Laboratory estimates of heritabilities and genetic correlations in nature.

A lower bound on heritability in a natural environment can be determined from the regression of offspring raised in the laboratory on parents raised in nature. An estimate of additive genetic variance in the laboratory is also required. The estimated lower bounds on heritabilities can sometimes be used to demonstrate a significant genetic correlation between two traits in nature, if their genetic and phenotypic correlations in nature have the same sign, and if sample sizes are large, and heritabilities and phenotypic and genetic correlations are high.

Genetics of mandible form in the mouse.

The underlying determination of phenotypic variability and covariability is described for 14 traits that define the morphological size and shape of the mature mouse mandible. Variability is partitioned into components due to direct additive and dominance genetic effects, indirect maternal additive genetic effects, genetic covariance between direct additive and indirect maternal additive effects and common and residual environmental effects. Multivariate analyses of the dimensionality of genetic variability indicate several complex and independent genetic components underlie the morphological form of the mandible. The multidimensional nature of the genetic components suggests a complex picture with regard to the consequences of selection on mandibular form.

Genetic analysis of size-scaling patterns in the mouse mandible.

The relationship between multidimensional form of the adult mouse mandible and body size is examined from an ontogenetic perspective. The origin and ontogeny of phenotypic correlations are described in terms of genetic and environmental covariance patterns between adult skeletal morphology and growth in body weight. Different ontogenetic patterns are observed in the genetic correlations, and these can be related to the developmental as well as the functional aspects of mandibular form. The quantitative genetic aspects of craniomandibular growth and morphogenesis are explored, together with an examination of the impact of ontogenetic changes in the genetic variance-covariance structure on morphogenetic integration and evolution by selection.

Genetics of growth predict patterns of brain-size evolution.

Experimental evidence is presented supporting a developmental model that explains the genetic basis for brain and body size associations. Evolutionary change in body size causes correlated change in brain size because some genes affect both traits. The commonly observed correlation between brain and body size results from genetic variation in growth determinants affecting both traits simultaneously during fetal and early postnatal growth. Later growth reduces brain-body correlation because of changes in the underlying causal components of growth in each trait. Brain-body size evolution shows a different pattern at higher taxonomic levels from that seen within and between closely related species because body-size evolution among higher taxa occurs primarily by change in early portions of growth, which share more genetic growth determinants with brain size.

Genetic analysis of crossfostering data with sire and dam records.

A method is presented for the analysis of data from crossfostering experiments in which parts of litters are reciprocally interchanged at birth. Observed variances and covariances of differently related individuals are expressed as functions of theoretical causal components of phenotypic variance (additive direct, dominance direct, additive maternal, dominance maternal, direct-maternal covariance, and environmental). Causal components are estimated by weighted least squares analysis of this system of equations, including a ridge-regression procedure to examine consequences of correlation between observed components. Ridge regression suggests that dominance direct genetic variance is generally underestimated, but that narrow-sense heritability estimates are reliable.

A genetic analysis of targeted growth in mice.

Effects of normal growth regulation on components of phenotypic variance and covariance of body weight were examined in a cross-fostering study of growth between 2 and 10 wk of age in ICR randombred mice. Different early growth rates caused genetic, postnatal maternal and residual environmental variances to increase, but these variances were subsequently reduced by negative autocorrelation between early and later growth. Postnatal maternal variance continued to increase for about 1 wk after weaning but then decreased substantially. Genetic variance caused by preweaning growth followed a pattern of increase and decrease very similar to that of postnatal maternal variance, but this pattern was masked by new genetic variance. Normal growth regulation affects the magnitudes of genetic variances and serial autocorrelations . The timing of these changes suggests that regulation of cell numbers reduces variance near the end of exponential growth, but this may be obscured by subsequent increase in cell size. In contrast with earlier studies, we find that targeted growth reduces both genetically and environmentally determined differences among early growth trajectories. Final size may be determined by an antagonistic balance between early growth rate and age at initiation of puberty.

Effects of the muscular dysgenesis gene on developmental stability in the mouse mandible.

Muscular dysgenesis (mdg) is an autosomal recessive gene in mice affecting primarily the skeletal musculature. mdg/mdg mice exhibit developmental arrest of myogenesis and degenerative changes in all skeletal muscles. In addition, there are pronounced abnormalities in skeletal traits, including the shape of the skull and mandible. Herein, we examine the phenotypic consequences of a single mdg allele in the heterozygous condition (+/mdg) on the size, shape, and developmental stability in 14 osteometric traits from the mouse mandible. Developmental stability in the mandible is measured by fluctuating asymmetry in bilateral traits. There are no statistically significant differences in the size or shape of the mandible between +/+ and +/mdg mice. However, compared to +/+ mice, +/mdg individuals exhibit less developmental stability for several mandible traits. The more unstable traits include height at the mandibular notch, height at the incisive process, condyloid width, height and area of the coronoid process, and size of the tooth-bearing region. All of these latter traits are closely associated with areas of muscle attachment and/or the muscular dysgenesis phenotype, suggesting that the presence of a single mdg allele is sufficient to alter developmental pathways. Traits not showing significantly increased instability in +/mdg mice bear no clear relationship to either muscle attachment areas or to the mdg/mdg phenotype.