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J C Thomson

Publications and source records attributed to J C Thomson.

6 recordsLinked to original sources
PubMed1992

Cloning and partial sequencing of an operon encoding two Pseudomonas putida haloalkanoate dehalogenases of opposite stereospecificity.

We have cloned fragments of DNA (up to 13 kb), from Pseudomonas putida AJ1, that code for two stereospecific haloalkanoate dehalogenases. These enzymes are highly specific for D and L substrates. The two genes, designated hadD and hadL, have been isolated and independently expressed in Escherichia coli and P. putida hosts by using broad-host-range vectors. They are closely adjacent and inducible in what appears to be an operon with an upstream open reading frame of unknown function. Nucleotide sequence determination of hadD predicts a mature, cytoplasmic protein of 300 amino acid residues (molecular weight of 33,601). This has no significant homology with the L-specific haloalkanoate dehalogenases from Pseudomonas sp. strain CBS3 (B. Schneider, R. Muller, R. Frank, and F. Lingens, J. Bacteriol. 173:1530-1535, 1991) nor with any other known DNA or protein sequences.

Amino Acid Sequence↗
PubMed1992

Sickle and thalassemic erythroid progenitor cells are different from normal.

Blood erythroid progenitors (BFU-E) from patients with sickle and thalassemic syndromes were compared with those from normal individuals. The day of maximal colony formation in methyl cellulose was slightly later in the cultures from the patients with hemoglobinopathies than in the normal cultures. The number of colonies/100,000 mononuclear cells was similar in all cultures on day 13, but was higher in the hemoglobinopathy cultures on the day of maximal growth. The number of BFU-E/mL of blood was significantly higher than normal at all times in both sickle cell anemia and thalassemia. The proportional synthesis of gamma globin was twice normal in all sickle cultures, and 4 times normal in those from beta+-thalassemia. Hemin and interleukin-3 increased the numbers of erythroid colonies in all cultures, but did not consistently alter the globin synthesis patterns. Each progenitor population has a unique pattern in terms of time course, number of BFU-E, and level of gamma globin synthesis. These features indicate distinct types of BFU-E, or differences in accessory cells, or both, which distinguish blood-borne erythropoiesis in normals and those with hemoglobinopathies.

Adolescent↗