Biomedical subjects

Lucio Vinicius

Publications and source records attributed to Lucio Vinicius.

3 recordsLinked to original sources

PubMed2005

Human encephalization and developmental timing.

Human evolution is frequently analyzed in the light of changes in developmental timing. Encephalization in particular has been frequently linked to the slow pace of development in Homo sapiens. The "brain allometry extension" theory postulates that the progressive extension of a conserved primate brain allometry into postnatal life was the basis for brain enlargement in the human lineage. This study shows that published primate and human growth data do not corroborate this model. Instead, the unique encephalization of H. sapiens is alternatively described as the result of evolutionary changes in three aspects of developmental timing. The first is a moderate extension in the duration of brain growth relative to our closest extant relatives, contrary to the view that human brain growth is drastically prolonged into postnatal life. Second, humans evolved a derived brain allometry in comparison with chimpanzees and early hominins. Third, humans (and other anthropoid primates to a lesser degree) display a significant retardation in early postnatal body growth in comparison with other mammals, which directly affects adult encephalization in our species. The rejection of the "brain allometry extension" model may require a reevaluation of the adaptive scenarios proposed to explain how human encephalization evolved.

Animals↗

PubMed2005

The temporal requirements for insulin signaling during development in Drosophila.

Recent studies have indicated that the insulin-signaling pathway controls body and organ size in Drosophila, and most metazoans, by signaling nutritional conditions to the growing organs. The temporal requirements for insulin signaling during development are, however, unknown. Using a temperature-sensitive insulin receptor (Inr) mutation in Drosophila, we show that the developmental requirements for Inr activity are organ specific and vary in time. Early in development, before larvae reach the "critical size" (the size at which they commit to metamorphosis and can complete development without further feeding), Inr activity influences total development time but not final body and organ size. After critical size, Inr activity no longer affects total development time but does influence final body and organ size. Final body size is affected by Inr activity from critical size until pupariation, whereas final organ size is sensitive to Inr activity from critical size until early pupal development. In addition, different organs show different sensitivities to changes in Inr activity for different periods of development, implicating the insulin pathway in the control of organ allometry. The reduction in Inr activity is accompanied by a two-fold increase in free-sugar levels, similar to the effect of reduced insulin signaling in mammals. Finally, we find that varying the magnitude of Inr activity has different effects on cell size and cell number in the fly wing, providing a potential linkage between the mode of action of insulin signaling and the distinct downstream controls of cell size and number. We present a model that incorporates the effects of the insulin-signaling pathway into the Drosophila life cycle. We hypothesize that the insulin-signaling pathway controls such diverse effects as total developmental time, total body size and organ size through its effects on the rate of cell growth, and proliferation in different organs.

Animals↗

PubMed2003

Morphometric heterochrony and the evolution of growth.

Heterochrony has been an influential perspective on the evolution of morphologies, a circumstance mostly due to a strategic shift of the theory to the analysis of growth and measurable traits. A difficulty in testing hypotheses of heterochrony in the morphometric realm, and therefore in establishing its evolutionary relevance, has been the absence of an explicit criterion of homology in comparisons supposed to reveal paedomorphosis and peramorphosis. Based on the formalism of ontogenetic and allometric trajectories, we defined a criterion of primary homology in the context of morphometric characters that requires only a comparison between metric traits from ontogenetic series of two or more taxa. On the one hand, such a criterion allows for the calculation of values of shape slopes and allometric coefficients in descendants supposedly affected by changes in ontogenetic timing, thereby supplying an analytical tool for testing hypotheses of heterochrony. On the other hand, the concept of morphometric homology establishes the descriptive limits of paedomorphosis and peramorphosis, showing, for example, that the model of sequential hypermorphosis applied to the evolution of human encephalization is not within the descriptive scope of the morphological markers of heterochrony. Sequential hypermorphosis is a successful model of morphometric evolution, as further illustrated by the match between our mathematical deductions and the empirical results obtained by analyses of brain growth data. By exploring the properties of multiphasic polynomial functions, we deduce equations that define the relationship between developmental delay or acceleration and their effect on adult brain size. Together with the primary criterion of homology, we demonstrate that sequential hypermorphosis could generate the large modern human brain, but such brain is neither paedomorphic nor peramorphic. Our approach based on homology and allometry indicates that the evolution of growth is richer in phenomena than heterochrony can account for, and accordingly we argue that morphometric theory can expand its descriptive and heuristic scope by looking beyond the limits imposed by paedomorphosis and peramorphosis.

Biological Evolution↗