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J N Prebble

Publications and source records attributed to J N Prebble.

5 recordsLinked to original sources

The philosophical origins of Mitchell's chemiosmotic concepts: the personal factor in scientific theory formulation.

Mitchell's formulation of the chemiosmotic theory of oxidative phosphorylation in 1961 lacked any experimental support for its three central postulates. The path by which Mitchell reached this theory is explored. A major factor was the role of Mitchell's philosophical system conceived in his student days at Cambridge. This system appears to have become a tacit influence on his work in the sense that Polanyi understood all knowledge to be generated by an interaction between tacit and explicit knowing. Early in his life Mitchell had evolved a simple philosophy based on fluctoids, fluctids and statids which was developed in a thesis submitted for the Ph.D. at the University of Cambridge, England. This aspect of his work was rejected by the examiners and became a tacit element in his intellectual development. It is argued from his various publications that this philosophy can be traced as an underlying theme behind much of Mitchell's theoretical writing in the 50's leading, through his notion of vectorial metabolism, to the formulation and amplification of the chemiosmotic theory in the sixties. This philosophy formed the basis for Mitchell of his understanding of biological systems and gave him his unique approach to cell biology.

Biology↗

Successful theory development in biology: a consideration of the theories of oxidative phosphorylation proposed by Davies and Krebs, Williams and Mitchell.

The chemiosmotic theory is normally attributed to Peter Mitchell's formulation published in Nature in 1961. However, the essential elements of the theory were published 9 years earlier by Davies and Krebs. Why, then, was this earlier formulation overlooked? The success of Mitchell's theory is examined in comparison with those of Davies and Krebs and of Williams.

Biochemistry↗

Protection of cell viability and respiratory quinone levels by carotenoid in Micrococcus lysodeikticus (M. luteus).

Viability and respiratory activity of post-exponential phase cultures of Micrococcus lysodeikticus (M. luteus) decreased with time more rapidly in carotenoidless mutants than in a parent pigmented strain. The concentration of menaquinone, the respiratory quinone, was found to be low in carotenoidless mutants and in cultures of the pigmented strain where carotenoid synthesis had been partially blocked by diphenylamine. Cell suspensions incorporated [2-14C]mevalonate into menaquinone. Carotenoidless strains incorporated label at substantially higher rates than did the pigmented wild-type strain. Gently prepared membranes of M. lysodeikticus also incorporated mevalonate into menaquinone suggesting that the enzymes for the isoprenoid pathway are bound (loosely) to the membrane. Carotenoidless membranes with low concentrations of menaquinone incorporated radioactivity from [2-14C]mevalonate into quinone more rapidly than did membranes from the wild-type. Azide inhibited the incorporation but n-heptyl-4-hydroxyquinolone-N-oxide did not. It is concluded that the low concentrations of menaquinone in carotenoidless strains are due to rapid breakdown of the quinone. Carotenoid is therefore seen as protecting menaquinone from breakdown by factors as yet unidentified.

Carotenoids↗