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Title
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Human fetuses and limb asymmetry: no evidence for directional asymmetry and support for fluctuating asymmetry as a measure of developmental instability
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Author
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Abstract
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| The often observed directional asymmetry in human limb bones could have a genetic basis. Alternatively, differences in limbs across sides could emerge from different mechanical loadings on the left and right side as a result of behavioral lateralization. Because handedness in itself has a genetic basis, it has been suggested that directional asymmetry in limbs could develop prenatally as a pre-adaptationto adult life. The developmental origins of limb asymmetry and the presence of directional asymmetry have important implications for the use of directionally random asymmetry (i.e., fluctuating asymmetry) as a measure of developmental instability (the inability of an organism to buff er its development against random noise). We study asymmetry in limb bones of deceased fetuses. We predict that if the direct effects of handedness (asymmetric mechanical loadings) would predominantly affect directional asymmetry, it would be absent in fetal limbs. However, because genes involved in the asymmetrical positioning of internal organs (situs solitus) also play a role in limb development, directional asymmetry may also emerge during early fetal stages. In a sample of over 500 fetuses, no indication of directional asymmetry was found in several limb bones. In addition, directional asymmetry did not emerge in the older fetuses either. We suggest that morphological asymmetries in fetal limb bones corresponded to fluctuating asymmetry measuring developmental instability. High levels of developmental integration found in our dataset could explain the overall low levels of asymmetry found in our study. |
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Language
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English
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Source (journal)
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Animal biology / Royal Dutch Zoological Society. - Leiden, 2003, currens
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Publication
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Leiden
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Brill
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2010
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ISSN
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1570-7555
[print]
1570-7563
[online]
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Volume/pages
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60
:2
(2010)
, p. 169-182
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ISI
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000279161400006
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Full text (Publisher's DOI)
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Full text (publisher's version - intranet only)
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