Regulation of the β-ketoadipate pathway in Rhizobium japonicum and bacteroids by succinate

Rhizobium japonicum 61-A-101 and its bacteroids catabolize phenol and p-hydroxybenzoate. With phenol as a carbon source, utilization started only after a prolonged lag phase while p-hydroxybenzoate was almost instantancously metabolized. Succinate, which supports rapid growth of Rhizobium japonicum, completely repressed respication of phenol; the oxidation of p-hydroxybenzoate was partially inhibited. Pyruvate, supporting slower growth than succinate, retarded the onset of phenol consumption but did not affect its maximum rate.Catabolite repression of phenol utilization by succinate appears to be a characteristic feature of rhizobia. In Pseudomonas putida which also actively metabolizes phenol, succinate had no effect on phenol utilization.     

Molecular cloning of the F8 fimbrial antigen from Escherichia coli

Abstract The genetic determinant coding for the P-specific F8 fimbriae was cloned from the chromosome of the Escherichia coli wild-type strain 2980 (O18:K5:H5:F1C, F8). The F8 determinant was further subcloned into the Pst I site of pBR322 and a restriction map was established. In a Southern hybridization experiment identity between the chromosomally encoded F8 determinant of 2980 and its cloned counterpart was demonstrated. The cloned F8 fimbriae and those of the wild type strain consist of a protein subunit of nearly 20 kDa. F8 fimbriated strains were agglutinated by an F8 polyclonal antiserum, caused mannose-resistant hemagglutination and attached to human uroepithelial cells. The cloned F8 determinant was well expressed in a variety of host strains.     

Guaianolides from Saussurea affinis

Cynaropicrin, 11βH-11,13-dihydrodesacylcynaropicrin, aguerins A and B, isoamberboin and the new guaianolides saussureolide and 11βH-11,13-dihydrodesacylcynaropicrin 8-β-d-glucoside were isolated from Saussurea affinis.     

Inactivation of a newly transferred gene in recombination-deficient recipients of Escherichia coli

Summary The expression of a newly transferred lacZ ⁺ gene in lacZ recipients carrying various mutations in the recA and recB genes was studied by measuring the rates of induced synthesis of -galactosidase in zygotes formed after mating with either F or Hfr donors. The ability to synthesize -galactosidase decreases with time in both recA and recB zygotes when the lacZ ⁺ gene is transferred from an Hfr donor, but not when the lacZ gene is transferred from an F donor. There is no such inactivation of the newly transferred lacZ ⁺ gene in Rec⁺ zygotes. We conclude that the functioning of the transferred DNA is progressively inactivated in rec recipients unless the DNA is contained in an episome such as F.     

Inhibition of Replication of an F′lac Episome in Hfr Cells of Escherichia coli

Hfr strains of Escherichia coli K-12 were found capable of accepting a F'lac episome during mating, with a frequency approximating that of F(-) strains. However, the F'lac episome was unable to replicate in the Hfr cells, and was diluted out during the growth of the culture. The lac(+) gene of the episome can be "rescued" by recombination into the host chromosome, as shown by the appearance of variegated recombinant colonies on a lactose-fermentation indicator medium. In recA Hfr strains, however, no lac(+) offspring were obtained in crosses with F'lac donors. The induced synthesis of beta-galactosidase in F'lac(+) x Hfr zygotes was studied. Rates of enzyme synthesis were approximately constant with respect to time as expected from unilinear inheritance of the F'lac episome. However, the rate of synthesis eventually increased, presumably due to integration of the lac(+) gene in some of the zygotes. In F'lac(+) x recA Hfr zygotes the rate of beta-galactosidase synthesis remained constant with respect to time, as expected.