Abstract
While chemiosmotic principles garnered endorsements, however reluctant, Mitchell’s mechanisms met persisting resistance, with skepticism bolstered by experimental challenges. This chapter traces the course to reformulating one of those mechanisms, that for the reversible ATPase. Although anaerobic bacteria may use this enzyme as a H+ pump (creating electrochemical gradients that drive secondary active transport systems), oxidizing and photosynthetic bacteria as well as mitochondria and chloroplasts use the enzyme routinely to make ATP: as an ATP synthase. Identifications of this ATP synthase with the reversible F0F1-ATPase, cited in preceding chapters, were also linked to the working assumption, supported by accumulating evidence, that active sites catalyzing ATP hydrolysis by F1 and by F0F1 were the active sites catalyzing ATP synthesis by F0F1.
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Notes to Chapter 18
Boyer (1965).
Ibid., p. 1011.
Slater (1971).
Harris et al. (1968); Green and Baum (1970).
See, for example, Chance et al. (1969).
Boyer et al. (1973).
R. A. Mitchell et al. (1967).
Ibid., p. 1799. They also argued that ATP-driven reactions of mitochondria occur over routes separate from that for oxidative phosphorylation.
Jones and Boyer (1969).
Harris et al. (1973), p. 152. Later studies showed that these tightly bound nucleotides were not at catalytic sites, however.
Bagshaw and Trentham (1973).
Jencks (1975).
Kayalar et al. (1976).
Boyer (1979).
Rosing et al. (1977).
Boyer (1975).
This argument was developed in Boyer (1981a).
Boyer (1975); Williams (1975).
Mitchell (1975).
See, for example, Mitchell and Koppenol (1982).
Boyer et al. (1973); Kayalar et al. (1977), p. 2490; voyer (1979).
Senior and Brooks (1971). Penefsky and Warner (1965) had shown that F1 contains subunits, and MacLennan and Tzagaloff (1968) published photographs showing multiple bands after gel electrophoresis.
Senior (1975).
Amzel and Pedersen (1978).
Bragg and Hou (1975); Vogel and Steinhart (1976).
Esch and Allison (1979).
Foster and Fillingame (1982).
Lünsdorf et al. (1984).
Cross and Nalin (1982).
These results were described in a series of papers beginning with Kanazawa et al. (1981); Nielsen et al. (1981); Gay and Walker (1981); and Walker et al. (1985).
See, for example, Bullough and Allison (1986); Xue et al. (1987); Lunardi and Vignais (1982).
Foster and Fillingame (1982).
Okamoto et al. (1977).
Beechey et al. (1966).
See, for example, Stekhoven et al. (1972); Sebald et al. (1980).
See, for example, Glaser et al. (1980); Negrin et al. (1980).
Woelders et al. (1985).
Williams (1982), p. 2.
Ivey and Krulwich (1992).
Grubmeyer et al. (1982); Cross et al. (1982).
Penefsky (1985b).
Penefsky (1985c).
See, for example, Penefsky (1985a); Matsuno-Yagi et al. (1985).
Boyer and Kohlbrenner (1981).
Cox et al. (1984).
Silverman and Simon (1974); Larsen et al. (1974); Manson et al. (1977); Matsuura et al. (1977). Previously, speculations about the mechanism covered an imaginative range, including formulations by Ling (1969) in terms of his protein induction model, and by Mitchell (1972) in terms of electrophoresis of ions from the bacterium along the outside of a hollow flagellum, with a return flow through that tube.
Chernyak et al. (1983).
Cross and Duncan (1996) note two technical advances that furthered the idea of rotary mechanisms. (1) New mass spectroscopic techniques permitted analysis of the reaction pathways, demonstrating that the rate constants at each of the three catalytic sites was the same, i.e., the asymmetry of the enzyme did not cause asymmetries in the reaction pathways. (2) Methods for amino acid sequence determination permitted demonstrations that neither a nor /3 had a tripartite structure (which would have allowed each to react identically with y, (5 and e). Furthermore, several approaches provided evidence for cyclical changes in enzyme conformation; see, for example, Kandpal and Boyer (1987); Shapiro and McCarty (1988); and Gogol et al. (1990).
Abrahams et al. (1994).
Ibid., p. 628.
Duncan et al. (1995).
Hilpert et al. (1984).
Laubinger and Dimroth (1987, 1988).
Laubinger et al. (1990).
Absence of E-P intermediates in F-type ATPases is concluded from direct evidence against this (Webb et al., 1980) as well as the lack of evidence for it.
Pedersen and Carafoli (1987).
Kirshner (1962).
Taugner (1971).
Bashford et al. (1975), p. 155.
Apps and Schatz (1979). Cidon and Nelson (1983) criticized these experiments for their contamination with mitochondria. However, subsequent studies-showing similarities in amino acid sequences between the vesicular ATPase and mitochondrial ATPase-supported Apps and Schatz’s conclusion.
Xie et al. (1984). Their starting material was “clathrin-coated vesicles,” cytoplasmic vesicles formed from invaginations of the plasma membrane.
For general reviews see volume 122, Journal of Experimental Biology (1992).
Boyer (1981b).
Ibid., p. 239.
Ibid., p. 237.
See, for example, Kinkaid (1990).
Mayr (1982).
Mitchell (1961a), p. 598.
Lehninger (1960), p. 952.
Mitchell (1961d).
Gilbert and Mulkay (1984).
Ibid., p. 119.
Ibid., p. 117.
Boyer (1981b), p. 236.
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© 1997 American Physiological Society
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Robinson, J.D. (1997). Oxidative Phosphorylation: F1, F0F1, and ATP Synthase. In: Moving Questions. People and Ideas Series. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-7600-9_18
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DOI: https://doi.org/10.1007/978-1-4614-7600-9_18
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