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Balanced Polymorphism

There are frequently populations of Batesian mimics that are polymorphic, often with one cryptic morph. If one assumes that the mimetic pattern is superior, the existence of the cryptic appears paradoxical. Actually, in such populations at equilibrium, all morphs are equally fit through density-dependent selection. The common supposition (which often is true), that the mimetic morphs are less successful at courtship is unnecessary, and may even be misleading. No superiority on the part of the cryptic morph need be shown - by overabundance the mimetic morphs negate their initial advantage at low frequencies. See Ford (1975), Ayala and Campbell (1974), and Barrett (1976) and references therein. [Pg.289]

Finally, all too often aposematic mimetic adaptations have been assumed to form an ecological and evolutionary panacea for the possessor. This they certainly do NOT, no more than any other adaptation. Thus, as we have seen, in polymorphic Batesian mimicry, a Batesian morph is not better protected than a cryptic morph, it is just differently protected. At equilibrium, all morphs will be equally protected. Once multiple species are involved, it is quite possible for a Batesian mimic to become so tied to its model that an independent existence is impossible. Furthermore, even its own numbers will be governed by the abundance and deterrence of its model. In fact, as I have said elsewhere (Huheey, 1980b), If, indeed, a Batesian mimic courts extinction by its rarity, it would not be the first example of selective forces which have led species into evolutionary dead ends from which they could not emerge.  [Pg.289]


Beutler E, Gelbart T, Demina A. Racial variability in the UDP-glucuronosyltrans-ferase 1 (UGT1A1) promoter a balanced polymorphism for regulation of bilimbin metabolism Proc Natl Acad Sci USA 1998 95 8170-8174. [Pg.306]

Furthermore, it has been observed that placental PGP is of great importance in limiting the fetal penetration of various potentially harmful or therapeutic compounds [64]. High PGP levels may have a role in the protection of fetuses from harmful tropical plant metabolites (from which many drugs are derived). An originally balanced polymorphism may have been preferentially selected by improved prenatal growth and development as well as improved postnatal health. This selective pressure may maintain the C allele in populations of African descent. [Pg.501]

I hypothesised (Baker and Beilis 1995 Baker 1996) that the within-population frequency distribution of testes size reflects a balanced polymorphism. In this hypothesis, men with larger testes were programmed to spend less time with partners, ejaculate often, and expose their sperm more often to sperm competition. Men with smaller testes were programmed to invest more in mate guarding and only infrequently to expose their sperm to competition. Between the two extremes, the intermediate men were programmed to pursue a more mixed strategy. [Pg.177]

This polymorphism, which was not related to the geographical origin of the infected fish hosts, is typical of a genetic polymorphism under the control of two co-dominant alleles. This type of balanced polymorphism indicates that cross-fertilisation must also occur, at least transiently, in L. intestinalis. The use of enzymes as markers in genetic studies in cestodes is clearly an important method for the detection of cross-fertilisation in this group. [Pg.164]

Dean M, Carrington M, O Brien SJ. Balanced polymorphism selected by genetic versus infectious human disease. Annu Rev Genomics Hum Genet 2002 3 263-292. [Pg.92]

Drug-sensitive hemolytic anemia is a hereditary disease, transmitted by a sex-linked dominant trait with low penetrance. The disease is widely distributed, and it is estimated that at least one hundred million people are affected by it. The anemia has been observed among many groups including Negroes, Jews, and Caucasians. It is prevalent in areas endemic for malaria. This association between malaria and drug-sensitive anemia results from a situation similar to that observed in sickle cell anemia, namely balanced polymorphism. [Pg.170]


See other pages where Balanced Polymorphism is mentioned: [Pg.491]    [Pg.176]    [Pg.178]    [Pg.185]    [Pg.1855]    [Pg.21]    [Pg.220]    [Pg.942]    [Pg.200]    [Pg.143]    [Pg.149]    [Pg.289]    [Pg.501]    [Pg.218]   
See also in sourсe #XX -- [ Pg.149 ]




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