Genetic regulation of a constitutive operon in E. coli B-r

Complementation analysis, using a regulatory mutant in the constitutive d-ribose operon of $\text{E. coli}\text{B}\text{r}$, have shown that the genetic regulation of constitutive operon may follow a truly positive control mechanism whereby the expression of the operon requires an active constitutive initiation protein to allow the synthesis of the structural genes products.     

Primary structure of the E. coli DNA region preceding the tryptophan operon genes

The nucleotide sequence of 1179 b.p. preceding the trp operon genes has been established. There are no open reading frames large enough to code for proteins containing more than 97 amino acid residues. In all cases the coding sequences do not contain the initiation codons. The determined sequence is concluded to represent an intercistronic region.     

Interaction of the trp repressor from Escherichia coli with a constitutive trp operator.

The mechanisms of the requirement of glucose for steroidogenesis were investigated by monitoring the uptake of the glucose analogue 2-deoxy-D-glucose by rat testis and tumour Leydig cells. The characteristics of glucose transport in both of these cell types were found to resemble those of the facilitated-diffusion systems for glucose found in most other mammalian cells. The Leydig cells took up 2-deoxy-D-glucose but not L-glucose, and the uptake was inhibited by both cytochalasin B and forskolin. In the presence of luteinizing hormone, the rate of 2-deoxy-D-glucose uptake by both cell types was increased by approx. 50%. In addition to D-glucose, it was shown that the Leydig cells could also utilize 3-hydroxybutyrate or glutamine to maintain steroidogenesis.     

Release of nascent trp mRNA from the operon DNA in chloramphenicol-treated cells of Escherichia coli.

Summary A synergistic effect of combined UV and -ray exposure was observed for inactivation of wild-type Schizosaccharomyces pombe. A recombinational repair process, known to be important in restitution of damage induced by both radiations, appears to be involved; a radiation-sensitive mutant defective in this repair pathway showed essentially no synergistic interaction between UV and -rays.Recovery from the synergistic effect of pre-exposure in wild-type cells did not display the expected fast -recovery and slow UV-recovery kinetics previously observed for regain of resistance to further exposure to the same radiation. Rather, UV-irradiated cells recovered quickly from synergistic inactivation on subsequent -exposure, while -irradiated cells recovered UV-resistance slowly. Recovery from synergism thus appears to reflect the nature of the second, and not the initial, radiation.AECL Reference No. 6154