Search

We identify a species of experiment—Kon-Tiki experiments—used to demonstrate the competence of a cause to produce a certain effect, and we examine their role in the historical sciences. We argue that Kon-Tiki experiments are used to test middle-range theory, to test assumptions within historical narratives, and to open new avenues of inquiry. We show how the results of Kon-Tiki experiments are involved in projective (rather than consequentialist) inferences, and we argue (against Kyle Stanford) that reliance on projective inferences does not provide historical scientists with any special protection against the problem of unconceived alternatives.

Eukaryotes exhibit a great diversity of cellular and subcellular morphologies, but their basic underlying architecture is fairly constant. All have a nucleus, Golgi, cytoskeleton, plasma membrane, vesicles, ribosomes, and all known lineages but one have mitochondrion-related organelles. Moreover, most eukaryotes undergo processes such as mitosis, meiosis, DNA recombination, and often perform feats such as phagocytosis, and amoeboid and flagellar movement. With all of these commonalities, it is obvious that eukaryotes evolved from a common ancestor, but it is not obvious how eukaryotes came to have their diverse structural phenotypes. Are these phenotypes adaptations to particular niches, their evolution dominated by positive natural selection? Or is eukaryotic cellular diversity substantially the product of neutral evolutionary processes, with adaptation either illusory or a secondary consequence? In this paper, we outline how a hierarchical view of phenotype can be used to articulate a neutral theory of phenotypic evolution, involving processes such as gene loss, gene replacement by homologues or analogues, gene duplication followed by subfunctionalization, and constructive neutral evolution. We suggest that neutral iterations of these processes followed by entrenchment of their products can explain much of the diversity of cellular, developmental, and biochemical phenotypes of unicellular eukaryotes and should be explored in addition to adaptive explanations.

Biological science uses multiple species concepts. Order can be brought to this diversity if we recognize two key features. First, any given species concept is likely to have a patchwork structure, generated by repeated application of the concept to new domains. We illustrate this by showing how two species concepts (biological and ecological) have been modified from their initial eukaryotic applications to apply to prokaryotes. Second, both within and between patches, distinct species concepts may interact and hybridize. We thus defend a semantic picture of the species concept as a collection of interacting patchwork structures. Thus, although not all uses of the term pick out the same kind of unit in nature, the diversity of uses reflects something more than mere polysemy. We suggest that the emphasis on the use of species to pick out natural units is itself problematic, because that is not the term’s sole function. In particular, species concepts are used to manage inquiry into processes of speciation, even when these processes do not produce clearly delimited species.

Charles Darwin, in his species notebooks, engaged seriously with the quinarian system of William Sharp Macleay. Much of the attention given to this engagement has focused on Darwin's attempt to explain, in a transmutationist framework, the intricate patterns that characterized the quinarian system. Here, I show that Darwin's attempt to explain these quinarian patterns primarily occurred before he had read any work by Macleay. By the time Darwin began reading Macleay's writings, he had already arrived at a skeptical view of the reality of these patterns. What most interested Darwin, as he read Macleay, was not the quinarian system itself. Rather, Darwin's notes on his reading primarily concerned certain background principles animating Macleay's work, in particular: (a) the non-existence of a saltus between human and animal minds, (b) the difficulty of establishing boundaries between species and varieties, and (c) Macleay's method of variation. Darwin's interest in the last of these left a mark on his discussion of taxonomic methodology in the Origin.

This paper investigates the complexity hypothesis in microbial evolutionary genetics from a philosophical vantage. This hypothesis, in its current version, states that genes with high connectivity (more functional connections to other genes) are likely to be resistant to being horizontally transferred. We defend four claims. (1) There is an important distinction between two different ways in which a gene family can persist: vertically and horizontally. There is a trade-off between these two modes of persistence, such that a gene better at achieving one will be worse at achieving the other. (2) At least some genes are likely to experience selection favoring increased transferability. One consequence of this can be encapsulated as the “simplicity hypothesis”: horizontally persisting genes will experience selection favoring reduced connectivity. (3) In order to make sense of the simplicity hypothesis, we need to consider evolutionary populations that transcend species boundaries. Vertical and horizontal persistence are therefore not two competing ways of succeeding at the same game, but involve playing two different games altogether. (4) The complexity hypothesis can be understood in terms of two related notions: entrenchment and Cuvierian functionalism. This framing reveals previously unrecognized and philosophically interesting connections between reasoning about deep conservation and horizontal transfer.

L.A. Paul has recently defended the methodology of metaphysics on the grounds that it is continuous with the sciences. She claims that both scientists and metaphysicians use inference to the best explanation (IBE) to choose between competing theories, and that the success of science vindicates the use of IBE in metaphysics. Specifically, the success of science shows that the theoretical virtues are truth-conducive. I challenge Paul’s claims on two grounds. First, I argue that, at least in biology, scientists adhere to the vera causa ideal, which allows the theoretical virtues to play a much more limited role in scientific reasoning than Paul requires for metaphysical reasoning. The success of biology thus does not vindicate the methodology of metaphysics. Second, I argue that, at least in many cases, the successful reliance on the theoretical virtues in scientific contexts shows only that the theoretical virtues are truth-conducive within those local contexts, and not that they are truth-conducive generally. The upshots are (1) that Paul’s defense of the methodology of metaphysics fails, and (2) that any attempt to rescue her defense must pay more careful attention to what precisely is vindicated by successful science.

Amphibians are among the most endangered organisms on Earth; however, few monitoring studies have been conducted in the tropics despite high amphibian diversity in these regions. To help fill this gap, we completed fieldwork to reassess the status of the Bloody Bay Poison Frog (Mannophryne olmonae, an endemic from the island of Tobago), classified as “Critically Endangered” by the original IUCN Global Amphibian Assessment, though recently downgraded to “Vulnerable.” To assess occupancy patterns and population stability, we used occupancy modeling with three years of listening survey data (2011–2013) from 35 sites. To examine patterns of relative abundance and recruitment, we gathered frog encounter rate and body size data from 18 stream-side transects. To assess current distributional limits, we conducted listening surveys at and beyond the known range limits. Together, these data suggest that M. olmonae is more widely distributed than previously reported (we found 23 extralimital populations), i...

Kyle Stanford has recently given substance to the problem of unconceived alternatives, which challenges the reliability of inference to the best explanation (IBE) in remote domains of nature. Conjoined with the view that IBE is the central inferential tool at our disposal in investigating these domains, the problem of unconceived alternatives leads to scientific anti-realism. We argue that, at least within the biological community, scientists are now and have long been aware of the dangers of IBE. We re-analyze the nineteenth-century study of inheritance and development (Stanford’s case study) and extend it into the twentieth century, focusing in particular on both classical Mendelian genetics and the studies by Avery et al. on the chemical nature of the hereditary substance. Our extended case studies show the preference of the biological community for a different methodological standard: the vera causa ideal, which requires that purported causes be shown on non-explanatory grounds to exist and be competent to produce their effects. On this basis, we defend a prospective realism about the biological sciences.

There is long-standing conflict between genealogical and developmental accounts of homology. This paper provides a general framework that shows that these accounts are compatible and clarifies precisely how they are related. According to this framework, understanding homology requires both (a) an abstract genealogical account that unifies the application of the term to all types of characters used in phylogenetic systematics and (b) locally enriched accounts that apply only to specific types of characters. The genealogical account serves this unifying role by relying on abstract notions of ‘descent’ and ‘character’. As a result, it takes for granted the existence of such characters. This requires theoretical justification that is provided by enriched accounts, which incorporate the details by which characters are inherited. These enriched accounts apply to limited domains (e.g. genes and proteins, or body parts), providing the needed theoretical justification for recognizing characters within that domain. Though connected to the genealogical account of homology in this way, enriched accounts include phenomena (e.g. serial homology, paralogy, and xenology) that fall outside the scope of the genealogical account. They therefore overlap, but are not nested within, the genealogical account. Developmental accounts of homology are to be understood as enriched accounts of body part homology. Once they are seen in this light, the conflict with the genealogical account vanishes. It is only by understanding the fine conceptual structure undergirding the many uses of the term ‘homology’ that we can understand how these uses hang together.

William Sharp Macleay developed the quinarian system of classification in his Horae Entomologicae, published in two parts in 1819 and 1821. For two decades, the quinarian system was widely discussed in Britain and influenced such naturalists as Charles Darwin, Richard Owen, and Thomas Huxley. This paper offers the first detailed account of Macleay's development of the quinarian system. Macleay developed his system under the shaping influence of two pressures: (1) the insistence by followers of Linnaeus on developing artificial systems at the expense of the natural system and (2) the apparent tension between the continuity of organic nature and the failure of linear classification schemes (which continuity seemed to require). Against what he perceived as dogmatic indolence on the part of the Linnaeans, Macleay developed a philosophy of science in which hypotheses that exceeded the available evidence should be proposed and subjected to severe tests. He also developed a novel comparative anatomical methodology, the method of variation, to aid in his search for the natural system. Using this method, he developed an intricate system that showed how organic nature could be continuous without being linear. A failure to appreciate these facets of Macleay's thought has led to several misunderstandings of him and his work, most notably that he was an idealist. These misunderstandings are here rebutted.

MIND FROM MATTER?: An Essay on Evolutionary Epistemology by Max Delbruck; edited by Gunther S. Stent

The oxidation of isopropyl alcohol by chromic acid is a reaction first order with respect to the acid chromate ion, HCrO4−, first order with respect to the alcohol, and second order with respect to hydrogen ion. Evidence has been obtained that the reaction proceeds by way of a compound of tetravalent or of pentavalent chromium. On the basis of these facts, a mechanism for the oxidation has tentatively been suggested.

From physiological and genetic evidence, it is concluded that the repressor for β-galactosidase (EC 3.2.1.23) synthesis in a mutant bacterium, E-103, is thermolabile. The apparent inactivation of repressor is first order and irreversible; however, paradoxically, only a characteristic fraction can be inactivated at a given temperature, suggesting some heterogeneity of repressor in this strain. Following inactivation of repressor, there is a delay in reappearance of repression that is believed to be caused by the time required to establish synthesis of repressor.

Advantage is taken of the properties of a mutant in which the production of repressor for the Lac operon is temperature-sensitive to show that the formation of this repressor is not appreciably inducible by inducers (IPTG) under conditions in which the rate of β-galactosidase synthesis is increased one-thousandfold.

A procedure is described for the isolation of bacteria able to make unusually large quantities of β-galactosidase. A number of such hyper strains, as they are called, have been isolated and some have been found to make protein containing as much as 25% β-galactosidase. This enzyme in these strains appears to be identical with that in normal strains with respect to Michaelis constant, heat sensitivity, sedimentation constant, and ratio of antigenic sites to enzymic sites. The ability to make β-galactosidase at hyper rates is genetically determined in the lac region of the bacterial chromosome, and this ability can be transferred by genetic recombination.

The effects of ethanol on the growth of a wild-type Escherichia coli K-12 are described. These effects include a reduction of the steady-state growth rate and an interference with the division process. They appear as an immediate response to the addition of ethanol and are rapidly reversed by removal of ethanol. Mutants were selected that could grow at a concentration of ethanol that stopped wild-type growth. The growth of one of the mutants we studied (strain S9L100) is stimulated by the presence of ethanol, methanol, or dimethyl sulfoxide. This strain exhibits pleiotropic growth defects including abnormal cell division and morphology. It also appears to have an altered lac permease function which is not due to a mutation in the Y gene itself. We conclude that this mutant has an altered membrane and that the membrane defect may be the cause of the abnormal growth properties. The use of compounds which serve as general membrane perturbants and mutants resistant to these perturbants form a system accessible to both genetic and physical-biochemical techniques.

By experiments with mutants having temperature-sensitive repression systems for the Lac operon, it has been possible to provide evidence indicating that: (a) the i -gene product is the repressor, or physically included in it; (b) the rate of enzyme synthesis varies inversely with the first power of repressor concentration; (c) the repressor is “growth unstable” with a mean life of 1/5 to 1/10 generation; (d) inducers cause structural changes in repressor, manifested by altered thermal stability; (e) and the repressor is composed of subunits, which have a site for combination with inducers.

The nature of the repressors which control gene expression and the mechanism of their action promise to be clarified very soon largely because of the recent successful development of in vitro assays for the lac repressor (Gilbert and Muller-Hill, 1966) and for the repressor controlling the temperate phage λ (Ptashne, 1967). These developments have followed earlier experiments with whole cells which originally led to the postulation of repressors and which continued to provide further support for their existence. In the present report, I would like to describe some studies in whole cells of the interaction of galactoside inducers with the lac repressor.

Delbruck and Bailey (1) noticed an anomaly in the lysate of bacteria which was obtained by mixedly infecting the B strain of coli with the bacterial viruses T2 and T4. Subsequently, Luria (2) found this anomaly to be even more pronounced when he repeated Delbruck's experiment-using, however, virus T2 that had been exposed to ultraviolet irradiation. When we undertook experiments in an attempt to understand this anomaly, we were led to the following result: If we infect a culture of the B strain of coli mixedly with the bacterial viruses T2 and T4 and incubate to permit lysis of the bacteria, there are present in the lysate 3 easily distinguishable types of bacterial viruses. Two of these, as expected, behave like the original parent strains T2 and T4, i.e., one of them behaves like T2 inasmuch as it is unable to attack the mutant strain B/2 (which is resistant to T2) but is able to grow in the mutant strain B/4 (which is sensitive to T2); the other behaves like T4, being unable to attack B/4 (which is resistant to T4) but is able to grow in B/2 (which is sensitive to T4). The third type of virus present is phenotypically like T4 inasmuch as it is capable of multiplying in the strain B/2 (which is sensitive to T4), but it is genotypically like T2 inasmuch as, after one passage in the strain B/2, it is no longer capable of growing in it but is capable of growing in the strain B/4 (which is sensitive to T2). The presence of this third type of virus, which may be called "latent T2," can be demonstrated in the following manner: We add to a culture of the B strain of coli viruses T2 and T4 in ratios corresponding to 10 T2 and 10 T4 virus particles per bacterium, incubate to permit lysis of the bacteria, and then filter the lysate. If we plate a sample of this lysate on agar that is inoculated with the strain B/4 (which is sensitive to T2 but resistant to T4), those virus particles contained in the lysate which have the phenotype T2 will show up as plaques on these plates. T4 virus particles will not give plaques on this plate because B/4 is resistant to T4. The number of plaques is thus a measure of the number of T2 particles in the lysate. Using a sample of the lysate, we determine in this manner the number of plaques obtained on an agar plate inoculated with the strain B/4. When we repeat this experiment-with the difference that before plating on the B/4 plate we add to the sample of our lysate a certain quantity of the strain B/2, allow 5 min for absorption, dilute with broth, and incubate for 1 hr to permit lysis of the bacteria-then we obtain a ten to twenty-five times larger number of plaques on the B/4 plate. This phenomenon appears to show that there is present in our lysate a virus (the "latent T2") which is capable of multiplying in B/2 and subsequently forming plaques on B/4. In order to account for our observation, the concentration of the "latent T2" in the lysate would have to be about 10% of the concentration of T2. We were not able to obtain, after one passage in B/2, any appreciable further growth in B/2 of our hypothetical "latent T2." Before drawing the conclusion that the presence of a "latent T2" is in fact responsible for our phenomenon, it is necessary to exclude alternative explanations. As an alternative explanation of our observation, it appeared a priori conceivable that our lysate contains aggregates of virus particles formed by a T2 and a T4 particle that stick together. Such aggregates might then perhaps be capable of entering into a bacterium of the strain B/2 (by virtue of their T4 component) and, once inside, both virus particles T2 and T4 might then be able to multiply, and thus to produce the observed phenomenon. We were able to rule out this possibility, however, by performing the following experiment. We add to a sample of our lysate a certain quantity of B/2, using an excess of B/2 so that independent infection of one bacterium by more than one virus particle can be neglected. We then allow 5 min for absorption and plate on an agar plate that has been inoculated with both B/2 and B/4. If there are present any B/2 bacteria into which has entered an aggregate of virus particles composed of T2 and T4, and in which both viruses will grow, then a certain number of clear plaques centering around such bacteria (which yield both T2 and T4) should develop on the agar plate. We were not able to find any such clear plaques, however, and found only turbid plaques (in which either the B/2 is lysed by T4 or the B/4 is lysed by T2). This rules out the alternative explanation of our phenomenon. We ascertained that our phenomenon is produced under conditions in which we use an excess of B/2, so that independent infection of one bacterium by more than one virus particle can be neglected. We also ascertained that our phenomenon is not produced if, in place of our lysate, we use a mixture of T2 and T4. We are thus led to conclude that the phenomenon described is due to virus particles that have the phe