Abstract
The purpose of this paper is to examine some conceptual aspects of the controversy over the possibility of directed mutagenesis in bacteria that has erupted since the publication of some provocative results by Cairns, Overbaugh and Miller [2]. The paper by Foster in this volume takes up more “empirical” issues, surveys the experimental literature, and offers occasionally different interpretations of the results. The conceptual issues that are important here occur at least at two levels, the first of which is, in a sense, metaphysical and the second, epistemological. First, the possibility of directed mutagenesis challenges the core of the current orthodox framework of evolutionary theory. Thus the sense in which mutations can indeed be “directed” is of considerable foundational importance to evolutionary theory. To the extent that such foundational issues are “metaphysical,” in the sense that they concern the most general and universal underlying features of the world explored by science, these conceptual issues properly belong to metaphysics. Second, much of the evidence on which the current controversy thrives is statistical evidence about the number of mutant bacteria. Experimental methods which rely on such evidence are non-reductive in the sense that they attempt to understand what occurs at a lower level—for instance, that within a bacterial cell—by making observations at a higher level—in the example, that of the cell.
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Notes
Cairns, J., J. Overbaugh, and S. Miller. The origin of mutants. Nature 335: 142–145, 1988.
Cairns, J. et al., The origin of mutants. Nature 335: 142–145, 1988;
Sarkar, S. Reductionism and molecular biology: a reappraisal. Ph. D. Dissertation. Department of Philosophy, University of Chicago, 1989.
Sarkar, S., Reductionism and molecular biology: a reappraisal. Ph. D. Dissertation. Department of Philosophy, University of Chicago, 1989;
Kauffman, S.A. Articulation of parts explanation in biology and the rational search for them. Boston Studies in the Philosophy of Science 8: 257–272, 1972;
Lewontin, R.C. The units of selection. Annual Review of Ecology and Systematics 1: 1–18, 1970.
Lewontin, R.C., The units of selection. Annual Review of Ecology and Systematics 1: 1–18, 1970, p. 1.
Lewontin, R.C., The units of selection. Annual Review of Ecology and Systematics 1: 1–18, 1970, p. 1.
Note that this explication of evolution by natural selection makes no mention of what the individuals of the population are. They could be molecules, organelles within a cell, cells, individuals (which in multi-cellular organisms would not be identical with cells), kins, groups, populations or species. What the appropriate units of selection are is a matter of considerable biological and philosophical controversy. In the case of bacteria, which is all that is directly of concern in this article, the levels of cells and individuals are identical thus partly avoiding this controversy. For details of this controversy, see Brandon, R. N. and R. N. Burian (eds.). Genes, Organisms, Populations: Controversies Over the Units of Selection. Cambridge, MA: MIT Press, 1984.
See Wimsatt, W.C. Randomness and perceived randomness in evolutionary biology. Synthese 43: 287–329, 1980, for an attempt to analyze the difficulties with the notion of randomness appropriate for evolutionary biology.
Kimura (Kimura, M. The Neutral Theory of Molecular Evolution. Cambridge: Cambridge University Press, 1983), in his more polemical moments seems to suggest such a viewpoint.
See Provine, W. The Origins of Theoretical Population Genetics. Chicago: University of Chicago Press, 1971, for details of this fascinating history.
See Maynard Smith, J. Evolutionary Genetics. Oxford: Oxford University Press, 1989, for an emphasis on natural selection and
Lewontin’s review (Lewontin, R.C.A natural selection. Nature 339: 107, 1989) for a critique.
Haldane, J.B.S. The Causes of Evolution. London: Harper & Brothers, 1932;
Huxley, J. 1942. Evolution: The Modern Synthesis. London: George Allen & Unwin.
Not one of the figures discussed by Hull (Hull, D. Lamarck among the Anglos. In J.B. Lamarck, Zoological Philosophy. Chicago: University of Chicago Press, 1984, pp. xl—lxvi) in his colorful, though short, account of the history of neo-Lamarkism seems to have suggested that all mutations were directed.
For details of Lysenkoist claims, see Hudson, P.S., and R.H. Richens. The New Genetics in the Soviet Union. Cambridge: Imperial Bureau of Plant Breeding and Genetics, 1946.
Among those at least partly sympathetic to Lysenko’s claims, only Haldane (Haldane, J.B.S. Lysenko and genetics. Science and Society 4: 433–437, 1940) seems to have been fully clear that all that was needed to explain the kind of effects Lysenko claimed to be observing was that some mutations could be induced in such a fashion.
This strong notion of directedness has been championed by Lenski, R.E. Are some mutations directed? Trends in Ecology and Evolution 4: 148–150, 1989.
This weaker definition has been used by Sarkar, S. On the possibility of directed mutations in bacteria: statistical analyses and reductionist strategies. In PSA 1990. A. Fine, editor, 1990. Philosophy of Science Association, East Lansing. In press.
Many of the participants in the controversy would also reject the use of “neo-Lamarckism” on various grounds including vagueness. However, vagueness, at least, has been removed if the distinctions and definitions elaborated in the text are clear enough. For responses to some other objections to the use of “neo-Lamarckism,” see Sarkar, S., On the possibility of directed mutations in bacteria: statistical analyses and reductionist strategies. In PSA 1990. A. Fine, editor, 1990. Philosophy of Science Association, East Lansing. In press.
However, for an important treatment of the possible inheritance of acquired characteristics where the concept is not used vaguely, see Jablonka, E., and M.J. Lamb. The inheritance of acquired epigenetic variations. Journal of Theoretical Biology 139: 69–83, 1989.
Cullis, C.A. The generation of somatic and heritable variation in response to stress. American Naturalist 130: S62–S73, 1987.
The reasons given for not using the notion of the inheritance of acquired characteristics are also those for not using another related distinction due to Mayr, namely, that between “hard” and “soft” inheritance (Mayr, E. The Growth of Biological Thought. Cambridge, MA: Harvard University Press, 1982), pp. 687–689). These choices, however, are made for the purpose of conceptual clarification. No suggestion is being made here that these other construals of the differences between neo-Darwinism and neo-Lamarckism can be avoided when the history of these disputes, especially during the first half of this century, is considered.
Lamarck, J.B. Zoological Philosophy. Chicago: University of Chicago Press, 1984, p. 113.
Darwin, C. On the Origin of Species. London: John Murray, 1859.
Darwin, C., On the Origin of Species. London: John Murray, 1859, pp. 134–139.
Mayr lists nine other examples (Mayr, E. Introduction. In C. Darwin, On the Origin of Species. Cambridge, MA: Harvard University Press, 1964, p.xxvi).
See Eiseley, L. Darwin’s Century. New York: Doubleday Anchor, 1961, and
Ruse, M., The Darwinian Revolution: Science Red in Tooth and Claw. Chicago: University of Chicago Press, 1979, for details of these developments.
See, for example, Weismann, A. Das Keimplasma: Eine Theorie der Vererbung. Jena: Gustav Fischer, 1892.
Romanes, G.J. Life and Letters. London: Longmans, Green, 1896.
For details of this history, Sarkar, S, Reductionism and molecular biology: a reappraisal. Ph. D. Dissertation. Department of Philosophy, University of Chicago, 1989, and
Fischer, E.P., and C. Lipson. Thinking About Science: Max Delbrück and the Origins of Molecular Biology. New York: Knopf, 1988, and references therein.
Though the terms, “mutant” and “mutation” were routinely used for this transformation, it remained an open question whether these “mutations” were mutations of genes. In 1943, for example, Luria and Delbück carefully observe: “Naming such hereditary changes ‘mutations’ of course does not imply a detailed similarity with any of the classes of mutations that have been analyzed in terms of genes for higher organisms. The similarity may be merely a formal one (Luria, S.E., and M. Delbrück. Mutations of bacteria from virus sensitivity to virus resistance. Genetics 28: 491–511, 1943, p. 492).”
Even in the late 1950’s a few skeptics such as Hinshelwood (for example, in Dean, A.C.R., and C.N. Hinshelwood. Aspects of the problem of drug resistance in bacteria. In Drug Resistance in Microorganisms. G.E.W. Wolstenholme, and C.M. O’Connor, editors. London: J. & A. Churchill, 1957, pp. 4–24) would maintain that any reference to genes in bacteria would actually be a reference to complex chemical reaction networks.
d’Herelle, F. The Bacteriophage and Its Behavior. Baltimore: Williams and Wilkins, 1926;
Gratia, A. Studies on the d’Herelle phenomenon. Journal of Experimental Medicine 34: 115–131, 1921;
Burnet, F. M. “Smooth-rough” variation in bacteria in its relation to bacteriophage. Journal of Pathology and Bacteriology 32: 15–42, 1929.
Luria, S.E. and M. Delbrück, Mutations of bacteria from virus sensitivity to virus resistance. Genetics 28: 491–511, 1943, p. 492. According to Luria, he was led to the idea of the fluctuation test while watching the operation of slot machines during a faculty dance at the Bloomington Country Club in Indiana. If these machines were programmed to return money at random, the returns would form a Poisson distribution clustered around a mean and there would be virtually no jackpots. If, however, the machines were programmed so that they return occasional jackpots with many very tiny returns, the returns would fluctuate much more widely. The average return would be the same in both cases. The way in which the machines were programmed could only be determined by actually observing the actual distribution of the returns and not from the mean alone. Luria immediately applied this insight to the question of the distribution of mutants in bacteria.
For further details see Luria, S.E. A Slot Machine, a Broken Test Tube: An Autobiography. New York: Harper and Row, 1984, pp. 74–79.
Yang, Y.N., and P. Bruce Wright. Rough variation in V. cholerae and its relation to resistance to cholera-phage (Type A). Journal of Pathology and Bacteriology 38: 187–200, 1934.
Luria, S. E. and M. Delbruck (Mutations of bacteria from virus sensitivity to virus resistance. Genetics 28: 491–511, 1943, p. 492) do not cite them.
Neither do Newcombe, H. B. Origin of bacterial variants. Nature 164: 150–151, 1949,
Lederberg, J., and E. Lederberg. Replica plating and indirect selection of bacterial mutants. Journal of Bacteriology 63: 399–406, 1952, or
Cavalli-Sforza, L.L., and J. Lederberg. Isolation of preadaptive mutants by sib selection. Genetics 41: 367–381, 1956,
which were critical papers in the establishment of the neo-Darwinian view. Cavalli-Sforza and Lederberg do list them in their bibliography in an earlier paper (Cavalli-Sforza, L.L., and J. Lederberg. Genetics of resistance to bacterial inhibitors. In Symposium: Growth Inhibition and Chemotherapy. Rome: Istituto Superiore di Sanita, 1953, pp. 108–142) but do not discuss them in the text.
A recent article by Lederberg is responsible for drawing attention to the contribution of Yang and Bruce White (Lederberg, J. Replica plating and indirect selection of bacterial mutants: isolation of preadaptive mutants in bacteria by sib selection. Genetics 121: 395–399, 1989).
Luria, S.E. and M. Delbrück, Mutations of bacteria from virus sensitivity to virus resistance. Genetics 28: 491–511, 1943, p. 492, p. 493.
Luria, S.E. and M. Delbrück, Mutations of bacteria from virus sensitivity to virus resistance. Genetics 28: 491–511, 1943, p. 492, p. 493.
Lea, D.E., and C.A. Coulson. The distribution of the number of mutants in bacterial populations. Journal of Genetics 49: 264–285, 1949. As a historical curiosity, it is worth noting that it is possible that Fisher might have solved the Luria-Delbrück distribution first.
Crow (Crow, J.F., R.A. Fisher, a centenniel view. Genetics 124: 207–211, 1990)
recalls that while he found the Luria-Delbrück argument convincing, he thought that the mathematical treatment “shoddy and confusing (Crow, J.F., R.A. Fisher, a centenniel view. Genetics 124: 207–211, 1990 p. 210).”
Consequently, in 1946, he approached Fisher with the problem. Fisher “leaned back in his chair, thought for perhaps a minute, took a scrap of paper, and wrote a generating function (Crow, J.F., R.A. Fisher, a centenniel view. Genetics 124: 207–211, 1990 p. 210).” Crow, not understanding the formula yet, put that scrap of paper aside, intending to work on it later and then lost it!
Stewart, F., D. Gordon, and B. Levin. Fluctuation analysis: the probability distribution of the number of mutants under different conditions. Genetics 124: 175–185, 1990. There were many previous attempts to generalize the Luria-Delbrück distribution but none to this extent.
For example, phenotypic lag is considered in Armitage, P. The statistical theory of bacterial populations subject to mutation. Journal of the Royal Statistical Society B 14: 1–40, 1952, and
Koch, A.L. Mutation and growth rates from Luria-Delbrück fluctuation tests. Mutation Research 95: 129–143, 1982.
The latter and Mandelbrot, B. A population birth-and-mutation process I: explicit distributions for the number of mutants in an old culture of bacteria. Journal of Applied Probability 11: 437–444, 1974 also consider differential fitnesses (growth rates), of the original and mutant strains. The effect of these factors on the distributions will be considered in Section 5.
Newcombe, H.B. Delayed phenotypic expression of spontaneous mutations in Escherichia coli. Genetics 33: 447–476, 1948;
Demerec, M., and U. Fano. Bacteriophage-resistant mutants in Escherichia coli. Genetics 30: 119–136, 1945.
Witkin, E.M. Genetics of resistance to radiation in Escherichia coli. Genetics 32: 221–248, 1947;
Ryan, F.J. On the stability of nutritional mutants of bacteria. Proceedings of the National Academy of Sciences (USA) 34: 425–435, 1948.
Demerec, M. Production of staphylococcus strains resistant to various concentrations of penicillin. Proceedings of the National Academy of Sciences (USA) 31: 16–24, 1945;
Oakberg, E.F., and S.E. Luria. Mutations to sulfonamide resistance in Staphylococcus aureus. Genetics 32: 249–261, 1947
Demerec, M. Origin of bacterial resistance to antibiotics Journal of Bacteriology 56: 63–74, 1948.
Ryan, F.J., L.K. Schneider, and R. Ballentine. Mutations involving the requirement of uracil in Clostridium. Proceedings of the National Academy of Sciences (USA) 32: 261–271, 1946;
Alexander, H.E., and J. Leidy. Mode of action of streptomycin on type b Hemophilus influenzae. Journal of Experimental Medicine 85: 607–621, 1947;
Curcho, M. de la G. Mutation to tryptophan independence in Erbethella typhosa. Journal of Bacteriology 56: 374–375, 1948.
Newcombe, H.B., Delayed phenotypic expression of spontaneous mutations in Escherichia coli. Genetics 33: 447–476, 1948;
Ryan, F.J. Distribution of numbers of mutant bacteria in replicate cultures. Nature 169: 882–883, 1952.
Newcombe, H.B., Origin of bacterial variants. Nature 164: 150–151, 1949;
Witkin, E.M., Genetics of resistance to radiation in Escherichia coli. Genetics 32: 221–248, 1947.
Ryan, F.J, K. Schneider, and R. Ballentine et al., Mutations involving the requirement of uracil in Clostridium. Proceedings of the National Academy of Sciences (USA) 32: 261–271, 1946.
Ryan, F.J. Distribution of numbers of mutant bacteria in replicate cultures. Nature 169: 882–883, 1952.
Ryan, F.J. Distribution of numbers of mutant bacteria in replicate cultures. Nature 169: 882–883, 1952;
Ryan, F.J. Adaptation to use lactose in Escherichia coli. Journal of General Microbiology 7: 69–88, 1952.
This mutation is particularly relevant here because it is one of those studied by Cairns, J., J. Overbaugh, and S. Miller et al.,. The origin of mutants. Nature 335: 142–145, 1988. In fact, that work used Ryan’s studies as one of its starting points.
Ryan, F.J. Distribution of numbers of mutant bacteria in replicate cultures. Nature 169: 882–883, 1952.
Armitage, P., The statistical theory of bacterial populations subject to mutation. Journal of the Royal Statistical Society B 14: 1–40, 1952. Note that Ryan does not explicitly invoke phenotypic lag or any other specific mechanism.
Dean, A.C.R. and C.N. Hinshelwood, Aspects of the problem of drug resistance in bacteria. In Drug Resistance in Microorganisms. G.E.W. Wolstenholme, and C.M. O’Connor, editors. London: J. & A. Churchill, 1957, pp. 4–24.
Eriksen, K.R. Studies on the mode of origin of penicillin resistant staphylococci. Acta Pathologica et Microbiologica Scandinavica 26: 269–279, 1949.
However, Eriksen’s experimental results were not particularly convincing because small samples were taken from the cultures which made the statistical tests inefficient as Cavalli-Sforza L.L. and J. Lederberg. Genetics of resistance to bacterial inhibitors. In Symposium: Growth Inhibition and Chemotherapy. Rome: Istituto Superiore di Sanita, 1953, pp. 108–142 point out.
For Hinshelwood’s position, see, for example, Hinshelwood, C.N. Chemistry and bacteria. Nature 166: 1089–1092, 1950;
and Dean, A.C.R., and C.N. Hinshelwood. 1952. The resistance of Bact. Lactis aerogenes to proflavine (2: 8-diaminoacri-dine). I: the applicability of the statistical fluctuation test. Proceedings of the Royal Society B 139: 236–250, 1952.
Cavalli, L.L. Genetic analysis of drug-resistance. Bulletin of the World Health Organization 6: 185–206, 1952;
Michison, D.A. The occurrence of independent mutations to different types of streptomycin resistance in Bacterium coli. Journal of General Microbiology 8: 168–185, 1953.
Mitchison, D.A., The occurrence of independent mutations to different types of streptomycin resistance in Bacterium coli. Journal of General Microbiology 8: 168–185, 1953, studied three types of strains of Bacterium coli which had differences in growth rates while being selected for streptomycin resistance by fluctuation analysis.
Cavalli, L.L., Genetic analysis of drug-resistance. Bulletin of the World Health Organization 6: 185–206, 1952.
Newcombe, H.B., Origin of bacterial variants. Nature 164: 150–151, 1949.
Newcombe, H.B., Origin of bacterial variants. Nature 164: 150–151, 1949, p. 150.
Lederberg, J. and E.M. Lederberg, Replica plating and indirect selection of bacterial mutants. Journal of Bacteriology 63: 399–406, 1952;
Cavalli-Sforza, L.L. and J.L. Lederberg, Genetics of resistance to bacterial inhibitors. In Symposium: Growth Inhibition and Chemotherapy. Rome: Istituto Superiore di Sanita, 1956, pp. 108–142.
In practice Cavalli-Sforza L.L. and J. Lederberg. Genetics of resistance to bacterial inhibitors. In Symposium: Growth Inhibition and Chemotherapy. Rome: Istituto Superiore di Sanita, 1956, pp. 108–142 had to increase cell concentration in each cycle because of slow selection.
Stahl, F. Bacterial genetics: a unicorn in the garden. Nature 335: 112–113, 1988.
Lederberg was certainly aware of this but seems not to have regarded it as particularly relevant Cavalli-Sforza L.L. and J. Lederberg. Genetics of resistance to bacterial inhibitors. In Symposium: Growth Inhibition and Chemotherapy. Rome: Istituto Superiore di Sanita, 1953, p. 121).
Ryan, F.J. On the stability of nutritional mutants of bacteria. Proceedings of the National Academy of Sciences (USA) 34: 425–435, 1948.
Ryan, F.J. Distribution of numbers of mutant bacteria in replicate cultures. Nature 169: 882–883, 1952.
Ryan, F.J. Adaptation to use lactose in Escherichia coli. Journal of General Microbiology 7: 69–88, 1952.
This does not, of course, endorse in any way criticisms of the sort made by Hinshelwood, C.N., Aspects of the problem of drug resistance in bacteria. In Drug Resistance in Microorganisms. G.E.W. Wolstenholme, and C.M. O’Connor, editors. London: J. & A. Churchill, 1957, pp. 4–24
Hinshelwood, C.N. Chemistry and bacteria. Nature 166: 1089–1092, 1952.
Luria, S.E. and M. Delbrück, Mutations of bacteria from virus sensitivity to virus resistance. Genetics 28: 491–511, 1943, p. 492. Note that they do not explicitly state that one alternative is the negation of the other; they simply ignore intermediate possibilities.
Lea, D.E. and C.A. Coulson, The distribution of the number of mutants in bacterial populations. Journal of Genetics 49: 264–285, 1949.
Armitage, P. The statistical theory of bacterial populations subject to mutation. Journal of the Royal Statistical Society B 14: 1–40, 1952.
The objection just noted in the text is independent of whether the last one, that of the selective media being lethal for non-mutants, is valid. Indeed, phenotypic lag had already been invoked by Newcombe, H.B. Origin of bacterial variants. Nature 164: 150–151, 1949, even before Lea and Coulson had calculated the Luria-Delbrück distribution.
Cavalli-Sforza, L.L. and J. Lederberg, Genetics of resistance to bacterial inhibitors. In Symposium: Growth Inhibition and Chemotherapy. Rome: Istituto Superiore di Sanita, 1956, pp. 108–142.
Lederberg, J., and M. Ledergerg. Replica plating and indirect selection of bacterial mutants. Journal of Bacteriology 63: 399–406, 1952;
Newcombe, H.B. Origin of bacterial variants. Nature 164: 150–151, 1949. Both experiments rely on visual recognition and make no quantitative arguments whatsoever. What they do show, however, is that some mutations were spontaneous (random).
The discussion in this section is not intended to be complete. For details, see the paper by Foster in this volume and Sarkar, S. On the possibility of directed mutations in bacteria: statistical analyses and reductionist strategies. In PSA 1990. A. Fine, editor, 1990. Philosophy of Science Association, East Lansing. In press.
Shapiro, J. Observations on the formation of clones containing araB-lacZ cistron fusions. Molecular and General Genetics 194: 79–90, 1984.
Cairns, J., J. Overbaugh, and S. Miller. et al., The origin of mutants. Nature 335: 142–145, 1988.
Ryan, F.J. Distribution of numbers of mutant bacteria in replicate cultures. Nature 169: 882–883, 1952;
Ryan, F.J. Adaptation to use lactose in Escherichia coli. Journal of General Microbiology 7: 69–88, 1952.
This mutation is particularly relevant here because it is one of those studied by Cairns, J., J. Overbaugh, and S. Miller. et al., The origin of mutants. Nature 335: 142–145, 1988. In fact, that work used Ryan’s studies as one of its starting points.
Hall, B. Adaptive evolution that requires multiple spontaneous mutations I. Genetics 120: 887–897, 1988.
Lenski, R.E. Are some mutations directed? Trends in Ecology and Evolution 4: 148–150, 1989, emphasizes the importance of this point.
Cairns, J., et al., The origin of mutants. Nature 335: 142–145, 1988.
Mittler, J.E. and R.E. Lenski. New data on excisions of Mu from E. coli MCS2 cast doubt on directed mutation hypothesis. Nature 334: 173–175, 1990;
Shapiro, J. Observations on the formation of clones containing araB-lacZ cistron fusions. Molecular and General Genetics 194: 79–90, 1984;
Cairns, J., et al., The origin of mutants. Nature 335: 142–145, 1988.
Mittler, J.E. and Lenski, R.E., New data on excisions of Mu from E. coli MCS2 cast doubt on directed mutation hypothesis. Nature 334: 173–175, 1990.
Cairns, J., et al. The origin of mutants. Nature 335: 142–145, 1988. Note that these authors interpret the shift as a Poisson component added on to a Luria-Delbrück distribution, but this is an interpretation and, therfore, subject to legitimate questioning.
Stewart, F., D. Gordon, and B. Levin et al., Fluctuation analysis: the probability distribution of the number of mutants under different conditions. Genetics 124: 175–185, 1990.
The second and the last of these cannot be shown using the analysis of Stewart, F., et al., Fluctuation analysis: the probability distribution of the number of mutants under different conditions. Genetics 124: 175–185, 1990.
The importance of this case has been particularly emphasized by Charlesworth, D., B. Charlesworth, and J.J. Bull. Origin of mutants disputed. Nature 336: 525, 1988,
and Tessman, I. Origin of mutants disputed. Nature 336: 527, 1988.
Cairns has replied to this objection by observing that there did not appear to be any difference in fitness between mutant and non-mutant types in his experiments (Cairns, J. Origin of mutants disputed. Nature 336: 527–528, 1988.)
Stewart, F., D. Gordon, and B. Levin et al., Fluctuation analysis: the probability distribution of the number of mutants under different conditions. Genetics 124: 175–185, 1990.
Lenski, R.E., M. Slatkin, and F.J. Ayala. Mutation and selection in bacterial populations: alternatives to the hypothesis of directed mutation. Proceedings of the National Academy of Sciences (USA) 86: 2775–2778.
Lenski, R.E., M. Slatkin, and F.J. Ayala, Mutation and selection in bacterial populations: alternatives to the hypothesis of directed mutation. Proceedings of the National Academy of Sciences (USA) 86: 2775–2778;
Lenski, R.E., M. Slatkin, and F.J. Ayala. Another alternative to directed mutation. Nature 337: 123–124, 1989.
Levin, B., D, Gordon, and F. Stewart. Is natural selection the composer as well as the editor of genetic variation? Forthcoming, 1990.
Cairns, J. et al., The origin of mutants. Nature 335: 142–145, 1988. These mechanisms will be discussed in detail in the text.
Stahl, F., Bacterial genetics: a unicorn in the garden. Nature 335: 112–113, 1988;
Davis, B.D. 1989. Transcriptional bias: a non-Lamarckian mechanism for substrate-induced mutations. Proceedings of the National Academy of Sciences (USA) 86: 5005–5009, 1989.
For example, the mechanism suggested by Davis, B. D., Transcriptional bias: a non-Lamarckian mechanism for substrate-induced mutations. Proceedings of the National Academy of Sciences (USA) 86: 5005–5009, 1989, can be ruled out (in part due to the experimental reports of Davis himself).
Cairns, J. et al., The origin of mutants. Nature 335: 142–145, 1988.
Cairns, J. et al., The origin of mutants. Nature 335: 142–145, 1988, require the same organelle to contain the reverse transcriptase and monitor the performance of the RNA molecules. Thus the interaction from the feedback process to the organelle is automatically ensured. However, there is no conceptual reason to require the same organelle to do all this. Hence, the three requirements have been separated in the version presented in the text.
Stahl, F., Bacterial genetics: a unicorn in the garden. Nature 335: 112–113, 1988.
Davis, B.D., Transcriptional bias: a non-Lamarckian mechanism for substrate-induced mutations. Proceedings of the National Academy of Sciences (USA) 86: 5005–5009, 1989.
It should perhaps be emphasized that probably none of the proponents of these mechanisms, especially Davis, B.D., Transcriptional bias: a non-Lamarckian mechanism for substrate-induced mutations. Proceedings of the National Academy of Sciences (USA) 86: 5005–5009, 1989, would choose to call the mechanisms “neo-Lamarckian.” Moreover, all that is being suggested here is that they are only “neo-Lmarckian” in the sense that they satisfy the criteria of the explication of the term given in Section 2.
Cairns, J. et al., The origin of mutants. Nature 335: 142–145, 1988. It is, perhaps, worth emphasis that there is no evidence, as yet, in favor of these mechanisms
Davis, B.D., Transcriptional bias: a non-Lamarckian mechanism for substrate-induced mutations. Proceedings of the National Academy of Sciences (USA) 86: 5005–5009, 1989, has argued that such a mechanism, itself, would have adaptive value. This is quite likely and such a mechanism might well have arisen in a thoroughly neo-Darwinian fashion. However, the new mutations that such a mechanism would make possible would still show the characteristics of being neo-Lamarckian. Thus the basic question, whether there is any neo-Lamarckian mutagenesis, remains the same.
Sarkar, S. Reductionism and molecular biology: a reappraisal. Ph. D. Dissertation. Department of Philosophy, University of Chicago, 1989, for a detailed examination of this issue.
For details, Sarkar, S., Reductionism and molecular biology: a reappraisal. Ph. D. Dissertation. Department of Philosophy, University of Chicago, 1989, and
Wimsatt, W.C. Reductive explanation: a functional account. Boston Studies in the Philosophy of Science 32: 671–710, 1976.
Cairns, J. Overbaugh, and S. Miller et al., The origin of mutants. Nature 335: 142–145, 1988, p. 145.
Sarkar, S. Reductionism and molecular biology: a reappraisal. Ph. D. Dissertation. Department of Philosophy, University of Chicago, 1989, and
Wimsatt, W. C. Reduction and reductionism. In Current Research in the Philosophy of Science. P.D. Asquith and H. Kyburg, editors. Philosophy of Science Association, pp. 352–377, 1978.
Sarkar, S. Reductionism and molecular biology: a reappraisal. Ph. D. Dissertation. Department of Philosophy, University of Chicago, 1989.
Kauffman, S.A., S.A. Articulation of parts explanation in biology and the rational search for them. Boston Studies in the Philosophy of Science 8: 257–272, 1972;
Wimsatt, W.C., Reductive explanation: a functional account. Boston Studies in the Philosophy of Science 32: 671–710, 1976.
The classic accounts of “theory reduction” are Nagel, E. The Structure of Science: Problems in the Logic of Scientific Explanation. New York: Harcourt, Brace & World, 1961, and
Schaffner, K. Approaches to reduction. Philosophy of Science 34: 137–147, 1967.
For arguments that attempt to show that such classic accounts of “theory reduction” cannot capture the flavor of research in molecular biology, Sarkar, S. Reductionism and molecular biology: a reappraisal. Ph. D. Dissertation. Department of Philosophy, University of Chicago, 1989.,
Wimsatt, W.C., Reductive explanation: a functional account. Boston Studies in the Philosophy of Science 32: 671–710, 1976, and,
especially, Hull, D. Reduction in genetics—biology or philosophy? Philosophy of Science 39: 491–499, 1972.
Luria, S.E. and M. Delbrück, Mutations of bacteria from virus sensitivity to virus resistance. Genetics 28: 491–511, 1943, p. 492. The same point can be made about most of the research of the Phage Group which usually tried to infer informations about processes within the virus by looking at interactions of the virus, as a whole, with other entities. Though, the present article argues for reductionist research in the context of the problem being considered here, examples such as this clearly show the value of non-reductionist research in biology in other contexts. Of course it is almost trivial to assert the same value for non-reductionist research in most of evolutionary biology.
Cairns, J., J. Overbaugh, and S. Miller et al., The origin of mutants. Nature 335: 1988, p. 145.
Delbrück, M. A physicist looks at biology. Transactions of the Connecticut Academy of Sciences 38: 173–190,1949;
Stent, G.S. That was the molecular biology that was. Science 160: 390–395, 1968;
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The important point is that the willingness to use such tests show that there was no prior commitment only to investigate biological problems in a reductionist fashion. It is not being suggested that Luria and Delbrück were deliberately attempting to keep their research strategy non-reductionist. In fact, Delbrck at least partly operated with an assumption that the only way in which his non-reductionist hopes might be realized is by pushing reductionist physical methods to the extreme and finding a paradox that defied such explanation. For details of this history, Sarkar, S., Reductionism and molecular biology: a reappraisal. Ph. D. Dissertation. Department of Philosophy, University of Chicago, 1989, and
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The only class of exceptions to the general reductionist explanations offered by molecular biology, at present, is that of functional explanations. For details of the problems that functional explanations pose for reductionist accounts, Sarkar, S., Reductionism and molecular biology: a reappraisal. Ph. D. Dissertation. Department of Philosophy, University of Chicago, 1989, and
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Sarkar, S. (1991). Lamarck Contre Darwin, Reduction Versus Statistics: Conceptual Issues in the Controversy over Directed Mutagenesis in Bacteria. In: Tauber, A.I. (eds) Organism and the Origins of Self. Boston Studies in the Philosophy of Science, vol 129. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-3406-4_11
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