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Journal Article

A Quantitative Genetic Analysis of Brain and Body Size Associations, Their Origin and Ontogeny: Data From Mice

William R. Atchley, Bruce Riska, Luci A. P. Kohn, A. Alison Plummer and J. J. Rutledge
Evolution
Vol. 38, No. 6 (Nov., 1984), pp. 1165-1179
DOI: 10.2307/2408625
Stable URL: http://www.jstor.org/stable/2408625
Page Count: 15
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A Quantitative Genetic Analysis of Brain and Body Size Associations, Their Origin and Ontogeny: Data From Mice
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Abstract

The heritability of brain size is approximately .6 at both 38 and 70 days of age, a value which is almost identical with other studies on mice. Ontogenetic data indicates that the genetic correlation between brain size and body weight is highest during early post-natal development and decreases as the organism ages. The genetic correlation between brain size and body weight gain is positive for periods of early growth but becomes negative for later periods of growth. The various environmental components of the correlation between brain and body size are reasonably constant during ontogeny. The high genetic correlation between brain size and body weight early in postnatal growth suggests that brain size is most strongly associated with the cell multiplication phase of growth in body size. Later growth in body size occurs primarily by cell enlargement and shows a much lower correlation with brain size. A model is presented to explain the origin and ontogeny of the genetic correlation between brain and body size. It is suggested that a genetic correlation can arise between two traits if they are responding simultaneously to one or more systematic stimuli, such as embryonic somatomedin which is a systematic mitogen acting on brain growth as well as on most other body tissues during early development. Changes in concentration of embryonic somatomedin would act on both brain and body size producing a positive genetic correlation between them. Growth in brain size slows greatly after about two weeks post-natal age at a time when the concentration of embryonic somatomedin level is also rapidly decreasing. There is a decrease in genetic correlation between brain and body size during ontogeny as brain size growth in mice slows and eventually stops. Growth in log transformed body weight occurring after cessation of brain growth in these mice has been shown to decrease the variance in body weight as well as the covariance of brain size and body weight. Thus, the early pattern of variation shared by brain and body size is being reduced as new patterns of body size variation appear. If selection were focused on the cell multiplication phase of growth, a more pronounced correlated change in brain size should occur than if selection occurred on the cell enlargement component. Such differential selection intensity could explain the steeper allometric slope seen between higher categories as compared to between populations and species.

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