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was to test the Oparin-Haldane hypothesis…

It is clear that infection has selected a mutant showing alterations in a highly relevant physiological trait such as respiration. The disequilibrium in the expected distribution of alleles of genes involved in genetically inherited diseases is the basis of Haldane's hypothesis. A trait (such as a genetically inherited disease) that reduces the fitness of the progeny can only be selected by an alternative selective force. In fact, it was suggested that the higher-than-expected frequency of these diseases in human populations is probably a side effect of the selection of lineages more resistant to infection (). In a similar way, the selection of a C. elegans strain with less proficient respiration must be the consequence of an alternative selective force. In this case, the selective force is resistance to P. aeruginosa infection. This resistance not only allows the nematode to be more resistant to cyanide poisoning but also to gain access to a new food resource, P. aeruginosa. Obviously, those changes (mainly the utilization of novel food resources) may allow the evolved C. elegans AN1 strain to colonize novel environments previously forbidden for the wild-type strain C. elegans N2. At first sight, this observation might be an example of shearing evolution. The nematode will be killed as a consequence of P. aeruginosa infection and, besides, it will die because there is not any other food resource to feed the worm. Nevertheless, C. elegans can feed on nonvirulent P. aeruginosa cells (), whereas mixed cultures of nontoxic E. coli (food resource) and P. aeruginosa (infective agent) kill the nematode (A.N. and J.L.M., unpublished results). This observation clearly shows that the deadly selective force for the evolution of the worm is infection, not the lack of food, and the exploitation of an alternate food resource is just an unexpected, beneficial consequence of this evolution.

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Two interesting additional points: sympatric species show greaterprezygotic isolation than allopatric species pairs. This pattern isconsistent with the reinforcement hypothesis and suggest that reinforcementcan act (see figs. 16.14 - 16.16, pg. 454-455). A second observation:less genetic distance between species pairs that produce sterileor inviable males than between species pairs that produce sterileor inviable females (D).

and often is attributed as the Oparin–Haldane hypothesis

08/01/2018 · In 1924, Aleksandr Oparin (and John Haldane separately in 1929) hypothesized that the formation of amino acids and proteins from non-living chemicals,.

The role of infections in the evolution of their hosts was proposed early by Haldane. In 1932, he wrote “A study of the causes of death in man, animals and plants leaves no doubt that one of the principal characters possessing survival value is immunity to disease” (). Later on, in 1949, the idea was stated more clearly: “the struggle against disease, and particularly infectious diseases, has been a very important evolutionary agent” (). This hypothesis has been backed by epidemiological data showing that some human populations have a much higher than the expected percentage of some genetically inherited diseases. More recently, it has been argued that any harmful trait that is too frequent to be explained by mutation or balanced polymorphism is probably selected by infection (). One of the first studied cases was thalassemia. It was found that there was a high prevalence of this disease in the Mediterranean region and that this phenomenon reflects heterozygote advantage against malaria (). The demonstration of malaria resistance came on 1954, when it was described that young children with the sickle cell trait had significant fewer Plasmodium falciparium parasites than normal homozygotes (). Recent works indicate that the picture is more complex than expected previously because P. falciparium infection might have selected changes in different human loci that contribute to resistance to the disease (). That way, malaria could be a selective force shaping the genetic structure of human populations in the Mediterranean and other geographic regions ().

The full reconciliation was achieved in the 1920s and early 30s,thanks to the mathematical work of Fisher, Haldane and Wright. Each ofthese theorists developed formal models to explore how naturalselection, and other evolutionary forces such as mutation, would modifythe genetic composition of a Mendelian population over time. This workmarked a major step forward in our understanding of evolution, for itenabled the consequences of various evolutionary hypotheses to beexplored quantitatively rather than just qualitatively. Verbalarguments about what natural selection could or could not achieve, orabout the patterns of genetic variation to which it could give rise,were replaced with explicit mathematical arguments. The strategy ofdevising formal models to shed light on the process of evolution isstill the dominant research methodology in contemporary populationgenetics.

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