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Biomedical subjects

J Parker

Publications and source records attributed to J Parker.

At least 343 records · Page 19Linked to original sources
PubMed1975

New chromosomal location for structural genes of ribosomal proteins.

An Escherichia coli mutant, ts9, previously reported by Flaks et al. (Cold Spring Harbor Symp. Quant. Biol. 31, 623-631, 1966) to have an electrophoretically altered ribosomal protein, has been further characterized and the altered component has been identified as L7/L12. Although mutant ts9 is temperature sensitive for growth (rts-), the rts and L7/L12 mutations are genetically separable and are both located between argH and rif. The L7/L12 mutation (rpyL) maps very close to relC, mutants of which have a defect in the 50S ribosomal subunit. The gene order is argH-rts-(rpyL,relC)-rif. Protein synthesis directed by bacteriophage lambdacI857S7drifd18 in ultraviolet-irradiated cells indicates that L7/L12, As well as L1, L10, L11, and possibly L8 or L9 are coded by the phage DNA. Our results indicate that rpyL is the structural gene for L7/L12 and that this region of the E. coli chromosome contains a cluster of structural genes for ribosomal proteins.

Bacterial Proteins↗
PubMed1975

The fine structure of proliferating cartilage cells: structural changes in an experimental model.

Extensive development of the rough endoplasmic reticulum and comparatively less developed Golgi membranes were seen in the cells of chondrocyte clusters which had formed in the vicinity of cartilage defects produced by intra-articular papain and cortisone injections. These cells frequently showed myelin-like membranous figures. These figures were seen either close to the cell membrane, or between cells, or connected to the nuclear envelope or the endoplasmic reticulum. The hypothesis is advanced that the myelin figures are made from redundant material which was not used for membrane formation. Cortisone, which is known to interfere with mitochondrial function and general metabolic processes, could have been responsible for the deficiency in membrane differentiation and transfer. This investigation was supported by grants from the Orthopaedic Research and Education Foundation and from the Research Evaluation and Allocation Committee of the School of Medicine, Univeristy of California, San Francisco.

Animals↗