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Predictive adaptive responses (PARs) are a form of developmental plasticity in which the developmental response to an environmental cue experienced early in life is delayed and yet, at the same time, the induced phenotype anticipates (i.e., is completely developed before) exposure to the eventual environmental state predicted by the cue, in which the phenotype is adaptive. We model this sequence of events to discover, under various assumptions concerning the cost of development, what lengths of delay, developmental time, and anticipation are optimal. We find that in many scenarios modeled, development of the induced phenotype should be completed at the exact same time that the environmental exposure relevant to the induced phenotype begins: that is, in contrast to our observed cases of PARs, there should be no anticipation. Moreover, unless slow development is costly, development should commence immediately after the cue: there should be no delay. Thus, PARs, which normally have non-zero delays and/or anticipation, are highly unusual. Importantly, the exceptions to these predictions of zero delays and anticipation occurred when developmental time was fixed and delaying development was increasingly costly. We suggest, therefore, that PARs will only evolve under three kinds of circumstances: (i) there are strong timing constraints on the cue and the environmental status, (ii) delaying development is costly, and development time is either fixed or slow development is costly, or (iii) when the period between the cue and the eventual environmental change is variable and the cost of not completing development before the change is high. These predictions are empirically testable.
Digenean parasites infecting four Cominella whelk species (C. glandiformis, C. adspersa, C. maculosa and C. virgata), which inhabit New Zealand's intertidal zone, were analysed using molecular techniques. Mitochondrial 16S and cytochrome oxidase 1 (COI) and nuclear rDNA ITS1 sequences were used to infer phylogenetic relationships amongst digenea. Host species were parasitized by a diverse range of digenea (Platyhelminthes, Trematoda), representing seven families: Echinostomatidae, Opecoelidae, Microphallidae, Strigeidae and three, as yet, undetermined families A, B and C. Each parasite family infected between one and three host whelk species, and infection levels were typically low (average infection rates ranged from 1·4 to 3·6%). Host specificity ranged from highly species-specific amongst the echinostomes, which were only ever observed infecting C. glandiformis, to the more generalist opecoelids and strigeids, which were capable of infecting three out of four of the Cominella species analysed. Digeneans displayed a highly variable geographic range; for example, echinostomes had a large geographic range stretching the length of New Zealand, from Northland to Otago, whereas Family B parasites were restricted to fairly small areas of the North Island. Our results add to a growing body of research identifying wide ranges in both host specificity and geographic range amongst intertidal, multi-host parasite systems.
Models of host–parasite co-evolution suggest that parasites can exert frequency-dependent selection on their hosts, favouring rare alleles that confer resistance against widespread parasites and thus contributing to the maintenance of genetic variation, at some loci at least. If parasites are important in maintaining variation at many loci, then host species incurring a high prevalence of parasite infections should exhibit greater levels of genetic variation than host species incurring a lower prevalence. Using data from electrophoretic studies and from field surveys of haematozoan infections, we constructed a dataset including 103 species of North American and European birds to test this prediction. After controlling for sampling effort and phylogenetic influences, we found no relationship between parasite prevalence and either heterozygosity or polymorphism. These results do not support a role for parasites in the overall maintenance of genetic variation via frequency-dependent selection.
The bitterness and protracted character of the biometrician–Mendelian
debate has long
aroused the interest of historians of biology. In this paper, we focus
on another and much
less discussed facet of the controversy: competing interpretations of the
mental defect. Today, the views of the early Mendelians, such as Charles
B. Davenport and
Henry H. Goddard, are universally seen to be mistaken. Some historians
assume that the
Mendelians' errors were exposed by advances in the science of genetics.
Others believe that
their mistakes could have been identified by contemporaries. Neither interpretation
account of the fact that the lapses for which the Mendelian eugenicists
are now notorious
were, in fact, mostly identified at the time by the biometricians David
Heron and Karl
Pearson. In this paper we ask why their objections had so little impact.
We think the answer
illustrates an important general point about the social prerequisites for
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