Cell numbers and cell sizes in organs of mice selected for large and small body size

Falconer, D. S.; Gauld, I. K.; Roberts, R. C.

doi:10.1017/s0016672300018061

Cited by 64 publications

(48 citation statements)

References 13 publications

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“…Results showing differserved in this experiment relative to those reported by Smith Richards et al (2002). The three QTL found ences in cell number and cell size at different ages have been observed in several selection experiments in mice in this study for intake at specific weekly intervals show, for the first time, age-dependent genomic regulation of (Falconer et al 1978;Atchley et al 2000), including the M16 line (Eisen and Leatherwood 1978).…”

Section: Or Between Lines Divergentlycontrasting

confidence: 55%

Genomic Mapping of Direct and Correlated Responses to Long-Term Selection for Rapid Growth Rate in Mice

2005

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Understanding the genetic architecture of traits such as growth, body composition, and energy balance has become a primary focus for biomedical and agricultural research. The objective of this study was to map QTL in a large F 2 (n ϭ 1181) population resulting from an intercross between the M16 and ICR lines of mice. The M16 line, developed by long-term selection for 3-to 6-week weight gain, is larger, heavier, fatter, hyperphagic, and diabetic relative to its randomly selected control line of ICR origin. The F 2 population was phenotyped for growth and energy intake at weekly intervals from 4 to 8 weeks of age and for body composition and plasma levels of insulin, leptin, TNF␣, IL6, and glucose at 8 weeks and was genotyped for 80 microsatellite markers. Since the F 2 was a cross between a selection line and its unselected control, the QTL identified likely represent genes that contributed to direct and correlated responses to longterm selection for rapid growth rate. Across all traits measured, 95 QTL were identified, likely representing 19 unique regions on 13 chromosomes. Four chromosomes (2, 6, 11, and 17) harbored loci contributing disproportionately to selection response. Several QTL demonstrating differential regulation of regional adipose deposition and age-dependent regulation of growth and energy consumption were identified.

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Section: Or Between Lines Divergentlycontrasting

confidence: 55%

Genomic Mapping of Direct and Correlated Responses to Long-Term Selection for Rapid Growth Rate in Mice

2005

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“…Thus, it is reasonable to suggest that biphasic size-scaling of metabolism is produced by the joined effects of ontogenetic shifts in energy expenditure for growth and changes in the relative roles of hyperplasia and hypertrophy in ontogenetic growth. Changes in the size and number of cells are also known to underlie responses to selection for growth traits (Medrano and Gall, 1976a;Falconer et al, 1978;Stevenson et al, 1995;Atchley et al, 1997;Atchley et al, 2000;Calboli et al, 2003). Partridge et al (Partridge et al, 1999), for example, demonstrated that lab evolution of larger Drosophila melanogaster proceeded mainly through increasing cell number, and an evolutionary decrease in size was achieved mostly by reduction of cell size.…”

Section: Linking Metabolic Scaling Growth and Cell Size -Future Prosmentioning

confidence: 99%

“…Our results favor the view that some part of this variability can be linked to variable growth rates, but we stress that this concept in its original form (sensu Wieser, 1994;Riisgård, 1998) overlooks the potential metabolic consequences of cellular processes associated with growth rate changes. Most organisms increase body size mainly through cell proliferation (hyperplasia) during early postembryonic development and thus with relatively little change in average cell size, but later in life mainly by cell growth and/or hypertrophy (Falconer et al, 1978;Atchley et al, 2000;Glazier, 2005). Given that larger cells require less energy per protoplasm volume than smaller cells for maintenance of ion gradients across cell membranes (Davison, 1955;Kozlowski et al, 2003), cellular changes through ontogeny alone should lead to nearly isometric scaling of metabolism early in life and to negative allometry of metabolism later in life, a phenomenon already postulated (Kayser and Heusner, 1964) and quoted (Medrano and Gall, 1976b).…”

Section: Linking Metabolic Scaling Growth and Cell Size -Future Prosmentioning

confidence: 99%

Scaling of metabolism inHelix aspersasnails: changes through ontogeny and response to selection for increased size

Czarnołęski

Kozłowski

Dumiot

et al. 2008

Journal of Experimental Biology

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SUMMARYThough many are convinced otherwise, variability of the size-scaling of metabolism is widespread in nature, and the factors driving that remain unknown. Here we test a hypothesis that the increased expenditure associated with faster growth increases metabolic scaling. We compare metabolic scaling in the fast-and slow-growth phases of ontogeny of Helix aspersa snails artificially selected or not selected for increased adult size. The selected line evolved larger egg and adult sizes and a faster sizespecific growth rate, without a change in the developmental rate. Both lines had comparable food consumption but the selected snails grew more efficiently and had lower metabolism early in ontogeny. Attainment of lower metabolism was accompanied by decreased shell production, indicating that the increased growth was fuelled partly at the expense of shell production. As predicted, the scaling of oxygen consumption with body mass was isometric or nearly isometric in the fast-growing (early) ontogenetic stage, and it became negatively allometric in the slow-growing (late) stage; metabolic scaling tended to be steeper in selected (fast-growing) than in control (slow-growing) snails; this difference disappeared later in ontogeny. Differences in metabolic scaling were not related to shifts in the scaling of metabolically inert shell. Our results support the view that changes in metabolic scaling through ontogeny and the variability of metabolic scaling between organisms can be affected by differential growth rates. We stress that future approaches to this phenomenon should consider the metabolic effects of cell size changes which underlie shifts in the growth pattern.

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“…Body weight at necropsy is strongly correlated with the target of selection in original lines, the body weight at 60 days (Falconer et al 1978;Vaughn et al 1999). All phenotypic measurements were taken at necropsy and were corrected for the effect of sex, age at necropsy, and litter size (,10 vs. .10) by partialing out the effect of these factors using the general linear model prior to further analysis.…”

Section: Datamentioning

confidence: 99%

Directionality of Epistasis in a Murine Intercross Population

et al. 2010

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Directional epistasis describes a situation in which epistasis consistently increases or decreases the effect of allele substitutions, thereby affecting the amount of additive genetic variance available for selection in a given direction. This study applies a recent parameterization of directionality of epistasis to empirical data. Data stems from a QTL mapping study on an intercross between inbred mouse (Mus musculus) strains LG/J and SM/J, originally selected for large and small body mass, respectively. Results show a negative average directionality of epistasis for body-composition traits, predicting a reduction in additive allelic effects and in the response to selection for increased size. Focusing on average modification of additive effect of single loci, we find a more complex picture, whereby the effects of some loci are enhanced consistently across backgrounds, while effects of other loci are decreased, potentially contributing to either enhancement or reduction of allelic effects when selection acts at single loci. We demonstrate and discuss how the interpretation of the overall measurement of directionality depends on the complexity of the genotype-phenotype map. The measure of directionality changes with the power of scale in a predictable way; however, its expected effect with respect to the modification of additive genetic effects remains constant. E PISTASIS is present when the effect of a genetic substitution depends on the genotypes at other loci. At the population level, this means that average allelic effects change as allele frequencies at other loci change, and thus that gene effects can evolve. The evolutionary significance of epistasis has been recognized mainly in relation to the allele-frequency changes that are caused by genetic drift (e.g

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Cell numbers and cell sizes in organs of mice selected for large and small body size

Cited by 64 publications

References 13 publications

Genomic Mapping of Direct and Correlated Responses to Long-Term Selection for Rapid Growth Rate in Mice

Genomic Mapping of Direct and Correlated Responses to Long-Term Selection for Rapid Growth Rate in Mice

Scaling of metabolism inHelix aspersasnails: changes through ontogeny and response to selection for increased size

Directionality of Epistasis in a Murine Intercross Population

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