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J R Yates

Publications and source records attributed to J R Yates.

210 records · Page 12Linked to original sources
PubMed1982

Resistance to inhibitors of mammalian cell protein synthesis induced by preincubation in hypertonic growth medium.

Incubation of L-929 cells in growth medium containing excess NaCl induces cellular protein synthesis to become resistant to the inhibitory action of growth medium made hypertonic by the addition of Na-acetate, KCl, choline chloride, D-alanine, or sucrose. Hypertonic preincubation also induces resistance to the inhibitory action of the drugs dimethyl sulfoxide, ethanol, and L-1-tosylamido-2-phenylethyl chloromethyl ketone, but not to the action of NaF or the inhibitors of polypeptide chain elongation, emetine and cycloheximide. Induction is independent of the solute used to make the induction medium hypertonic and is not mediated by an elevated intracellular Na+ concentration. In a separate series of experiments, it was determined that the formation of functional methionyl-tRNAf.40 S ribosomal complexes is not impaired by exposure of uninduced cells to hypertonic growth medium. The combined results are evaluated with respect to the mechanism of action of hypertonic growth medium in the inhibition of polypeptide chain initiation and the adaptive mechanisms that animal cells have evolved to deal with alterations in their extracellular environments.

Animals↗
PubMed1982

Time-dependent increase in the resistance of mammalian cell protein synthesis to inhibition by hypertonic medium.

As a result of continued incubation of cultured L-929 fibroblasts in growth medium containing excess NaCl, protein synthesis became resistant to the inhibitory effect of hypertonic medium. Protein synthesis became progressively resistant in a linear fashion during the first 6 h of incubation. The level of resistance attained was directly related to the concentration of excess NaCl to which the cells were exposed during the incubation period. Actinomycin D did not prevent the expression of resistance, indicating that de novo synthesis of RNA is not required. Finally, resistance declined to near the preinduction level by 4 h after resistance cells were returned to isotonic medium.

Animals↗
PubMed1981

Cell-to-substrate contacts in an adhesion-defective mutant of Balb/c3T3 cells.

The cell-to-substrate contacts of the adhesion-defective mutant, AD6, have been examined by interference reflexion microscopy and compared with those of the wild-type Balb/c3T3 cell. The 2 cell-types differed in their ability to produce focal contacts with the substrate (10-15 nm separation distance). Only 10% of AD6 versus 92% of Balb/c3T3 cells formed these contacts. When present in AD6 the focal contacts were smaller and fewer in number per cell than in Balb/c3T3. Close contact with the substrate (approx. 30 nm separation distance) was formed by both cell types. The absence of the stronger focal contacts accounts for the reduced substrate adhesion of the mutant cells and for other phenotypic characteristics such as reduced spreading, rounded shape, altered pattern of movement, and absence of stress fibres. The reduced adhesion of the mutant has been attributed to a change in the pattern of glycoproteins exposed at the cell surface, which results from a defect in glycosylation. This suggests that normal glycosylation and correct exposure of one or more cell surface components are required for the formation of a specific substrate adhesion, the focal contact, and offers the possibility of identifying individual surface components involved in formation of this adhesion. Attention is drawn to zero-order minima originating from cell thickness and not cell-to-substrate separation distance in the interference reflexion image.

Animals↗
PubMed1980

The effects of acidosis on canine hepatic and renal oxidative phosphorylation.

The intracellular effects of acidosis remain poorly defined. To examine the effects of acidosis on oxidative phosphorylation, liver biopsies and weight nephrectomies were performed on 10 adult German shepherd dogs. The mitochondria were isolated from each tissue and their respiratory activity was studied by the polarographic technique with the pH of the reaction media varied from 5.5 to 8.0. Glutamate and succinate substrates were employed. Results showed a dramatic reduction in the efficiency of oxygen utilization by mitochondria with glutamate as the reaction medium became more acidic. The efficiency of succinate oxidation was significantly (P less than 0.01) preserved. These findings were confirmed by both the respiratory control indices and by ADP:O ratios. Acidosis appears to result in severe inhibition of NAD-linked energy substrate oxidation.

Acidosis↗
PubMedDate not supplied

Stickler syndrome: further mutations in COL11A1 and evidence for additional locus heterogeneity.

Stickler syndrome (hereditary arthro-ophthalmopathy) is a dominantly inherited connective tissue disorder with ocular, oro-facial, auditory and skeletal manifestations. It is genetically and phenotypically heterogeneous with the majority of families having mutations in the gene encoding type II collagen (COL2A1) and exhibiting a characteristic 'membranous' or type 1 vitreous phenotype. More recently a novel mutation in the gene encoding the alpha1 chain of type XI collagen (COL11A1) was reported in a Stickler syndrome pedigree with a different 'beaded' or type 2 vitreous phenotype. In the present study five more families with the type 2 vitreous phenotype were examined for linkage to four candidate genes: COL2A1, COL5A2, COL11A1 and COL11A2. Two families were linked to COL11A1 and sequencing identified mutations resulting in shortened alphal(XI) collagen chains, one via exon skipping and the other via a multiexon deletion. One of the families showed weak linkage to COL5A2 but sequencing the open reading frame failed to identify a mutation. In the remaining two families all four loci were excluded by linkage analysis. These data confirm that mutations in COL11A1 cause Stickler syndrome with the type2 vitreous phenotype and also reveal further locus heterogeneity.

Abnormalities, Multiple↗