found that flagellar and PhoP-regulated proteins were affected by the tdcA mutation. The results of beta-galactosidase assays and FACS analysis showed that, among the four PhoP-dependent genes tested, the expression of ssaG, which is located in Salmonella pathogenicity island 2 (SPI2), was reduced in the tdcA mutant, especially in the intracellular environment of macrophages. Taken together, our data suggest that tdcA plays an important role in the pathogenesis of Salmonella.
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PMID:A mutation in tdcA attenuates the virulence of Salmonella enterica serovar Typhimurium. 2039 61