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An adaptationist programme has dominated evolutionary thought in England and the United States during the past 40 years. It is based on faith in the power of natural selection as an optimizing agent. It proceeds by breaking an organism into unitary ‘traits’ and proposing an adaptive story for each considered separately. Trade-offs among competing selective demands exert the only brake upon perfection; non-optimality is thereby rendered as a result of adaptation as well. We criticize this approach and attempt to reassert a competing notion (long popular in continental Europe) that organisms must be analysed as integrated wholes, with Baupläne so constrained by phyletic heritage, pathways of development and general architecture that the constraints themselves become more interesting and more important in delimiting pathways of change than the selective force that may mediate change when it occurs. We fault the adaptationist programme for its failure to distinguish current utility from reasons for origin (male tyrannosaurs may have used their diminutive front legs to titillate female partners, but this will not explain why they got so small); for its unwillingness to consider alternatives to adaptive stories; for its reliance upon plausibility alone as a criterion for accepting speculative tales; and for its failure to consider adequately such competing themes as random fixation of alleles, production of non-adaptive structures by developmental correlation with selected features (allometry, pleiotropy, material compensation, mechanically forced correlation), the separability of adaptation and selection, multiple adaptive peaks, and current utility as an epiphenomenon of non-adaptive structures. We support Darwin’s own pluralistic approach to identifying the agents of evolutionary change.

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Abstract. Robustness is the invariance of phenotypes in the face of perturbation. The robustness of phenotypes appears at various levels of biological organization, including gene expression, protein folding, metabolic flux, physiological homeostasis, development, and even organismal fitness. The mechanisms underlying robustness are diverse, ranging from thermodynamic stability at the RNA and protein level to behavior at the organismal level. Phenotypes can be robust either against heritable perturbations (e.g., mutations) or nonheritable perturbations (e.g., the weather). Here we primarily focus on the first kind of robustness-genetic robustness-and survey three growing avenues of research: (1) measuring genetic robustness in nature and in the laboratory; (2) understanding the evolution of genetic robustness; and (3) exploring the implications of genetic robustness for future evolution.

Abstract.-If a population is growing in a randomly varying environment, such that the finite rate of increase per generation is a random variable with no serial autocorrelation, the logarithm of population size at any time t is normally distributed. Even though the expectation of population size may grow infinitely large with time, the probability of extinction may approach unity, owing to the difference between the geometric and arithmetic mean growth rates.A problem of recurrent interest to population ecology is the question of "density-dependent" control of population numbers. The literature on this subject is so vast and so well known to ecologists that it cannot and need not be referenced here. Briefly, the question is to what extent the actual growth rates of populations are affected by the population density, and so to what extent density and resource shortage must be taken into account in explaining the observed history of population numbers.The solution to this difficult and not always well-defined problem involves, among other things, an adequate description of how a population would change its numbers if its growth rate were not related to number, but only to variations in the independent environment (including other species, of course). Thus, we ask whether the observed variation in numbers of a species could be satisfactorily explained by supposing that at all times numbers are growing by the simple exponential growth law, but that the exponential rate of increase r is varying according to some extrinsic law unrelated to N, the population number. As stated, this proposition about variation in r is so general that no theoretical or experimental distinction could possibly be made between this hypothesis and that of density dependence. More specification is required. We assume a stationary distribution for r. Specifically, then, we want to ask how population numbers will change if the population is undergoing simple geometric increase or decrease with a rate that varies at random independently of both N and t.Although many sophisticated treatments of stochastic population growth exist for a variety of models,1' 2 it is our purpose in this note to point out a peculiarity of multiplicative population growth which is apparently not widely appreciated and which gives rise to some confusion.Consider a population of size Ne at time t, which in a single reproductive period has a multiplicative increase It so that Nt+1 = Ndl(1) and in general Nt = No Hi.