Organisms represent a complex arrangement of anatomical structures and individuated parts that must maintain functional associations through development. This integration of variation between functionally related body parts and the modular organization of development are fundamental determinants of their evolvability. This is because integration results in the expression of coordinated variation that can create preferred directions for evolutionary change, while modularity enables variation in a group of traits or regions to accumulate without deleterious effects on other aspects of the organism. Using our own work on both model systems (e.g., lab mice, avians) and natural populations of rodents and primates, we explore in this paper the relationship between patterns of phenotypic covariation and the developmental determinants of integration that those patterns are assumed to reflect. We show that integration cannot be reliably studied through phenotypic covariance patterns alone and argue that the relationship between phenotypic covariation and integration is obscured in two ways. One is the superimposition of multiple determinants of covariance in complex systems and the other is the dependence of covariation structure on variances in covariance-generating processes. As a consequence, we argue that the direct study of the developmental determinants of integration in model systems is necessary to fully interpret patterns of covariation in natural populations, to link covariation patterns to the processes that generate them, and to understand their significance for evolutionary explanation.
The hypothesis that variation in craniofacial shape within and among species is influenced by spatial packing has a long history in comparative anatomy, particularly in terms of primates. This study develops and tests three alternative models of spatial packing to address how and to what extent the cranial base angle is influenced by variation in brain and facial size. The models are tested using mouse strains with different mutations affecting craniofacial growth. Although mice have distinctive crania with small brains, long faces, and retroflexed cranial bases, the results of the study indicate that the mouse cranial base flexes to accommodate larger brain size relative to cranial base length. In addition, the mouse cranial base also extends, but to a lesser degree, to accommodate larger face size relative to cranial base length. In addition, interactions between brain size, face size, and the widths and lengths of the components of the cranial base account for a large percentage of variation in cranial base angle. The results illustrate the degree to which the cranial base is centrally embedded within the covariation structure of the craniofacial complex as a whole.
A new paracryptodiran turtle, Arundelemys dardeni, gen. et sp. nov., is described on the basis of an isolated, nearly complete skull from the Early Cretaceous Arundel Clay facies of Maryland, USA. The basicranial region exhibits the paracryptodiran condition of a single foramen for the canalis caroticus internus located midway along the basisphenoid. As revealed by CT scans, the basicranial region of Arundelemys is unusual in that the right and left canales carotici interni merge just before reaching the sella turcica and the canalis caroticus lateralis is very small or absent. A phylogenetic analysis places Arundelemys dardeni as the basal-most member of the Paracryptodira. Within the Paracryptodira, Arundelemys dardeni is most similar to Compsemys victa in general proportions.
Organisms exhibit an incredible diversity of form, a fact that makes the evolution of novelty seemingly self-evident. However, despite the “obvious” case for novelty, defining this concept in evolutionary terms is highly problematic, so much so that some have suggested discarding it altogether. Approaches to this problem tend to take either an adaptation or development-based perspective, but we argue here that an exclusive focus on either of these misses the original intent of the novelty concept and undermines its practical utility. We instead propose that for a feature to be novel it must have evolved both by a transition between adaptive peaks on the fitness landscape and that this transition must have overcome a previous developmental constraint. This definition focuses novelty on the explanation of apparently difficult or low probability evolutionary transitions and highlights how the integration of developmental and functional considerations is necessary to evolutionary explanation. It further reinforces that novelty is a central concern not just of evolutionary developmental biology (i.e., “evo-devo”) but of evolutionary biology more generally. We explore this definition of novelty in light of four examples that range from the obvious to subtle.
Elucidating the causes of congenital heart defects is made difficult by the complex morphogenesis of the mammalian heart, which takes place early in development, involves contributions from multiple germ layers, and is controlled by many genes. Here, we use a conditional/invertible genetic strategy to identify the cell lineage(s) responsible for the development of heart defects in a Nipbl-deficient mouse model of Cornelia de Lange Syndrome, in which global yet subtle transcriptional dysregulation leads to development of atrial septal defects (ASDs) at high frequency. Using an approach that allows for recombinase-mediated creation or rescue of Nipbl deficiency in different lineages, we uncover complex interactions between the cardiac mesoderm, endoderm, and the rest of the embryo, whereby the risk conferred by genetic abnormality in any one lineage is modified, in a surprisingly non-additive way, by the status of others. We argue that these results are best understood in the context of a model in which the risk of heart defects is associated with the adequacy of early progenitor cell populations relative to the sizes of the structures they must eventually form.
Mutations have the ability to produce dramatic changes to covariance structure by altering the variance of covariance-generating developmental processes. Several evolutionary mechanisms exist that may be acting interdependently to stabilize covariance structure, despite this developmental potential for variation within species. We explore covariance structure in the crania of laboratory mouse mutants exhibiting mild-to-significant developmental perturbations of the cranium, and contrast it with covariance structure in related wild muroid taxa. Phenotypic covariance structure is conserved among wild muroidea, but highly variable and mutation-dependent within the laboratory group. We show that covariance structures in natural populations of related species occupy a more restricted portion of covariance structure space than do the covariance structures resulting from single mutations of significant effect or the almost nonexistent genetic differences that separate inbred mouse strains. Our results suggest that developmental constraint is not the primary mechanism acting to stabilize covariance structure, and imply a more important role for other mechanisms. K E Y W O R D S :Cranial morphology, geometric morphometrics, Muroidea, morphological integration, phenotypic covariance.The importance of covariance structure patterning, and the resulting integration and observed modularity of the phenotype, for understanding the evolution of form was recognized early in the development of evolutionary theory (Darwin 1859). The modern study of these phenomena was formalized by Olson and Miller (1958) and has received extensive attention (e.g
The integration of the brain and face and to what extent this relationship constrains or enables evolutionary change in the craniofacial complex is an issue of long-standing interest in vertebrate evolution. To investigate brain-face integration, we studied the covariation between the forebrain and midface at gestational days 10-10.5 in four strains of laboratory mice. We found that phenotypic variation in the forebrain is highly correlated with that of the face during face formation such that variation in the size of the forebrain correlates with the degree of prognathism and orientation of the facial prominences. This suggests strongly that the integration of the brain and face is relevant to the etiology of midfacial malformations such as orofacial clefts. This axis of integration also has important implications for the evolutionary developmental biology of the mammalian craniofacial complex.
Background How developmental mechanisms generate the phenotypic variation that is the raw material for evolution is largely unknown. Here we explore whether variation in a conserved signaling axis between the brain and face contributes to differences in morphogenesis of the avian upper jaw. In amniotes, including both mice and avians, signals from the brain establish a signaling center in the ectoderm (the Frontonasal ectodermal zone or “FEZ”) that directs outgrowth of the facial primordia. Results Here we show that the spatial organization of this signaling center differs among avians, and these correspond to Sonic hedgehog (Shh) expression in the basal forebrain and embryonic facial shape. In ducks this basal forebrain domain is present almost the entire width, while in chickens it is restricted to the midline. When the duck forebrain is unilaterally transplanted into stage matched chicken embryos the face on the treated side resembles that of the donor. Conclusions Combined with previous findings, these results demonstrate that variation in a highly conserved developmental pathway has the potential to contribute to evolutionary differences in avian upper jaw morphology.
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