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W R Atchley

Publications and source records attributed to W R Atchley.

50 records · Page 3Linked to original sources

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.

Aging↗

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.

Age Factors↗

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.

Abnormalities, Multiple↗

A genetic analysis of the mandible and maxilla in the rat.

A quantitative genetic analysis of eight osteometric traits from the oral region together with femur length in the rat are described. The relevant questions being examined are (1) the heritability of each trait; (2) the relative contribution of genetic, maternal environmental, and residual environmental effects to the correlation between the oral traits, and (3) genetic and nongenetic components of the correlation between the oral traits and overall body size. Some quantitative genetic aspects of covarying traits is briefly reviewed with special emphasis on allometric variation. Phenotypic regression coefficients from log-transformed data (= allometry coefficients) of oral traits onto femur length are partitioned into components due to genetic, maternal environmental, residual environmental, and total environmental causes. All phenotypic regression coefficients and all but one based on an environmentally determined covariance component are significantly different from zero, suggesting a substantial body size effect in the oral region resulting from nonheritable causes. However, three genetic coefficients from regressions of oral traits to femur length are not different from zero, indicating a genetic correlation with body size in five traits but not in three others. A principal components analysis was carried out on the phenotypic, genetic, and environmental correlations of the eight oral traits to provide a multivariate depiction of the components of covariation in the maxilla and mandible of the rat. General multivariate effects due to body size together with group or special effects are demonstrated for each component of morphogenesis.

Animals↗

Evolutionary consequences of parthogenesis: evidence from the Warramaba virgo complex.

Comparative quantitative analyses of variability in closely related parthenogenetic and sexually reproducing species have been lacking. This paper reports results of comparative analyses of relative variability carried out on the obligate thelytokous grasshopper Warramaba virgo (Key) and three closely related sexually reproducing species. Consistent patterns of differences in variability in 14 morphometric traits were found between clones and races of the parthenogenetic species which were absent in populations and species of the related sexual forms. When variability in the parthenogenetic and sexual species was compared, the parthenogenetic taxa were shown to be at least as variable as and often more variable than the sexual species.

Animals↗

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.

Animals↗

Heterozygosity of F2 from two segregating populations.

Exact formulas that predict the average inbreeding coefficient and heterozygosity of an F2 generation derived from two segregating populations were developed. When population sizes are sufficiently large, the heterozygosity of the F2 is one-half of the heterozygosity of F1 plus one-half of the mean heterozygosity of the two parental populations. The importance of inferring heterozygosity of F2 is discussed from evolutionary perspective.

Animals↗

A quantitative genetic analysis of localized morphology in mandibles of inbred mice using finite element scaling analysis.

We analyzed patterns of mandibular genetic and phenotypic morphological integration and the relationship of genealogy to interstrain molecular and morphological differences in ten inbred strains of mice. Positions of mandibular landmarks in two-dimensional space were used to construct a finite element mesh for each individual, then all individuals from the ten strains were compared to the average mandible from a standard strain (SEA/GnJ). Measures of size and shape associated with finite element scaling analysis were then used in a quantitative genetic analysis of mandibular variation. Significant genetic variation for mandibular size and shape was uncovered. Patterns of both genetic and phenotypic correlation for measures of landmark-specific sizes were consistent with models of morphological integration based on the developmental origin of parts of the mandible and on the effects of muscle attachment on mandibular morphology. Shape differences local to particular landmarks did not show these forms of morphological integration. Although interstrain distances based on local shape magnitudes were significantly correlated with genealogical relationship, distances based on local size differences were not. Even higher than the correlation of genealogy with distances based on local shape magnitude was the genealogical-molecular distance correlation. Patterns of morphometric mandibular variation corresponded to expected effects of epigenetic developmental processes. Also, when detailed shape differences were considered, morphology served as a rough guide to genealogy, although molecular distances showed a stronger relationship.

Animals↗

The ontogeny of morphological differences in the mandible in two inbred strains of mice.

We have analyzed the postnatal ontogeny of the mandible of two inbred strains of mice (C3HeB and C57/BL) with conventional statistical analysis of area traits and with Euclidian Distance Matrix Analysis (EDMA). The relative contribution of the distal tooth-bearing part of the mandible to the area of the whole mandible decreases over time. The most prominent differences in shape between mice of 10 days and 25 days postnatal age are found in the lower posterior part of the mandible. Between angular and condylar process intramembranous ossification proceeds at a high rate and gradually fills the space between these two processes. The position of the proximal end of the molar tooth-row is relocated ventrally during this period. Morphological differences between C3H and C57 are most pronounced at 15 days postnatal age. Regions that discriminate best between the two strains change during development. While differences in the coronoid process separate the two groups clearly at 10 and 25 days postnatal age, no significant differences in the coronoid process are found at 20 days postnatal age. Similarly, masseter area shows significant differences at 15 and 25 days postnatal age, while C57 and C3H mice are equivalent for this trait at the other times. The same qualitative results are obtained by Euclidian Distance Matrix Analysis (EDMA): regions of major differences between strains are not consistent among ages. These results suggest that the ontogeny of morphological differences between closely related taxa is quite an erratic process; development of morphometric differences does not proceed smoothly and continuously. This unpredictable pattern of development of morphometric differences is expected if development of the mandible is tightly integrated by epigenetic and regulatory processes.

Age Factors↗